General Electrophysiology

doi:10.1002/joa3.12266

Result:

Among 202 patients with AHF, 23 (11.4%) patients had IFH. In our study, there are 118 (58.7%) viral hepatitis patients (hepatitis A, 83 patients, 41.3%; hepatitis B, 19 patients, 9.5%; hepatitis C, 15 patients, 7.5%) and alcoholic hepatitis patients (83 patients, 41.3%). Based on the ROC curve, we set the corrected QT interval (QTc) cutoff value of 425 milliseconds for prediction of IFH, which gave a sensitivity of 66.7% and a specificity of 66.0% (P = .002). In univariate analysis, age, QTc, diabetes mellitus (DM), heavy alcoholics, labile INR, hemoglobin, albumin, total bilirubin, sodium, and C‐reactive protein were significantly associated with IFH. In multivariate analysis, age, QTc, DM, heavy alcoholics, and total bilirubin were independent risk factors for IFH at the long‐term follow‐up.

Conclusion:

Longer QTc (>425 milliseconds) in patients with AHF was associated with higher IFH, suggesting close clinical and electrocardiographic follow‐up will be required.

AP19‐00012

Impact of alfa‐ and beta‐blocker, carvedilol on the long‐term clinical outcomes in benign prostatic hypertrophy patients with palpitation

Sung Il Im, Hansu park

Kosin University Gospel Hospital, South Korea

Introduction:

Benign prostatic hypertrophy (BPH) is associated with autonomic dysfunction. Purpose: There was limited data about the impact of alfa‐ and beta‐blocker (BB), Carvedilol on the long‐term clinical outcomes in BPH patients with palpitation.

Methods:

A total of 448 patients with BPH were consecutively enrolled (mean age; 69.2 ± 10.9 years) from 2015 to 2018. Inclusion criteria included patients taking BB in patients with BPH. We analyzed arrhythmic events and the voiding pattern, urinary symptoms.

graphic file with name JOA3-35-4-g002.jpg

Result:

Among 448 patients taking BB in patients with BPH, Carvedilol group (219 patients; 48.9%) and other BB group (bisoprolol, 183 patients, 80%; nevibolol, 45 patients, 20%) were enrolled. There was no difference of the baseline characteristics. During a mean follow‐up of 29.3 ± 12.4 months, there was no difference of total IPSS score in both group. However, there were increased voiding volume and maximal voiding velocity in the Carvedilol group. And there was higher incidence of additive prescription of alfa‐blocker in the other BB group (P = .004). There was higher event‐free survivals from urologic events associated with BPH (P = .030) in the Carvedilol group and the lower use of Carvedilol (P < 0.001), CHF (P < .001), and renal disease (P = .046) were independent risk factors for arrhythmic events in multivariate analysis.

Conclusion:

Although there was no difference of total IPSS score in both groups, Carvedilol can improve the voiding volume and maximal voiding velocity, and decrease the incidence of urologic events for BPH and the use of Carvedilol was associated with lower arrhythmic events in the long‐term follow up.

AP19‐00015

Too much for a single heart: Case report

Haseeb Raza

National Institute of Cardiovascular Diseases, Pakistan

Introduction:

Accessory pathway AP is the second most common substrate on young population and are more likely to have bidirectional conduction properties, 90 or 95% of the cases the anterograde conduction is over AV node—his purkinje tissue and retrograde conduction over AP “orthodromic AVRT”. But, in 5%‐10% the anterograde conduction is over AP and retrograde conduction over AV node—his purkinje tissue “antidromic AVRT”. Idiopathic Fascicular Left Ventricular Tachycardia represents 10%‐15% of cases of idiopathic ventricular tachycardia. It was first described by Zipes et al in 1979 and described a typical RBBB pattern with left axis deviation with relatively narrow QRS complex (120‐140 milliseconds) .

Methods:

Sometimes when we go into a EP study with a patient with a documented tachycardia, we preconceive some hypothesis about what the rhythm is, and what the mechanism might be. But, unexpected things sometimes happen. We can find a different tachycardia mechanism or even more, another unexpected arrhythmia substrate and at this point the question is. which is the clinical tachycardia? Should we ablate the other un‐ expected substrate too?.We present an atypical case of 35 years old male patient with history of recurrent palpitations, with normal structural heart, also normal CXR. The 12 lead ECG showed a regular wide complex tachycardia and on sinus rhythm a patent preexcitation.

Result:

In Electrophysiology Laboratory an orthodromic AVRT was induced with successful ablation of AP and then after ablation, another tachycardia was induced but not related to AP with clear AV dissociation RBBB pattern and left axis deviation making the diagnosis of Idiopathic Fascicular Left Ventricular Tachycardia (ILFVT).

Conclusion:

• Even when we have a substrate on resting tracing an AP , as in this case, we have to be sure that there is no other hidden potential substrate.In this is case we can point out that symptoms is not specific to make a differentiate between supraventricular or ventricular tachycardia because the ventricular tachycardia did not show any hemodynamic compromise therefore not any clinical sign.

• In this case the clinical tachycardia was the antidromic AVRT which was successfully ablated and the patient was discharged and programmed for long tern follow up looking for recurrence of LAFVT.

• Always expect another bystander tachyarrhythmia in the same patient which became obvious on giving extra‐stimulus.

• We did not find any report about the association of AP with left fascicular ventricular tachycardia as a common pathophysiological bases or random association between the substrates.

AP19‐00016

Evaluation of the accuracy of a single lead adhesive ECG patch monitoring device (S‐Patch) in patients post myocardial infarction

Tony Li, Toon Wei Lim

National University Hospital Singapore, Singapore

Introduction:

With technological advances and promulgation of smart devices, remote cardiac rhythm monitoring has garnered increasing interest. One population that stands to benefit are patients with a recent acute coronary syndrome (ACS) event and are at heightened risk of arrhythmias and sudden cardiac arrest. Till now, they can only be reasonably monitored for short periods with ward based systems. With an accurate yet portable system, monitoring may be done remotely and safely.

Methods:

This is a proof of concept study that aims to assess if a single‐lead adhesive ECG patch monitoring device (S‐Patch) can reliably detect arrhythmias in patients soon after an ACS event and become a potential tool for extended post‐discharge monitoring. We recruited 42 patients (mean age: 59.8 [40‐82], 29 male [69.0%]) post myocardial infarction who were admitted with telemetry beyond 24 hours. This included patients with STEMI post coronary angiogram and patients with NSTEMI on monitoring. Subjects were concurrently placed on conventional and S‐patch monitoring for 48 hours or till telemetry was discontinued. An in‐house machine‐learning algorithm was applied to identify notable arrhythmias on S‐patch recordings. Results were compared to conventional telemetry.

Result:

S‐patch performed favourably in identifying critical arrhythmias but was more sensitive to baseline noise. 17 VT and 15 SVT episodes were identified by S‐patch while conventional telemetry noted 2 VT and 1 SVT episodes. The SVT episode was correctly identified by both systems. For VT episodes on telemetry, one was correctly identified as noise by S‐patch whilst the other occurred after S‐patch had been terminated and was missed. Rest of events picked up by S‐patch were due to baseline noise.

Conclusion:

S‐patch demonstrated reasonable accuracy in detection of arrhythmias in patients post myocardial infarction. With further development and validation in broader populations, it could become an economical yet effective tool for diagnoses of arrhythmias and improve preventive healthcare.

AP19‐00021

Early repolarization pattern characterized by right precordial T‐wave inversion in a healthy African‐Japanese athlete

Yuki Sahashi, Takatomo Watanabe, Takashi Nakashima, Nobuhiro Takasugi, Hiroyuki Okura

Department of Cardiology, Gifu University, Japan

Introduction:

A 20‐year old asymptomatic professional football player with no past medical history was referred to our institute for early repolarization pattern and right precordial lead T‐ wave inversion (Figure). The football team doctor suspected a cardiomyopathy (e.g. arrhythmogenic right ventricular cardiomyopathy and hypertrophic cardiomyopathy) or an arrhythmogenic disorder such as Brugada syndrome. Family history was noncontributory, and echocardiography and blood tests did not suggest the presence of any cardiomyopathy nor arrhythmogenic disorder. In the Japanese population, precordial lead T‐wave inversion is considered to be abnormal findings and treatment is often necessary. However, according to previous reports, precordial lead T‐wave inversion subsequent to early repolarization is thought to be normal and frequently observed in African athletes. With the increasing number of foreign people living in and traveling to Japan, it is becoming crucial for Japanese physicians to know the abnormal ECG change in African athletes.

Methods:

N/A.

Result:

N/A.

Conclusion:

N/A.

graphic file with name JOA3-35-4-g003.jpg

AP19‐00045

Impact of oxidative stress on the long‐term heart rate variability: Linear vs nonlinear heart rate dynamics

Chan‐Hee Lee, Dong‐Gu Shin

Yeungnam University Medical Center, South Korea

Introduction:

Heart rate variability (HRV) is a widely used noninvasive and quantitative marker of the cardiac autonomic control. An elevated oxidative stress (OS) and reduced HRV have been proven in specific disease subsets. However, the impact of OS on the long‐term heart rate dynamics of both conventional linear and nonlinear origins in the general population is not known.

Methods:

The 24‐hour ambulatory electrocardiogram recordings and plasma 8‐iso‐Prostaglandin F2α (8‐iso‐PGF2α) as an OS marker were acquired simultaneously in 71 consecutive patients. The conventional time and frequency domain HRV parameters and nonlinear parameters were measured.

Result:

The 8‐iso‐PGF2α is a significant determinant of most long‐term conventional time and frequency domain HRV parameters and standard deviation (SD1, perpendicular to the line‐of‐identity; SD2, along the line‐of‐identity) descriptors from the Poincare plot analysis, but not of the nonlinear complexity and fractal parameters. Patients with a high OS burden had a lower absolute low frequency and high frequency (HF) power during both the night and morning periods, with a significant decrease in the HF power in the morning. Judging from the relationship between the OS severity and HF power, the estimated upper boundary value of the 8‐iso‐PGF2α was 57.35 through 73.10 pg/mL.

Conclusion:

OS is one of the significant determinants of the HRV. The severity of the OS is reflected in the conventional time and frequency domain HRV parameters, but not in the nonlinear measurements.

AP19‐00061

Diagnostic value of QTc dispersion and QT dispersion ratio changes in treadmill training test for detecting coronary lesion in stable angina pectoris patients

Putri Yeantesa, Hauda El Rasyid, Masrul Syafri

Dr. M. Djamil General Hospital, Indonesia

Introduction:

Treadmill exercise test remains an important method and often used in the initial evaluation of patients with chest pain and can be a filter for more expensive invasive diagnostic. Increased QT dispersion (QTD) occurs because of the heterogeneity of ventricular repolarization because transient ischaemia during a treadmill stress test can be a marker of coronary artery disease (CAD) and can improve the accuracy of exercise tests to diagnose CAD, but this parameter is still controversial.

Methods:

This is an analytic observational approach with a cross sectional study. Data was taken retrospectively at the Heart Centre Installation at RSUP Dr. M. Djamil Padang, from March to April 2019, stable angina pectoris patient with a positive treadmill stress test who underwent coronary angiography as the subject. Bivariate analysis was performed on changes in QTcD (∆QTcD) and QTdR (∆QTdR) variables on the significance of coronary lesions by the chi‐square method, after which a diagnostic test was based on receiver operating curve (ROC) analysis.

Result:

There were 113 subjects and found that older age, male and smoking were more common in groups with significant coronary lesions. Cut off point for ∆QTcD is ≥13 milliseconds with a sensitivity of 96.7% and specificity 98.0% and AUC 97.8%, while ∆QTdR ≥5.5% with sensitivity 95.1% and specificity 96.2% and AUC 96.6% are related to significance of coronary lesion. Obtained subjects with significant lesions generally had a value of ∆QTcD ≥13 milliseconds (P < .001) and ∆QTdR ≥5.5% (P < .001).

Conclusion:

The use of QTD parameters as ECG variables, which are easily obtained in evaluating stress tests, can improve the diagnostic accuracy of exercise tests. In addition, evaluation of QTD variables can provide information about the incidence of CAD.

Keywords: ∆QTcD, ∆QTdR, Treadmill Exercise Test, Coronary Lession Significancy, Stable Coronary Artery Disease

AP19‐00141

Initial genetic results for Brugada syndrome and hypertrophic cardiomyopathy patients in Brunei Darussalam

Bee Ngo Lau, Sofian Johar

Raja Isteri Pengiran Anak Saleha Hospital, Brunei

Introduction:

Mutations in at least 12 genes encoding the sodium, calcium and potassium channels are associated with Brugada syndrome (BrS), and mutations in 11 sarcomere protein genes are known to cause hypertrophic cardiomyopathy (HCM). We aim to look at the genetic results of our local patients having BrS and HCM.

Methods:

For BrS, probands with type 1 electrocardiograms (spontaneous or flecainide‐induced), and for HCM, probands with clinical diagnosis of HCM were included. For genetic tests, 1 mL of saliva was collected via self‐collection kit (Oragene‐DNA:OG‐500) after fasting for 30 minutes, or 3 mL blood was taken in 2 EDTA tubes. Informed consents were obtained. Salivary samples were sent to Genelabs Diagnostics, and blood samples to Cardiogenomics in Singapore for genetic tests.

Result:

30 patients had genetic tests (BrS: N = 24; HCM: N = 6) between December 2014 and April 2019 (mean age: 45.87 ± 14.58 years, 60% males) (Table 1). For the BrS cohort, 5 have genes associated with BrS. All are apparently unrelated. 3 (S1, 21, 23) have SCN5A, and 2 (S6, 8) have CACNA1C. S1 had recurrent palpitations, spontaneous type I ECG and reproducibly inducible ventricular fibrillation (VF) leading to primary prevention implantable cardioverter defibrillator (ICD) implant. S21 and S23 have asymptomatic flecainide‐induced Brugada type 1 ECG. S6 had syncope, family history of premature sudden death, fever‐induced type I ECG and reproducibly inducible VF aged 19 years. An ICD was recommended but patient declined it. S8 was asymptomatic. 5 BrS patients (S2, 4, 5, 15, 16) who were clinically deemed to be at high risk of sudden death had ICD implants but none had a pathogenic gene that is associated with BrS. Other genetic findings in BrS patients included genes that are associated with HCM (MYL2, MYH6, MYH7, MYBPC3), dilated cardiomyopathy (MYH6, MYL2, MYH7, DCS2, MYBPC3, HFE), arrhythmogenic right ventricular cardiomyopathy [ARVC] (DCS2), non compaction cardiomyopathy (MYH7, MYBPC3), and restrictive cardiomyopathy (MYL2, MYH7). For the HCM cohort, 1 (S26) has MYH7, a pathogenic gene associated with HCM. She had myomectomy for severe left ventricular outflow tract obstruction (LVOTO) aged 4 years. 1 (S25) has MYH6, a variant of uncertain significance. 1 asymptomatic patient (S27) having a likely clinical diagnosis of HCM, and a strong family history of premature sudden death has PKP2, a pathogenic gene associated with ARVC. 1 (S28) had myomectomy for HCM with severe LVOTO, and primary prevention ICD implant but his genetic test was negative. All patients are alive at follow‐up.

Conclusion:

In our local small cohort, pathogenic genes associated with BrS and HCM are seen. Hence we may offer genetic cascade testing in clinically unaffected first‐degree relatives with the aim of identifying asymptomatic relatives for clinical follow‐up, sudden death risk stratification and prevention.

TABLE 1 Genetic results

Subject (S)	BrS or HCM	Age (yr) / Gender	Test samples	History of cardiac arrest	ICD implant	ICD shock	Genetic variants
1	BrS	46 / M	Saliva	No	Yes	No	SCN5A (DNA coding c.5103G>C; variant p.M1701I)MYL2 (DNA coding c.4G>A; variant p.A2T)
2	BrS	32 / F	Saliva	No	Yes	No	MYH7 (DNA coding c.5326A>G; variant p.S1776G)
3	BrS	53 / M	Saliva	No	No	None
4	BrS	67 / F	Saliva	No	Yes	No	None
5	BrS	33 / F	Saliva	No	Yes	No	None
6	BrS	29 / M	Saliva	No	No	CACNA1C (DNA coding c.5731G>C; variant p.G1911R)
7	BrS	60 / M	Saliva	No	No	DSC2 (DNA coding c2368_2370delGGA; variant p.Gly790del)
8	BrS	71 / F	Saliva	No	No	CACNA1C (DNA coding c.5731G>C; variant p.G1911R)
9	BrS	33 / F	Saliva	No	No	MYH6 (DNA coding c.4727G>A; variant p.R1576Q)
HFE (DNA coding c.892+1G>T)
10	BrS	49 / M	Saliva	No	No	None
11	BrS	65 / M	Saliva	No	No	MYBPC3 (DNA coding c.2761c>G; variant p.Q921E)
12	BrS	67 / M	Saliva	No	No	MYH7 (DNA coding c.5326A>G; variant p.S1776G)
13	BrS	39 / F	Saliva	No	No	None
14	BrS	46 / M	Saliva	No	No	DCS2 (DNA coding c.1597C>A, variant p.L533M)
15	BrS	45 / M	Saliva	No	Yes	No	None
16	BrS	39 / F	Saliva	No	Yes	No	MYH6 (DNA coding c.3867G>T, variant p.L1289F)
17	BrS	32 / M	Blood	No	No	None
18	BrS	55 / F	Blood	No	No	None
19	BrS	41 / F	Blood	No	No	MYH7(DNA coding c.5326A>G, variant p.S1776G)
20	BrS	34 / F	Blood	No	No	None
21	BrS	47/M	Blood	No	No	SCN5A(DNA coding c.4860G>A, variant p.T1620T)
22	BrS	26/M	Blood	No	No	MYBPC3 (DNA coding c.2479C>A, variant p.Q827K)
23	BrS	52/M	Blood	No	No	SCN5A (DNA coding c.4452C>T, variant p.D1484D)
24	BrS	48/F	Blood	No	No	PCSK9 c.42_43insCTG p.Leu15dup
25	HCM	62 / M	Blood	No	No	MYH6 (DNA coding c.4430G>A; variant p.R1477H)
26	HCM	17 / F	Blood	No	No	MYH7 (DNA coding c.3149G>A; variant p.Arg1050Gln)
27	HCM	23 / M	Blood	No	No	PKP2 (DNA coding c.1848C>G; variant p.Try616Ter)
28	HCM	40/M	Blood	No	Yes	No	None
29	HCM	59/M	Blood	No	No	None
30	HCM	66/M	Blood	No	No	None

Seven studies incorporating 1685 patients were analyzed. Study period ranged between 2007 and 2017. The EST followed the standard Bruce protocol in all included studies. Two studies used nuclear myocardial perfusion imaging to define the extent of CAD, and five assessed the stenosis of epicardial coronary arteries by invasive coronary angiography. In terms of the detection of LMCA disease only, pooled sensitivity of aVR STE ≥1.0 mm was 0.72 (95% confidence interval [CI] 0.33‐0.93), specificity was 0.77 (95% CI 0.59‐0.89), with the area under the curve (AUC) for sROC was 0.81 (0.78‐0.84). For the detection of LMCA disease or 3VD, pooled sensitivity of aVR STE ≥1.0 mm was 0.63 (95% CI 0.31‐0.86), specificity was 0.79 (95% CI 0.64‐0.89), with the AUC for sROC was 0.79 (0.76‐0.83).

Conclusion:

In addition to the standard role of EST as a simple non‐invasive test in stable CAD, EST‐ induced STE ≥1.0 mm in lead aVR may provide significant diagnostic information for predicting high CAD burden as well as the presence of LMCA disease.

AP19‐00188

Near Zero X‐Ray mapping approach with a novel ablation technology in SVT procedures: Preliminary experience from the CHARISMA registry

Filippo Maria Cauti, Pietro Rossi, Luigi Iaia, Luca Rosario Limite, Matteo Anselmino, Natale Di Belardino, Agostino Piro, Gianfranco Tola, Domenico Pecora, Marco Scaglione, Stefano Pedretti, Luca Rossi, Francesco Solimene, Roberto Mantovan, Francesco Piccolo, Maurizio Malacrida, Stefano Bianchi

Fatebenefratelli Hospital, Italy

Introduction:

Electrophysiological studies and ablation procedures expose both physicians and patients to a significant amount of radiation. Nowadays, most of 3‐D mapping systems allow for improved tracking of catheters with possible reduction in radiation exposure. No data exists on the ability of a novel mapping system in minimizing fluoroscopy time and dose. To report preliminary data on feasibility and safety of a non‐fluoroscopic approach using the Rhythmia mapping systems (Boston Scientific) and novel navigation‐enabled ablation catheter in supraventricular tachycardia (SVT).

Methods:

The 3‐D atrial geometry was created from the navigation‐enabled small tip ablation catheter and the Rhythmia mapping system. First, a quadripolar catheter was inserted through the femoral vein and advanced by 20 cm, as a stable reference for the field map. Secondly, the sensor‐enabled ablation catheter was moved through the inferior vena cava into the right atrium (RA) creating 3‐D anatomy and field map of RA. The coronary sinus (CS) ostium was identified and a decapolar catheter was inserted up to postero‐lateral segments of mitral annulus. After reaching a stable position, the CS catheter was switched as the new internal reference for the field map. The anatomical map was completed through the ablation catheter and the quadripolar catheter was inserted in the right ventricle.

Result:

61 unselected consecutive cases of SVT were included in the study (33 AVNRT, 13 AFL, 10 AP and 5 other right atrial procedures). In all the cases, diagnostic EP and ablation catheters were positioned using only the near zero‐ray guided mapping approach. During the study, a total of 1570 seconds of fluoroscopy was needed in 61 patients (26 ± 73 seconds per procedure). Forty‐four procedures (72%) were completed without any use of fluoroscopy, i.e. a totally zero‐ray approach (ZFL). During the remaining 17 procedures (28%), 92 ± 116 seconds of fluoroscopy were used. ZFL approach was more frequently obtained in case of AVNRT ablation (28, 85%) compared with AFL (7, 54%; P = .05) and AP (4, 40%; P = .009). The median reconstructed RA volume was 110[100‐133] mL in a mean mapping time of 11 ± 5 minutes. The median number of radiofrequency ablations to terminate each arrhythmia was 4 [3‐7] (total RF delivery time of 189[145‐262] seconds). A 100% rate of acute success was observed in our case series. No complications occurred.

Conclusion:

In our preliminary experience, arrhythmias ablation through near zero fluoroscopy approach and the use of a novel ablation technology seems to be safe, feasible, and effective in common right atrial arrhythmias. Use of fluoroscopy can be completely avoided in most cases, without any reduction of the safety and effectiveness profile.

AP19‐00219

A case of mitral regurgitation deterioration via right ventricular apex constant pacing caused by pilsicainide hydrochloride induced impaired atrioventricular conduction

Kiyotaka Tsuyuki, Naoto Nishina, Masahiro Esato

Takeda General Hospital, Japan

Introduction:

We experienced a case of acute cardiac failure with mitral regurgitation deterioration caused by antiarrhythmic drug‐induced constant right ventricular apex pacing.

Methods:

A 88‐year female was admitted to our department, diagnosed as cardiac failure due to severe mitral regurgitation. She previously had experienced frequent syncopal attack under rhythm‐ control therapy using class I antiarrhythmic drug (AAD) for atrial tachycardia/fibrillation (AT/AF) and QT prolongation with TdP was documented. As rhythm‐control for AT/AF using AADs were still needed, permanent pacemaker implantation was therefore performed in order to prevent QT prolongation‐related fatal arrhythmia. Pilsicainide hydrochloride (Pil) was used in addition to bepridil, as AT/AF was uncontrollable during the follow‐up. 12‐lead ECG on regular check‐up under bepridil administration revealed pacemaker rhythm with atrial pacing followed by normal QRS morphology (Atrial pace‐Ventricular sense mode: ApVs mode). However, constant ventricular pacing (Vp) due to atrioventricular (AV) conduction delay was documented on admission. AAD induced impaired AV conduction as the major cause of Vp was suspected and therefore Pil was discontinued after admission.

graphic file with name JOA3-35-4-g004.jpg

Result:

ApVs pacemaker rhythm restoration with significant improvement of mitral regurgitation and cardiac failure was observed after Pill discontinuation (Figure).

Conclusion:

This case highlighted the potent inhibitory effect on AV conduction under Pill administration, although Pill is well known as class Ic AAD, with a pure sodium channel‐blocking pharmacokinetic property. Furthermore, deleterious effect on left ventricular function (i.e. mitral regurgitation deterioration in this case) may cause rapidly once a high burden of Vp is observed in patients with permanent cardiac electrical stimulation.

AP19‐00222

Fasciculoventricular accessory pathway unmasked by a pseudo gap phenomenon

Weizhuo Liu, Nanqing Xiong

Huashan Hospital, China

Introduction:

Fasciculoventricular bypass tracts (FVBT) are a rare form of preexcitation characterized by the fixed H‐V interval with decremental conduction over atrioventricular node. Since FVBTs are not associated with supraventricular tachycardia or preexcited atrial fibrillation, it is always important to differentiate FVBTs from atrioventricular bypass tracts. Here we report an FVBT with long refractory period, which was diagnosed with the help of a “pseudo gap phenomenon”.

Methods:

A 28 year old female with manifest preexcitation underwent electrophysiology study for multiple episodes of palpitation which had not ever been documented. Her baseline A‐H and H‐V interval was recorded. Programmed atrial extrastimuli were delivered from high right atrium

Result:

The delta wave of this patient had a left inferior axis with a highest amplitude of 1.7 mm in lead 2, and was almost isoelectric in lead V1‐V3 (Figure 1A). Preexcitation was found to be intermittent. H‐V interval was 14 milliseconds with delta wave and 33 milliseconds without preexcitation (Figure 1B). V potential on His recording was earlier than CS and RVa. There was no ventriculo‐atrial conduction during V pacing. An A1‐A2 of 350 milliseconds was associated with loss of delta wave and normalization of H‐V interval, indicating the refractoriness of the accessory pathway (Figure 2). Then A‐H interval remained constant until A1‐A2 was below 330 milliseconds, after which gradual prolongation of A‐H was observed, consistent with relative refractory period of AV node. When A1‐A2 was decreased to 280 milliseconds, an A‐H interval jump from 173 milliseconds to 390 milliseconds was observed. Simultaneously, the delta wave appeared again with an H‐V interval identical to that during sinus rhythm (Figure 3)

graphic file with name JOA3-35-4-g005.jpg

graphic file with name JOA3-35-4-g006.jpg

graphic file with name JOA3-35-4-g007.jpg

graphic file with name JOA3-35-4-g008.jpg

Conclusion:

Diagnosis of FVBT could be made based on the same H‐V interval before the pathway was blocked and after it recovered. This was clearly an example of gap phenomenon using fasciculoventricular pathway for initial block, while AV node played the role of proximal site, where the conduction was delayed and thus sufficient time was given for recovery of FVBT (Figure 4).

AP19‐00234

Radiation exposure reduction during catheter ablation by changing the setting of fluoroscopic system

Kazuaki Amami, Naoko Hijioka, Takashi Kaneshiro, Shinya Yamada, Masashi Kamioka, Takafumi Ishida, Yasuchika Takeishi

Fukushima Medical University, Japan

Introduction:

Reduction of ionized radiation dose during catheter ablation procedure is of benefit both for patients and staff in a catheterization laboratory. Currently, radiation exposure is reduced with various protective gears and by decreasing the amount of fluoroscopic time during ablation procedure utilizing an electro‐anatomical mapping system. Here, we attempted to reduce the radiation exposure by rearranging the setting of fluoroscopic system.

Methods:

We enrolled 699 patients who underwent catheter ablation and examined the effect of two attempts on the reduction in the radiation exposure; the removal of secondary radiation grid and the reduction in fluoroscopic pulse rate. The study subjects were divided into three groups. In group 1, 229 patients underwent catheter ablation with grid and fluoroscopic rate of 7.5 frame/s. We performed ablation in 255 patients without grid and with fluoroscopic rate of 6 frame/s (group 2), and in 215 patients without grid and with fluoroscopic rate of 4 frame/s (group 3).

Result:

Although the ratio of complex ablation (atrial fibrillation or ventricular tachyarrhythmia with structural heart disease, which needs the atrio/ventriculography during procedure) increased from group 1 through group 3 (37% vs 51% vs 53% in groups 1, 2 and 3, respectively, P = .0008), these attempts reduced the total radiation exposure (1323 ± 1112 vs 498 ± 449 vs 379 ± 349 mGy, P < .0001). These attempts also reduced the radiation dose (23.1 ± 15.3 vs 10.7 ± 9.2 vs 9.0 ± 8.0 mGy/min, P < .0001). To assess the pure effect of the grid removal, we compared the radiation dose per 100 fluoroscopic frames between grid (+) group (= group 1) and grid (–) group (= group 2 + 3). The radiation dose was significantly lower in grid (−) group than in grid (+) group (3.3 ± 3.0 vs 5.2 ± 3.4 mGy/100 frames, P < .0001).

Conclusion:

We could successfully reduce the radiation exposure during catheter ablation by removing secondary radiation grid and reducing fluoroscopic pulse rate. Rearranging the setting of fluoroscopic system may be alternative ways to further reduce radiation exposure in a catheterization laboratory.

AP19‐00255

When Wellens’ syndrome meets Brugada phenocopy

Haseeb Raza

National Institute of Cardiovascular Diseases, Pakistan

Introduction:

The Brugada electrocardiographic (ECG) pattern, can be dynamic being recorded in upper precordial leads, is basically the hallmark of Brugada syndrome. The differential diagnosis could include Brugada‐like pattern in the right precordial leads, especially athletes, right bundle‐branch block, arrhythmogenic right ventricular dysplasia or cardiomyopathy and pectus excavatum. Here it is important to mention the concept of Brugada phenocopies that ECG patterns are of characteristic Brugada pattern that may appear and disappear in relation with multiple causes but are not related with Brugada syndrome. The case which we're discussing here includes the clinical criteria and implications of Wellens’ syndrome and Brugada phenocopy

Methods:

A 53 year old male with Past Medical History of treated Pulmonary Tuberculosis, presented in the hospital with severe chest pain for 1 hour, started while he was working in his garden. The pain radiated to both arms associated with nausea and sweating. He denied use of illicit substances, drugs, smoking and alcohol. He had no family history of coronary artery disease. Patient was pain free when he reached the hospital emergency. Glasgow coma scale (GCS) was 15/15, blood pressure was 150/90 mm Hg, heart rate was 68 beat/min, respiratory rate was 18 breath/min, temperature was 98 F, and jugular venous pressure (JVP) was not raised. Rest of the physical examination was unremarkable. Written informed consent was taken and initial 12 lead ECG showed ST segment elevation in leads V1, V2, V3 with ST segment elevation similar to Brugada pattern (Type I), showed in Figure 1. Patient was admitted and given antiplatelet medication. Anti‐Ischemics and anticoagulants were started because the patient was started having chest pain on and off. Serial ECGs were done and the ECG done after 10 hours was consistent with ischemia (wellenoid pattern).

Result:

Patient underwent Coronary angiography which showed severe proximal LAD stenosis (Figure 3) and that brugada pattern came out to be brugada phenocopy seen in V1 and V2. PCI to LAD was done (Figure 4) with Drug eluting stent (DES)

Conclusion:

The purpose for presenting this case is that any patient with Brugada Pattern ECG can have underlying Wellens’ syndrome. Coronary angiogram should be performed to rule out the coronary artery disease. Ischemic changes can be confused with Brugada pattern. History and recognition of the ECG findings of both Type 1 and 2 Wellens’ syndrome is important for proper management and emergent intervention to avoid large anterior wall MI. Hence the definitive treatment for Wellens’ syndrome typically involves cardiac catheterization with percutaneous coronary intervention (PCI) to relieve the occlusion.

FIGURE 1 ECG on arrival in hospital emergency (Initial 12 lead ECG showed ST segment elevation in leads III, V1 ,V2, V3 with ST segment elevation)

graphic file with name JOA3-35-4-g009.jpg

FIGURE 2 ECG done after 3 hours of initial ECG (ECG done after 3 hours showed ST elevation in lead V3 and V4 with prominent Biphasic T wave consistent with ischemia (wellenoid pattern). There is Brugada like phenocopy in V1 and V2. There is also a prominent R wave with mild ST Elevation in two contiguous leads and biphasic T wave inversions suggestive of Wellens’ criteria )

graphic file with name JOA3-35-4-g010.jpg

FIGURE 3 Coronary Angiogram showing severe disease in Proximal LAD

graphic file with name JOA3-35-4-g011.jpg

FIGURE 4 After placing stent in Proximal LAD

graphic file with name JOA3-35-4-g012.jpg

FIGURE 5 Rechecked ECG after stented to LAD

graphic file with name JOA3-35-4-g013.jpg

AP19‐00271

Epicardial ablation of accessory pathways: Single centre experience

Suraya Hani Kamsani, Rohith Stanislaus, Mohd Faiz Faizul Fauzi, Surinder Kaur Khelae Atma SIngh, Azlan Hussin

Institut Jantung Negara, Malaysia

Introduction:

This case series addresses the feasibility, safety and complications of transvenous epicardial ablation of accessory pathways in a single centre in Malaysia.

Methods:

A total of nine patients underwent epicardial ablation procedures from 2000 to 2016 in our centre. Activation mapping was performed in all cases, with standard 3 or 4‐wire study. All patients had symptoms of palpitation, 3 with recurrent supraventricular tachycardia, and two with pre‐excited AF. Duration of symptoms were between 2 and 5 years. Epicardial ablation modality was radiofrequency (RF) in all patients; with five patients (55.5%) utilizing irrigated tip ablation catheter. Transseptal puncture was performed in four patients (44.4%).

Result:

Median age was 33 (range 18‐52) years. Two patients (22%) had underlying congenital heart disease. 12‐lead surface electrograms (ECG) showed WPW type A in three patients (33.3%) and type B in 6 patients (66.7%). Radiofrequency energy was delivered inside the coronary sinus for all the cases, with one patient into middle cardiac vein and one in posterior vein. Overall procedural success was 67% (six out of nine patients) with minimal complication of 0.1% (one in nine patients) developing coronary sinus perforation. There was one recurrence after a successful ablation, which was managed medically.

Conclusion:

Transvenous epicardial ablation of accessory pathways can be performed with acceptable success and minimal complications in a select group of patients.

AP19‐00286

Outcome of failed index and redo procedures in catheter ablation for arrhythmias—A single centre experience

Pradeep Hasija, Prashant Bhardwaj, Anup Banerji

Army Medical Corps, India

Introduction:

Catheter ablation for arrhythmias can be difficult, challenging and compelling to demand repeat procedure (Redo) in some patients. This observational study was done to evaluate the reasons of failed index procedure and final outcome of redo procedure at a tertiary care centre.

Methods:

Retrospective data of patients who underwent catheter ablation of arrhythmias at our centre from August 2012 to November 2016 was reviewed and a detailed analysis was done for the patients who failed initial index procedure and underwent redo procedures to study the procedural, technical or patients specific reasons for difficult ablation and its outcome.

Result:

Over 4 years and 4 months, a total 265 patients underwent catheter ablations for arrhythmia at our centre, of whom 63 procedures (45 patients) were categorised as redo procedure after initial failed ablation or recurrences after standard EP procedure. This cohort (age 24 ± 19 years, 56% male) had NQRST in 20 (44%) and WQRST in 25 (56%) of which 7 (16%) has initial ablation in other centres. The spectrum of arrhythmia and their success is summarised in Image‐1 and the reason of success or failure in redo procedure is shown in Image‐2. One patient with left fascicular VT masqueraded as AVNRT with aberrancy, was successfully ablated after review of previous ablation tracings. Of the 17 (40%) failed cases, 9 (20%) were further planned for repeat with alternate approach or under 3 D navigation but failed to undergo repeat procedure. In 3 patients (7%) the ablation was abandoned being high risk being close to LM, AV node and inside GCV. The true failure was in 5 (11%) patients only. The overall success was achieved in 251/256 (98%) whereas for redo procedures it was 31/36 (86%) with average procedural attempts of 1.4 times and fluoroscopy time of 22.88 + 4.55 minutes against overall 18.8 + 7.4 minutes.

graphic file with name JOA3-35-4-g014.jpg

Conclusion:

Redo procedure after failed index procedure have improved outcome with change in strategy. Trans‐septal access for left sided pathway, and 3 Dimensional Navigation in localisation of focus resulted in maximum success. Postero‐septal location of ablation was associated with maximum failure of ablation. Redo procedure are safe and can be achieved with comparable overall success rate with the use of additional hardware, and extra fluoroscopy time.

AP19‐00305

Ventricular late potentials measured by signal‐averaged electrocardiogram in young Korean professional soccer players

Jung Myung Lee, Jin‐Bae Kime

Kyung Hee University, South Korea

Introduction:

Athlete's heart is well recognized and characterized by structural cardiac changes including enlargement and hypertrophy. However, exercise‐induced cardiac remodeling is not well known in Asian athletes. We sought to evaluate the association between vigorous exercise and development of abnormal late potential on signal‐averaged electrocardiogram (SAECG).

Methods:

We enrolled 56 of Korean professional soccer players who underwent SAECG and transthoracic echocardiography in Kyung Hee University Hospital. To determine the incidence of abnormal SAECG in young athletes and compare with healthy control subjects, 72 controls with similar ages were analyzed. An SAECG was considered abnormal when any one of the three following criteria was met: filtered QRS duration of more than 114 milliseconds, root‐mean‐square voltage in the terminal 40 milliseconds of less than 20 μV, or a voltage of less than 40 μV for more than 38 milliseconds.

Result:

Mean age of control group was older than athletes (30.0 ± 2.2 years vs 21.1 ± 3.8 years, P < .01). Athletes showed significantly lower resting heart rate (67.9 ± 9.6 bpm vs 55.4 ± 6.9, P < .001), longer QRS duration (91.3 ± 9.2 milliseconds vs 96.9 ± 15.0 milliseconds, P = .014), and corrected QT interval (413.2 ± 23.4 milliseconds vs 438.1 ± 30.1 milliseconds, P < .001). Fragmented QRS was more commonly found in athletes (1.4% vs 12.3%, P = .021). Athletes demonstrated significantly higher proportion of long filtered QRS duration more than 114 milliseconds (8.3% vs 26.3%, P = .006), and lower terminal QRS room mean square voltage less than 20 μV (6.9% vs 21.1%, P = .019). Any one of abnormal SAECG finding was significantly more frequent in athletes (40.4% vs 16.7%, P = .003).

TABLE 1 Comparison of electrogram and signal‐averaged electrogram parameters between athletes and controls

Controls (n = 72)	Athletes (n = 56)	P value
Age	30.0 ± 2.2	21.1 ± 3.8	<.001
Female	27 (37.5)	21 (36.8)	.939
ECG parameters
Heart rate, bpm	67.9 ± 9.6	55.4 ± 6.9	<.001
PR interval, ms	157.9 ± 16.4	164.7 ± 34.9	.182
QRS duration, ms	91.3 ± 9.2	96.9 ± 15.0	.014
QTc, ms	413.2 ± 23.4	438.1 ± 30.1	<.001
R axis, degree	71.3 ± 25.9	84.8 ± 12.6	<.001
T axis, degree	51.9 ± 12.0	53.2 ± 21.4	.683
RBBB	1 (1.4)	1 (1.8)	1.0
RAE	0	1 (1.8)	.442
Q wave	1 (1.4)	0	1.0
T inversion	0	2 (3.5)	.193
Early repolarization	9 (12.5)	29 (50.9)	<.001
Fragmented QRS	1 (1.4)	7 (12.3)	.021
fQRS inferior	1 (1.4)	3 (7.0)	.169
fQRS anterior	0	3 (5.3)	.084
Sinus arrhythmia	1 (1.4)	7 (12.3)	.021
SAECG parameters
Filtered QRS duration, ms	104.5 ± 20.4	105.6 ± 33.9	.840
Terminal QRS RMS voltage, μV	65.0 ± 45.9	82.8 ± 56.9	.103
Low amplitude late potential duration, ms	28.8 ± 17.6	20.8 ± 17.0	.023
Filtered QRS > 114 ms	6 (8.3)	15 (26.3)	.006
Terminal QRS RMS voltage < 20 μV	5 (6.9)	12 (21.1)	.019
Low amplitude late potential duration > 38 ms	7 (9.7)	7 (12.3)	.643
1 positive criteria	12 (16.7)	23 (40.4)	.003
2 positive criteria	4 (5.6)	6 (10.5)	.336
3 positive criteria	2 (28.6)	5 (8.8)	.240

N/A.

FIGURE 1 Initial 12‐lead electrocardiogram showing isorhythmic AV dissociation, atrial rate 110 per min with ventriculophasic sinus arrhythmia, junctional escape rhythm 55 per minute with narrow QRS complex. Corrected QT interval was 549 milliseconds by using Bazett's formula

graphic file with name JOA3-35-4-g018.jpg

FIGURE 2 Subsequent 12‐lead electrocardiogram showing that PR interval became shortened and P wave was buried in the initial portion of the following QRS complex. P‐P and R‐R interval remained constant

graphic file with name JOA3-35-4-g019.jpg

FIGURE 3 Fluoroscopic image in RAO 30° view during electrophysiologic study. Three intracardiac catheters were inserted via the right femoral vein. Right atrial quadripolar catheter was placed in high right atrium near the sinoatrial node. His bundle quadripolar catheter was in close proximity to the compact atrioventricular node recording his bundle deflection. Right ventricular quadripolar catheter was positioned near the right ventricular apex. Transvenous temporary pacemaker was inserted via the right internal jugular vein and tip of the lead was seated at the right ventricular apex. (RA = Right Atrial Catheter, His = His Bundle Catheter, RV = Right Ventricular Catheter, TP = Temporary Pacemaker Lead)

graphic file with name JOA3-35-4-g020.jpg

FIGURE 4 Surface electrocardiogram in lead I, aVF, and V1 and intracardiac electrogram recorded from right atrial, His bundle and right ventricular catheters at a paper speed of 31 mm/second. P wave and QRS complex were completely dissociated in an isorhythmic fashion with an approximate integral ratio of 2:1. A‐A and V‐V interval were constant measuring 606 milliseconds and 1182 milliseconds respectively. Atrial rate was higher than ventricular rate. V‐A interval was progressively prolonged and variable. H‐V interval was short and fixed. Complete Heart Block was confirmed and diagnosed on both surface and intracardiac electrograms

graphic file with name JOA3-35-4-g021.jpg

FIGURE 5 Surface electrocardiogram in lead I, aVF, and V1 and intracardiac electrogram recorded from right atrial, His bundle and right ventricular catheters at a paper speed of 63 mm/second. Each of the ventricular signals was preceded by a His bundle deflection and completely dissociated from the atrial signals indicating that the level of block was above the His bundle. (A = Atrial electrogram, H = His bundle electrogram, V = Ventricular electrogram)

graphic file with name JOA3-35-4-g022.jpg

FIGURE 6 Surface electrocardiogram in lead I, aVF, and V1 and intracardiac electrogram recorded from right atrial, His bundle and right ventricular catheters at a paper speed of 63 mm/s. Rapid atrial pacing near the sinoatrial node at a constant cycle length of 400 milliseconds. Corrected Sinus Node Recovery Time (Sinus Recovery Time ‐ Sinus Cycle Length) was 98 milliseconds proving normal sinoatrial node function

graphic file with name JOA3-35-4-g023.jpg

First, for digitization, ECG are filtered by the specific cut‐off value of red, green and blue, then the filtered ECG image is changed into gray scale. In order to extract ECG signal, the algorithm fine the only one of the biggest white body throughout the X‐axis. The X and Y axis is matched with distance and amplitude, depending on dots per inch (DPI). Second, to detect PVC, ECG signal is filtered to eliminate baseline wandering. The characteristics of PVC is higher amplitude and longer duration than normal sinus rhythm, we set two criteria to detect the PVC: 1.5 times the duration, 1.2 points out of the amplitude. For the synchronization of timing, lead II rhythm strip was used by PVC detection and then the rest of 12‐lead ECG is matched based on lead II synchronization (Figure 1). We applied this algorithm to the three real patient's ECGs. Two of three ECGs are successfully digitalized signal and PVC detection. However, the other subject failed to detect PVC from because the algorithm confused ECG signal from the lead marking, such as V1 (Figure 2).

FIGURE 1 Process of PVC detection system from ECG paper records

graphic file with name JOA3-35-4-g025.jpg

FIGURE 2 (A) is successful to take digitalized ECG and PVC detection, and (B) fail to take it because the method confuse ECG signal and the lead name marking

graphic file with name JOA3-35-4-g026.jpg

Conclusion:

We successfully developed the algorithm analog ECG signal into digital signal to detect PVC. In the future, this method helps to gather big data from ECG papers to develop a new algorithm to localization of PVC.

AP19‐00448

Optimal contact force to minimize edema volume during radiofrequency ablation

Morio Ono, Kennosuke Yamashita, Wataru Igawa, Junpei Saito, Masahiko Ochiai

Showa University Northern Yokohama Hospital, Japan

Introduction:

Radiofrequency (RF) ablation results in creation of acute edema which can lead to temporary disruption of electrical propagation. The goal of this study was to find the optimal contact force (CF) to minimize edema formation in comparison to the chronic lesion size using magnetic resonance imaging (MRI).

Methods:

Forty‐nine ventricular RF lesions were created by a CF sensing catheter in a canine model (n = 10) with varying force for 30 seconds. Animals underwent T2‐weighted and late gadolinium enhancement MRI (LGE‐MRI) immediately and 12 weeks after ablation. Acute LGE, acute edema, and chronic LGE volume were segmented and measured (Panel A). Acute edema/LGE volume ratio (EL ratio) was used to divide the lesions into two groups.

Result:

Acute edema volume/LGE‐MRI volume ratio shows an inverse relationship with CF (Panel B). The lesions were divided into greater edema group (GE group, n = 8) and smaller edema group (SE group, n = 41) based on an EL ratio. When comparing the two groups, the CF and force time integral (FTI) in the GE group were significantly lower than those in the SE group (4.1 ± 4.2 vs 12.4 ± 4.9 g, P = .003; 390.2 ± 150.2 vs 802.8 ± 364.7 g, P = .003, respectively). Catheter power setting, tip temperature change, impedance drop, and bipolar electrogram voltage change were not significantly different. Acute LGE volume and chronic lesion depth were significantly smaller in the BE group. Moreover, ROC curve for the SE lesion group showed that the most discriminant cut‐off value for FTI was 584 g (Panel C).

Conclusion:

To minimize edema size while still forming permanent lesions, ablation should be performed with FTI >584 g or CF >12.4 g.

graphic file with name JOA3-35-4-g027.jpg

AP19‐00453

Anatomical and clinical features in patients underwent atypical coronary sinus cannulation

Sixian Weng, Min Tang, Pihua Fang, Shu Zhang

Fuwai Hospital, Chinese Academy of Medical Sciences, Peking Union Medical College, China

Introduction:

Clinical data in patients underwent atypical coronary sinus(CS)cannulation intraoperative has not been well described. We hypothesized that an atypical CS cannulation may clue to different kind of CS variation and aimed to retrospective analyze the anatomical and clinical features in patients with abnormal CS from viewpoint by whom underwent atypical coronary sinus cannulation during electrophysiology (EP) procedure.

Methods:

We retrospective analyzes 7,206 consecutive patients underwent CS cannulation during EP procedure from January 2011 to February 2019. The definition of atypical CS cannulation are as follow: (a) Cannot put inside or difficult to advance the CS catheter; (b) Even though we cannulate favorably, the CS catheter stay in an unusual place or an unstable situation such as outside cardiac border, inside left atrium, extremely deviate from atrioventricular valve ring, transposition, Large swing with heartbeat, incongruous movement, drop out easily, etc. These were all judged by at least two EP physician who operate greater than 200 EP procedures independently every year. After that, these patients were accepted CS angiography or cardiac imaging to confirm the detail situation of CS.

Result:

72 patients (mean age 41.9 ± 18.4 years, 61.1% male) included in the study were divided into two groups depended on the situation of CS cannulation: Group A contain 43 patients cannulated in an unusual place/unstable situation(UP/US); Group B contain 29 patients cannulated difficultly (CD). Compare to UP/US, CD has a higher body mass index (BMI; 25.7 ± 4.9 vs 22.3 ± 3.9, P = .001). 28 patients(38.9%)complicate with structural heart disease and 11 of them has a cardiac function grade(NYHA)≥2. A total of 74 arrhythmias induced during EP study and most of it(70/74) were supraventricular tachycardia(SVT). There is no difference in the type of arrhythmia between two groups except UP/US has a higher proportion of right accessory pathway (19% vs 0%, P = .025). After combined with CS angiography or cardiac imaging (computed tomography, CT; transthoracic echocardiography, UCG), we found that both two group have different kinds of CS variation. UP/US mainly subdivided into 23 persistent left superior vena cava (PLSVC), 11 abnormal CS position, 7 simple CS dilation and 2 unroof CS. CD can subdivided into 7 coronary sinus ostium atresia (CSA), 6 coronary sinus stenosis (CSS) and 16 undetermined/unknown (no obvious CS variation).

TABLE 1 Baseline characteristics

parameter	Total (n = 72)	CD (n = 29)	UP/US (n = 43)	P
Age (years, $\bar{x}$ ± s)	41.9 ± 18.4	39.5 ± 15.9	43.4 ± 19.9	.380
Gender (male/female)	44/28	20/9	24/19	.262
BMI (kg/m2, $\bar{x}$ ± s)	23.7 ± 4.6	25.7 ± 4.9	22.3 ± 3.9	.001
LVEDD (mm, $\bar{x}$ ± s)	47.8 ± 9.3	48.8 ± 8.0	47.1 ± 10.1	.139
LVEF (%, $\bar{x}$ ± s)	62.3 ± 8.1	63.2 ± 6.0	61.7 ± 9.2	.592
LAAD (mm, $\bar{x}$ ± s)	35.3 ± 7.1	36.6 ± 8.4	34.5 ± 6.0	.331
RVAD (mm, $\bar{x}$ ± s)	21.7 ± 6.1	21.5 ± 2.8	21.8 ± 7.5	.031
IVS(mm, $\bar{x} n n$ ± s)	10.4 ± 7.7	10.4 ± 5.7	10.3 ± 8.8	.752
Structural heart disease*(%)	28(38.9)	9(31.0)	19(44.2)	.262
NYHA(0‐4)_≥_2 (%)	11(15.3)	4(13.8)	7(16.3)	1
Arrhythmias(n)	74	32	42	—
AVNRT(n,%)	21(28.4)	9(28.1)	12(28.6)	.966
R‐AP(n,%)	8(10.8)	0(0)	8(19.0)	.025
L‐AP(n,%)	17(23.0)	10(31.3)	7(16.7)	.140
AFL/AT(n,%)	16(21.6)	6(18.8)	10(23.8)	.600
AF(n,%)	8(10.8)	5(15.6)	3(7.1)	.432
VAS(n,%)	4(5.4)	2(6.3)	2(4.8)	1

Open in a new tab

Note *Including congenital heart disease, cardiomyopathy, valvular heart disease; CD=cannulate difficultly; UP/US=unusual place/unstable situation; BMI=body mass index; LVEDD=left ventricular end‐diastolic dimension; LVEF=left ventricular ejection fraction; LAAD=left atrium anteroposterior diameter; RVAD=right ventricular anteroposterior diameter; IVS=interventricular septum; NYHA=heart function grade of New York heart association; AVNRT=atrioventricular nodal reentrant tachycardia; R‐AP=right accessory pathway; L‐AP=left accessory pathway; AFL/AT=atrial flutter/atrial tachycardia; AF=atrial fibrillation; VAS=ventricular arrhythmias.

graphic file with name JOA3-35-4-g028.jpg

Conclusion:

For patients underwent atypical coronary sinus cannulation may combine with abnormal coronary vein especially in patients with structural heart disease. When it comes to UP/US during EP procedure, abnormal CS position and PLSVC should be consider; As regard to CD, CSA or CSS cannot be neglected and apply CS angiography during procedure or CT scan after procedure may helpful for identify the cause of CD.

AP19‐00466

Clinical significance of cardiac arrhythmias on readmission and cardiac death in hospitalized patients with heart failure

Shinya Yamada, Masashi Kamioka, Takashi Kaneshiro, Yasuchika Takeishi

Fukushima Medical University, Japan

Introduction:

The parameters obtained from Holter monitoring provide useful information on the clinical management of various cardiac diseases. The present study aimed to clarify the impact of atrial fibrillation (AF) and non‐sustained ventricular tachycardia (NSVT) on risk stratification of heart failure (HF) patients.

Methods:

We studied 435 HF patients (males, 62%; mean age, 65 years). All patients were hospitalized for the treatment of acute decompensated HF. After optimal medications, 24‐hour Holter monitoring was performed in stable condition before discharge. The clinical characteristics, Holter ECG results and outcomes after discharge were investigated.

Result:

During the follow‐up (3.4 ± 2.1 years), there were 120 (27.5%) cardiac events (71 re‐ hospitalizations due to worsening HF and 49 cardiac deaths). The patients with cardiac events had higher prevalence of AF (>5 seconds) and NSVT (>3 beats) during the Holter monitoring compared to those without (AF, 36.6% vs 26.3%, P = .034; NSVT, 46.6% vs 26.3%, P < .001). The multivariable Cox proportional hazard analysis showed that AF and NSVT were significant risk factors of cardiac events with hazard ratios (HR) of 1.564 (P = .012) and 1.643 (P = .008), respectively, after the adjustment of multiple confounders. The study subjects were then divided into three groups based on their combination of AF and NSVT. The patients were given 1 point each for the presence of AF and/or NSVT: score 0 (n = 214), score 1 (n = 176) and score 2 (n = 45). Cardiac events were 18.6% in score 0, 34.0% in score 1 and 44.4% in score 2, respectively (P < .001, Figure 1A). When compared with score 0, the multivariable Cox proportional hazard analysis showed that scores 1 and 2 had hazard ratios of 2.091 and 2.913, respectively, for cardiac events (Figure 1B).

graphic file with name JOA3-35-4-g029.jpg

Conclusion:

The presence of AF and NSVT was significantly associated with cardiac events in hospitalized patients with HF.

AP19‐00472

Automated localization of accessory pathway by deep neural network interpretation of surface electrocardiography

Yu Liao, Mu‐Hsiang Huang, Ting‐Chun Huang

National Cheng Kung University Hospital, Taiwan

Andrew E P Sunardi, Evan Jim Gunawan, Setiadi Benny, Agnes L Panda

Faculty of Medicine, Sam Ratulangi University, Indonesia

Introduction:

Cardiovascular manifestations are a frequent finding in hyperthyroidism and hypothyroidism. While hypothyroidism may cause bradycardia, low voltage QRS and heart block, hyperthyroidism (HT) is commonly associated with sinus tachycardia and supraventricular tachyarrhythmia. But a rare complication of thyrotoxicosis is impaired atrioventricular (AV) conduction.

Methods:

A‐30 year old man with seizures was referred to cardiology for total AV block. He had fever since last week, weight loss in 1 month, frequent bowel movements, diaphoresis, palpitation and also fatigue was noted. No remarkable previous medical history. IMT was 20 kg/m², BP was 80/50 mm Hg, HR 40x/min, no fever. There were exophthalmos, enlarged symmetrical thyroid, mitral systolic murmur and diastolic murmur on the aorta. The extremity was warm, fine tremor and hyperhidrosis. Laboratory results was significant for TSHs <0.005 μIU/mL (0.30‐4.68 μIU/mL), FT4 4.45 ng/dL (0.70‐1.55 ng/dL), FT3 12.23 pmol/L (4.1‐6.7 pmol/L) and increase in leucocyte 16.100/μL. ASTO and electrolyte were normal. Echo findings were EF 63%, mild regurgitation on aorta, mitral and tricuspid. Patients were diagnosed with Graves disease with TAVB on TPM. Methimazole 10 mg twice a day was given along with antibiotics and patient discharged with AV block grade 1.

Result:

Cases of high‐grade AV block complicating HT have been reported as early as 1970. The possible etiology of AV block in HT is still controversial. One proposed mechanism was excessive thyroid hormone increases the automaticity of the AV node due to inflammation of the conduction system. An autoimmune response in Grave's disease, as a result of precipitating factors like infection, may cause inflammatory cells infiltrating myocardium and conduction pathway. Bradyarrhythmia leads to low cardiac output and blackout with abnormal movement mimicking epilepsy seizures. Control thyroid disease with antithyroid agents may help to restore to normal conduction. The pacemaker was rarely indicated unless there is a hemodynamic disturbance.

graphic file with name JOA3-35-4-g031.jpg

graphic file with name JOA3-35-4-g032.jpg

Conclusion:

The mechanism by which hyperthyroid may cause AV block is still unknown, but a direct thyroid hormone was allegedly involved in inflammation and infiltration on the conduction system. The principal management of conduction abnormalities in thyroid disease is antithyroid agent aiming to control thyroid level itself and eliminating precipitating factors.

AP19‐00550

Recurrent ventricular arrhythmia from left ventricular summit after ablation, what should we do next for ablation strategy?

Victor Bandana, Evan Jim Gunawan, Beny Hartono, Gunawan Yoga, Benny Setiadi, Janry Pangemanan, Agnes Lucia Panda, Muhammad Munawar

Sam Ratulangi University, Indonesia

Introduction:

The left ventricular summit (LVS) is a complex anatomical region located at the epicardial base of left ventricular outflow tract (LVOT) and approximately 14.5 % origin of idiopathic ventricular arrhythmias (VAs). There is a percentage of patients in whom successful ablation cannot be achieved because of anatomic limitations. In this regard, one of the most challenging clinical problems in electrophysiology (EP) is the approach to VAs arising from the LVS.

Methods:

Yuji Wakamatsu, Koichi Nagashima, Kazuki Iso, Ryuta Watanabe, Masaru Arai, Naoto Otsuka, Yagyu Seina, Toshiko Nakai, Yasuo Okumura

Nihon University School of Medicine, Japan

Introduction:

Entrainment pacing is a quick, useful method for locating reentrant atrial tachycardia (AT) circuits, but alteration or termination of the AT can derail the process. We hypothesized ATs reset by scanned single atrial pacing from a multielectrode catheter on the AT circuit at a downstream site during a period when the neighboring electrodes at an upstream site are refractory would be a diagnostic tool to avoid AT alterations (Figure A). This study was conducted to assess the relative value of commonly used entrainment pacing and this resetting maneuver in terms of diagnostic performance and risk of AT alteration or termination.

Methods:

Forty ATs with a cycle length (CL) of 232 ± 36 milliseconds were included (26 common flutters, 6 left atrial roof flutters, 4 perimitral flutters, 2 left atrial scar reentry tachycardias, 1 pulmonary vein‐gap reentry tachycardia, and 1 unknown circuit). Both entrainment pacing and scanned single atrial pacing were attempted for each AT at the cavotricuspid isthmus, LA roof, and mitral isthmus and/or critical AT isthmus.

Result:

On the circuit, the post‐pacing interval minus ATCL after entrainment pacing was <30 milliseconds for all ATs and reset of the AT cycle ≥10 milliseconds by scanned single atrial pacing occurred for 84% of the ATs (Figure B). No ATs were reset by scanned single atrial pacing outside the circuit. The positive predictive value of both maneuvers for locating the circuit was 100%, but the negative predictive value of scanned single atrial pacing was lower than that of entrainment pacing (89% vs. 100%, P = 0.02). The incidence of AT alteration was lower during scanned single atrial pacing than during entrainment pacing (1% vs. 11%, respectively; P = 0.003). For ATs with a CL <210 milliseconds, SP and entrainment frequently failed to detect the circuit, due to reset failure and AT alteration, respectively.

Conclusion:

AT reset by scanned single atrial pacing is a reliable diagnostic maneuver that avoids AT alteration and termination.

graphic file with name JOA3-35-4-g034.jpg

AP19‐00586

Quality of life and care giver burden in SND patients treated with guideline indicated pacemaker therapy in South Asia: Results from the IMPROVE Brady study

Fazila Tun Nesa Malik, Ajay Naik, Rishi Sethi, Nadeem Afroz, Dwight W Reynolds, Yogesh Kothari, Y Vijaya Chandra Reddy, Vinayakrishnan Rajan, Alexandra Dedrick, Ulhas Pandurangi, Kaiser Nasrullah Khan, Calambur Narasimhan

India Medtronic Pvt. Ltd., India

Introduction:

Pacemaker therapy for guideline indicated patients with sinus node dysfunction (SND) remains low in developing geographies. We sought to better understand the care pathways of bradycardia patients and to assess if a specific process improvement intervention could increase the adoption of pacemakers in this patient population.

Methods:

IMPROVE Brady was a quality improvement initiative conducted at centers in India and Bangladesh for bradycardia patients. The prospective study was conducted sequentially in two phases. Phase I assessed the existing care pathways for diagnosis and treatment of symptomatic SND. Phase II evaluated the impact of specific process improvement interventions consisting of education, diagnostic algorithms, and documentation tools on diagnosis and adoption of pacemaker therapy and quality of care. The study enrolled patients in both Phases with a heart rate of ≤ 50 beats per minute and symptoms including syncope, dizziness, and/or dyspnea. Patients were followed to identify the proportion diagnosed with symptomatic SND and subsequently treated with pacemaker therapy. SND patients implanted with a Medtronic family pacemaker in Phase II completed a quality of life survey (SF‐12) before the implant procedure and at 6 months post implant. The primary caregiver of the patients was asked to complete the Zarit Burden Interview at the same timepoints to assess caregiver burden.

Result:

A total of 470 patients were enrolled and met inclusion criteria in Phase II of the IMPROVE Brady study across 8 centers. Patients were on average 58 years of age, 73% were male, and 93% had completed at least a primary education. A SND diagnosis was made in 409 (87%) patients of whom 130 received pacemaker therapy and of whom 76 were implanted with a Medtronic family pacemaker. There was a statistically significant improvement in quality of life at 6 months, with approximately equal improvements in both mental and physical components (see Table). There was a significant reduction in caregiver burden following pacemaker therapy.

FIGURE 1 3D mapping and catheter ablation

graphic file with name JOA3-35-4-g035.jpg

Conclusion:

Among patients with symptomatic SND from South Asia, significant and clinically meaningful improvements in quality of life and reductions in caregiver burden were observed after receiving guideline‐indicated pacemaker therapy. This represents the first report on caregiver burden using the Zarit Interview in a bradycardia population.

AP19‐00597

The incidence Of QTc prolongation and its influencing factors in patients with breast cancer

Yan Ji, Hua Qian, Mingyue Tan, Guoliang LI, Yan Liu

Department of Cardiology, the First Affiliated Hospital of Xi'an Jiaotong University, China

Introduction:

Objective: To analyze the incidence of QTc prolongation and its influencing factors in hospitalization of breast cancer patients.

Methods:

Retrospective analysis of clinical baseline data of 296 patients with breast cancer diagnosed by pathology from January to December 2018 in First Affiliated Hospital of Xi'an Jiaotong University, aged 26‐84 years old, we observed all ECG of patients before February 2019, the corrected QT values by heart rate were taken as QTc max, QTc ≥450 milliseconds as the prolongation group, and QTc <450 milliseconds as the control group. Univariate and multivariate logistic regression analysis were used to analyze the factors that may cause QTc prolongation.

Result:

The incidence of QTc prolongation in breast cancer patients was 18%. Correlation factor analysis showed that the heart rate (OR: 1.04; P: .012), with hypertension (OR: 6.48; P: <.001), the use of anthracycline (OR: 3.96; P: .031) were statistically significant (all P < .05); whereas the age (OR: 1.01; P: .012), serum sodium (OR: 099; P: .869), potassium (OR: 0.69; P: .446), calcium (OR: 4.3; P: .254), with coronary heart disease (OR: 0.32; P: .344), diabetes (OR: 2.4; P: .377). The type of medical insurance (OR: 0.75; P: .603) and education degree (OR: 0.61; P: .312) were no statistical significance (P > .05).

Conclusion:

The increased heart rate, with hypertension and anthracycline use in breast cancer patients may be the risk factors for prolonged QTc.

Key Words: QTc; breast cancer; influencing factors

AP19‐00599

Unusually prolonged bradycardia in a child after percutaneous device closure of patent ductus arteriosus

Hnin Phyu

University of Medicine II, Myanmar, Burma

Introduction:

Profound bradycardia after large patent ductus arteriosus (PDA) closure is recognized and reported in dogs. In human, the condition was reported to occur after occlusion of large arteriovenous(AV) fistula, which, is very similar to large PDA in hemodynamics. The condition is explained by baroreceptor reflex activity called Nicoladoni‐Branham sign and is usually benign and self limiting. Understanding causal relations or possible mechanisms can alleviate unnecessary worries, medications or interventions.

graphic file with name JOA3-35-4-g036.jpg

Methods:

4 yrs boy was diagnosed as having large PDA and undergone percutaneous device closure. His baseline heart rate(HR) was 80 bpm and blood pressure(BP) was 97/43 mmHg. Pre‐op 12 leads ECG showed sinus rhythm with P‐wave axis at 0 degree. PDA size was 11 mm in echo and 10.3 mm in angiogram. PDA was closed with Lifetech PDA Occluder Device 22/20 mm. After procedure was successfully finished, his aortic pressure increased from (79/45/61) to (83/49/66) and HR was 124/min. Around 6 hr after procedure, sinus bradycardia was started to notice with HR 50 bpm. However, the child had no symptoms and vital signs are stable throughout. His BP increased to 100/60 mmHg. In 24 hr Holter ECG monitoring, sinus bradycardia was present throughout with resting HR 47–68 bpm. The child was sent home with no medication for bradycardia. Recheck ECG was done intermittently and only after 3 weeks of PDA closure, his resting HR increased to 74 bpm with sinus rhythm. We had similar experience in a 6 yr old boy who also received device closure for large PDA.

Result:

Closure of large PDA can be followed by transient bradycardia. This phenomenon can be explained by a reflex mechanism, in which increase in mean arterial pressure stimulate arterial baroreceptor causing decrease in heart rate via vagal activation. This condition required no treatment and can prolong for a few days, but except in our case, which lasted for 3 weeks. Another factor is traction or pressure on Vagal trunk by very large device although such mechanical injuries happened in surgical PDA ligation and not reported before to occur in percutaneous device closure.

Conclusion:

We reported an occurrence of profound bradycardia following occlusion of large PDA in 4 year boy. The condition was only transient and spontaneously resolved. Branham's sign of reflex bradycardia is considered to be underlying mechanism although pressure effect on Vagus nerve still cannot be totally excluded.

AP19‐00603

(CASE REPORT) Blacked out: Long QT syndrome in a young female with recurrent seizure and syncope diagnosed by epinephrine stress test

Roxanne Camina, Katrina Balcos, Angelica Dela Cruz, Giselle Gervacio

Philippine Heart Association, Philippines

Introduction:

Congenital Long QT syndrome (LQTS) is a rare congenital disorder of ventricular repolarization characterized by QT interval prolongation. The prevalence in Asia ranges from 0.02% to 0.04%. LQTS predisposes patients to seizure like activity, syncope, life threatening arrhythmias and sudden cardiac death. Diagnosis is based on a good clinical history and electrocardiographic findings. The epinephrine stress test provides a safe and reliable way of unmasking Type 1 LQTS.

Methods:

Objective: To present a case that will highlight the clinical utility of provocative testing with Epinephrine in a young female with history of recurrent seizure and syncope.

Result:

Case Presentation: A 27‐year old female who was having episodes of seizure and syncope for the past 2 months. Neurologic work‐up and initial cardiac work up were all negative and was managed with seizure disorder. She came in with another episode of seizure followed by syncope sustaining a hematoma on her right frontal area. She was documented having supraventricular tachycardia on monitor which reverted to sinus rhythm after giving doses of Adenosine and Verapamil. Given the history of seizure and syncope with associated arrhythmia in a young patient, long QT syndrome was highly suspected. An epinephrine stress test was done to induce long QT and catecholaminergic polymorphic ventricular tachycardia. Initial electrocardiogram before the stress test showed sinus rhythm with normal QTc interval of 401 milliseconds. Patient was started in graded Epinephrine infusion under continuous ECG monitoring and noted progressive prolongation of actual QT interval and QTc during stage 1 recovery. There was no note of arrhythmia. The QTc reverted to pretest level at the end of test. She was discharged on Beta‐blocker therapy and advised for ICD implantation.

Conclusion:

The diagnosis of seizure and syncope with documented associated arrhythmia is a challenge to every clinician, warrants a good clinical history and further investigation. Among these, congenital long QT syndrome as a cause in a young patient with recurrent seizure and syncope with negative initial diagnostic work up and normal QTc on initial electrocardiogram could pose a dilemma. Early diagnosis and treatment can prevent sudden cardiac death in patients with long QT syndrome. Provocative testing with catecholamine, such in this case, Epinephrine, can unmask concealed type 1 long QT syndrome with a high level of accuracy. It may help differentiate patients with suspected LQTS from normal and may distinguish one genetic defect from another.

AP19‐00615

Diffuse ST elevation myopericarditis in Leptospirosis: A case report

Denise Elaine Aguilar, Silverose Agustin, Marcellus Francis Ramirez

University of Sto. Tomas Hospital, Philippines

Introduction:

Leptospirosis is a complex zoonotic disease caused by spirochetes from the genus Leptospira commonly encountered in tropical and subtropical countries. Cardiac involvement is a common but underreported manifestation of leptospirosis. Common ECG changes involve atrial fibrillation, nonspecific ST‐T wave changes, and conduction delays.

Methods :

Case Report.

Result:

A previously well 32‐year old male from the Philippines was admitted at a tertiary care hospital with a one‐week history of generalized myalgia, fever, chills, and severe retrosternal chest pain. He was hypotensive, diaphoretic, jaundiced, with conjunctival suffusion and bibasal crackles. Initial 12LECG revealed ST elevation in leads V1, V2, and V3 after 1 hr showing resolution of ST elevation with early repolarization phenomenon. Patient was later noted to have recurrence of ST elevation now diffusely noted in leads II, III, aVF, V3, V4, and V5. Laboratory examinations revealed elevated troponin I, CKMB, and CK‐total, azotemia, and normal hepatic enzymes. Leptospirosis micro agglutination test (MAT) was positive up to the 1:1600 dilution. Patient was immediately started on intravenous Ceftriaxone 2 grams every 24 hours. By the third hospital day, patient was clinically improved with no recurrence of chest pain and resolution of hypotension. 12LECG now revealed normal sinus rhythm and labs revealed resolution of azotemia as well. He was discharged fully recovered on the seventh hospital day.

Conclusion:

Diffuse ST segment elevation is a rare cardiac manifestation in patients with leptospirosis. Limited studies have documented this phenomenon worldwide. This is the first report in the Philippines detailing such presentation.

TABLE 2 Summary of the patient's serial complete blood count measurements taken during admission. Gradual thrombocytopenia was noted by the third hospital stay, eventually resolving the sixth hospital day

Complete blood count	ReferenceRange	Day 1	Day 3	Day 5	Day 6	Day 7
Hgb	130‐180	125	150	132	124	121
RBC	4.5‐6.2	5.78	6.90	6.20	5.75	5.73
Hct	0.40‐0.50	0.39	0.45	0.40	0.38	0.38
MCV	85+/‐4	67.00	64.60	64.50	66.20	65.80
MCH	28+/‐2	21.70	21.80	21.30	21.60	21.10
MCHC	30+/‐2	32.40	33.70	33.0	32.60	32.10
RDW	11.6‐14.6	15.00	15.10	15.10	15.0	14.90
MPV	7.4‐10.4	9.40	9.10	9.10	8.70	9.00
Platelet Count	170‐400	223	184	136	182	225
WBC	4.0‐10	8.20	7.90	6.30	6.10	5.40
Neutrophils	0.50‐0.70	0.92	0.66	0.50	0.38	0.30
Segmenters	0.55‐0.66	0.92	0.66	0.42	0.38	0.30
Lymphocytes	0.25‐0.35	0.07	0.32	0.04	0.53	0.61
Monocytes	0.03‐0.06	0.07	0.02	0.04	0.03	0.03
Eosinophils	0.02‐0.04	—	—	—	0.06	0.06
Basophils	0.00‐0.01	—	—	—	—	—

Open in a new tab

TABLE 3 Tabulation of the blood chemistries done on patient from the first to third hospital day

Blood Chemistry	Reference Range	Day 1	Day 1
Urea Nitrogen	9‐23mg/dl	36.50
Uric Acid	4‐8.5mg/dl	6.10
Creatinine	0.67‐1.17mg/dl	2.73	0.97
Alkaline Phosphatase	40‐129U/L	97.00
SGOT—AST	0‐38U/L	37.50
SGPT—ALT	0‐41U/L	37.20
Total Bilirubin	0.5‐1.5mg/dL	1.96
Direct Bilirubin	0.1‐0.40mg/dL	1.22
Indirect Bilirubin	0.3‐1.1mg/dL	0.74
Sodium	136‐145mmol/L	132	142
Potassium	3.5‐5.1mmol/L	3.72	3.59
Magnesium	1.6‐2.59mg/dL	2.06
Ionized Calcium	1.12‐1.32mg/dL	1.12
Troponin I	0‐0.04ng/mL	5.50	69.25
CK Total	39‐308U/L	>2000
CKMB Activity	7‐25U/L	218.09

Open in a new tab

FIGURE 1 Initial echocardiogram (ECG) done at a primary hospital revealing ST elevation in leads V1, V2, V3

graphic file with name JOA3-35-4-g037.jpg

FIGURE 2 12 lead ECG done at 2nd hospital 55 minutes after 1st ECG was done revealing sinus rhythm, early repolarization phenomenon and complete resolution of ST elevation

graphic file with name JOA3-35-4-g038.jpg

FIGURE 3 Third 12‐lead ECG done almost 2 ½ hours after initial tracing revealing diffuse ST elevation in leads V2, V3, V4, V5, V6, II, III, and aVF

graphic file with name JOA3-35-4-g039.jpg

FIGURE 4 12 lead ECG done on the 4th hospital day revealing complete resolution of the diffuse ST elevation

graphic file with name JOA3-35-4-g040.jpg

graphic file with name JOA3-35-4-g041.jpg

AP19‐00632

Clinical utility of fluorodeoxyglucose positron emission tomography/ magnetic resonance imaging in assessment of non‐ischemic cardiomyopathy

Ching‐Han Liu, Chin‐Yu Lin, Isaiah Carlos Lugtu

Heart Rhythm Center and Division of Cardiology, Department of Medicine, Taipei Veterans General Hosp, Taiwan

Introduction :

Background: Drug‐refractory ventricular arrhythmia (VA) in non‐ischemic cardiomyopathy (NICM) remains to be challenging despite catheter ablation. Objective: To explore the value of hybrid magnetic resonance imaging (MRI) and positron emission tomography (PET) using 18F‐ fluorodeoxyglucose (FDG) for NICM with VA.

Methods:

Patients with NICM and drug refractory VA underwent hybrid MRI/PET with 18F‐FDG and late gadolinium enhancement (LGE) to assess the pattern of inflammatory activity and scar, respectively. The pattern of cardiac 18F‐FDG uptake were classified as pattern (1) no uptake, (2) diffuse uptake, (3) focal uptake, and (4) focal‐on‐diffuse uptake. Patterns 3 and 4 were considered positive findings. Patients underwent catheter ablation and were followed‐up for at least 6 months. Receiver‐ operating characteristic methods were used to identify imaging biomarkers.

Result:

Catheter ablation was performed in 12 out of 15 consecutive patients with drug refractory VA. Elimination and non‐inducibility of VA were achieved in all patients (100%). Recurrence after ablation were found in 4 patients (33.3%) after a mean follow‐up of 6.5 months. Comparing the LGE in the MRI, the presence of 18F‐FDG uptake at baseline better predict long‐term VA recurrence. Additional prednisolone successfully suppressed recurrent VA in 3 patients (20%) with increased 18F‐FDG uptake.

graphic file with name JOA3-35-4-g042.jpg

Conclusion:

MRI/PET imaging provided information about the pattern of injury and disease activity in a single scan. Furthermore, it holds a major promise of prognostic value in patients with NICM and drug refractory VA.

AP19‐00636

The comparison of characteristics of intraseptal pacing with and without left bundle branch capture confirmed by direct recruited proximal or distal conduction system

Weijian Huang, Xueying Chen, Shengjie Wu

Department of Cardiology, the First Affiliated Hospital of Wenzhou Medical University, Wenzhou, China

Ming Chu

Nanjing Medical University, China

Introduction:

Latest evidence indicates the association of atrial diseases with embolic strokes of undetermined source. This study aimed to investigate the relationship between advanced interatrial block (aIAB, an electrophysiological mark of atrial abnormality) and silent cerebral small vessel diseases (SVD) in the absence of atrial fibrillation (AF) and atrial flutter.

Methods:

This study included 499 patients with normal left ventricular ejection fraction (LVEF), who were free of AF, atrial flutter, stroke and acute coronary syndrome. aIAB was detected from digital electrocardiograms. Left atrial diameter, left ventricular ejection fraction (EF) and left ventricular posterior wall thickness (LVPWT) were measured on echocardiograms. Four manifestations of SVD, including white matter hyperintensity (WMH), lacunes, microbleeds and enlarged perivascular spaces (EPVS), were rated on magnetic resonance imaging. Regression models were used to explore the association of aIAB with these 4 manifestations after adjusting for confounding factors, respectively.

Result:

A total of 23 (4.6%) patients had aIAB and 67 (13.4%), 21 (4.2%) had lacunes and CMBs, respectively. The mean score/number of WMH and EPVS were 6.2 and 66.2, respectively. After adjusting for age, sex, hypertension, diabetes, hyperlipidemia, left atrial diameter, LVEF and LVPWT, regression models showed a significant association of aIAB with WMH (β = 1.463, 95% CI 0.310‐2.616), and with lacunes (OR = 3.647, 95% CI 1.174‐11.332), respectively. No association of aIAB with EPVS or CMBs was found.

Conclusion:

aIAB was independently associated with a high burden of WMH and lacunes in the brain.

TABLE 1 Characteristics of the patients with and without aIAB

	Patients with no aIAB (n = 476)	Patients with aIAB (n = 23)	P
Age	67.5 (13.7)	71.8 (11.4)	.136
Male, n (%)	311 (65.3)	16 (69.6)	.677
Hypertension, n (%)	326 (68.5)	12 (52.2)	.102
Diabetes, n (%)	145 (30.5)	7 (30.4)	.998
Hyperlipidemia, n (%)	385 (80.9)	20 (87.0)	.467
LAD (mm)	35.1 (4.7)	38.3 (4.4)	.001
LVEF	65.1% (3.5%)	63.1% (2.7%)	.007
LVPW (mm)	9.7 (1.4)	10.0 (0.9)	.427
WMH total score	6.1(3.3)	8.2 (2.9)	.003
Lacunes, n (%)	61 (12.8)	6 (26.1)	.107
CMBs, n (%)	20 (4.2)	1 (4.3)	.974
EPVS, n (%)	213 (44.7)	10 (43.5)	.898

Open in a new tab

Continues and categorical variables are presented as mean (SD) and percentages, respectively.

Aiab, advanced interatrial block; LAD, left atrial diameter; LVEF, left ventricular ejection fraction; LVPW, left ventricular posterior wall thickness; WMH, white matter hyperintensities; CMBs, cerebral microbleeds; EPVS, enlarged periventricular spaces

TABLE 2 Characteristics of the patients with and without lacunes, ePVS or CMBs, respectively

	lacunes		ePVS		CMBs
No (n = 432)	Yes (n = 67)	No (n = 276)	Yes (n = 223)	No (n = 478)	Yes (n = 21)
Age	66.6 (13.8)	74.7(9.6)*	64.2 (13.3)	74.7(9.6)*	67.1 (13.5)	80.8(9.4)*
Male, n (%)	276 (63.9)	51 (76.1)	185 (67.0)	141 (63.2)	309 (64.8)	17 (81.0)
HT, n (%)	279 (64.6)	59 (88.1)*	174 (63.0)	163 (73.1)*	319 (66.7)	18 (85.7)
Diabetes, n(%)	125 (28.9)	27 (40.3)	80 (29.0)	72 (32.3)	144 (30.1)	8 (38.1)
Hyperlipidemia, n(%)	346 (80.1)	59 (88.1)	214 (77.5)	190 (85.2)*	390 (81.6)	14 (66.7)
LAD (mm)	35.1 (4.7)	36.2 (4.7)	35.2 (4.6)	36.2 (4.7)	35.1 (4.7)	36.4 (4.7)
LVEF (%)	65.1 (3.5)	64.8 (3.4)	65.4 (3.6)	64.6 (3.3)*	65.0 (3.5)	66.6 (3.2)
LVPW (mm)	9.7 (1.4)	10.2 (1.3)*	9.6 (1.4)	9.9 (1.3)	9.8 (1.3)	9.4 (1.7)
aIAB, n(%)	17 (3.9)	6 (9.0)	13 (4.7)	10 (4.5)	22 (4.6)	1 (4.8)

Open in a new tab

Continues and categorical variables are presented as mean (SD) and percentages, respectively. *P < .05

TABLE 3 The association of aIAB with WMH, lacunes, EPVS or MBs, respectively

	Non‐adjusted model		Adjusted model
OR (95% CI)*	P	OR (95% CI) *	P
WMH
aIAB	2.078 (0.706‐3.449)	.003	1.463 (0.310‐2.616)	.013
Lacunes
aIAB	2.401 (0.911‐6.326)	.076	3.647 (1.174 ‐11.332)	.025
EPVS
aIAB	0.946 (0.407‐2.201)	.898	0.631 (0.257‐1.549)	.351
CMBs#
aIAB	1.034 (0.133‐8.060)	.974	0.819 (0.100‐6.689)	.852

graphic file with name JOA3-35-4-g044.jpg

graphic file with name JOA3-35-4-g045.jpg

Methods:

A 57‐year‐old male patient without history of cardiac disease was admitted to referral hospital for acute onset of chest pain. Hypertension was the only patient's risk factor for coronary artery disease. ECG at 30‐minute after symptom onset (Figure 1) showed significant ST‐segment depression at the J point in leads V4‐V6 with tall, positively symmetrical T waves with slight ST‐segment elevation (0.1 mm) in the aVR lead. The patient developed ventricular fibrillation and managed by defibrilation. The patient was referred for further treatment. On arrival the patient was hemodynamically stable and physical examination revealed no abnormalities. Repeated ECG showed normal sinus rhythm with normalization of the ST depression. Urgent coronary angiography showed total occlusion in the proximal LAD coronary artery (Figure 2). Percutaneous coronary intervention was performed with three drug eluting stent resulted TIMI‐2 graded flow. No complication developed in hospital after the procedure and the patient was discharged five days later.

Result:

de Winter described a novel ECG pattern in 2008. Specific criteria for this ECG pattern consistently include: 1‐3 mm upsloping ST‐segment depression at the J‐point in leads V1‐V6 that continue into tall, positive symmetrical T‐waves and 1‐2 mm ST‐ segment elevation in lead aVR. However, it is rare case that occurs in approximately 2% of patients with LAD occlusion. De winter et al purposed that there is an idiopathic anatomical variant of the Purkinje fibers, leading to delayed endocardial conduction. They also hypothesized the absence of ST‐segment elevation is due to lack of activation of sarcolemmal ATP‐sensitive potassium channels by ischemic ATP depletion. Controversy exists whether this pattern only occurs as a transient or persistent. That ECG changes may be missed or misdiagnosed as nonspecific, reversible ischemia. This can significantly lengthen reperfusion therapy. It is imperative that all practitioners learn to identify this ECG pattern to ensure appropriate intervention in the cardiac catheterization laboratory.

Conclusion:

Patient presenting with typical angina symptoms, ST‐segment depression and peaked T waves, combined with the absence of classic ST‐segment elevation in the precordial leads of the 12‐lead ECG, suggest that a significant LAD coronary artery occlusion is present. The de‐Winter T waves should be expressed clearly in educational courses and in the guidelines such that patients would receive appropriate treatment in time and morbidity and mortality can be reduced.

AP19‐00835

Prevalence of cardiac arrhythmia in hypothyroid and euthyroid patients

Pritam Kitey, Amitabh Yaduvanshi, Vikas Kataria, Mohan Nair

Holy Family Hospital, India

Introduction:

Thyroid hormone acts as a regulator of cardiac function and rhythm through genomic and non‐genomic actions of T3 on cardiac myocytes. Hypothyroidism is not considered as a risk factor for arrhythmia despite well‐known ECG changes associated with this condition. This study was conducted to evaluate the difference, if any, in the prevalence of cardiac arrhythmia between hypothyroid patient and euthyroid patients.

Methods:

One hundred consecutive patients attending the cardiac OPD of Holy Family Hospital with stable coronary artery disease were evaluated. Patients were divided into two groups depending on their thyroid status. Group 1—Euthyroid, Groud 2—Hypothyroid patients. All patients were subjected to 72 hours of Holter monitoring and their arrhythmia burden recorded.

Result:

There were 62 patients in the euthyroid group and 38 patients in the hypothyroid group. The two groups had no significant difference in baseline characteristic with respect to age, the prevalence of hypertension, DM, the extent of coronary artery disease. The mean age was 58.2 years and 57.3 years in the hypothyroid and euthyroid group respectively. Mean TSH level in hypothyroid patients group was 9.2 mL IU/L and the euthyroid group was 2.23 mL IU/L. There was a statistically high prevalence of ventricular arrhythmia in the hypothyroid group as compared to the euthyroid group (P = .03).

Conclusion:

Our study revealed the high prevalence of ventricular arrhythmia in patients with hypothyroidism. Increase in ventricular arrhythmia in the hypothyroid patient group, suggest that they require early detection of hypothyroidism and optimal medical treatment for hypothyroidism, to decrease arrhythmia burden. Further large scale studies are needed to better define the risk of such ventricular arrhythmia

AP19‐00838

Repetitive shock therapy of subcutaneous implantable cardioverter defibrillators in a patient with idiopathic ventricular fibrillation: What is the mechanism?

Kanae Hasegawa, Shinsuke Miyazaki, Kenichi Kaseno, Hiroshi Tada

University of Fukui, Japan

Introduction:

The efficacy and safety of the subcutaneous ICD (S‐ICD) has been demonstrated sudden cardiac death. However, the presence of inappropriate shocks observed.

Methods:

N/A.

Result:

A 45‐year‐old man was admitted to our hospital due to repetitive shock therapies from a S‐ ICD without syncope during the daytime. When he was 35‐years‐old, he was resuscitated from ventricular fibrillation (VF) during sleep. He was diagnosed with idiopathic VF (J wave syndrome), and a dual chamber transvenous ICD was implanted in another hospital. When he was 44‐years‐old, he received repetitive inappropriate ICD shocks due to lead dysfunction, and therefore a S‐ICD was implanted. Since he received several appropriate ICD shock therapies at midnight, cilostazol was prescribed to suppress the VF episodes. All previous VF episodes had been successfully terminated by a single ICD shock. As shown in Fig A, repetitive ICD shock therapies were required to terminate the tachyarrhythmia. What was the mechanism of the arrhythmia and what should we do next?

Conclusion:

As shown in the S‐ICD tracing (Figure A), the tachyarrhythmia exhibited a regular tachycardia with a cycle length of 240 milliseconds and the QRS complex did not seem to be relatively wide, which differed from VF episodes. In addition, the polarity of the QRS complex differed during sinus rhythm and the tachycardia. The additional important differences from the previous appropriate shock episodes was (a) the VF was always terminated by a single ICD shock, while the tachyarrhythmia required multiple ICD shocks to terminate it, and (b) VF always occurred at midnight, while the tachyarrhythmia occurred in the daytime without syncope. The possible diagnoses seemed to be (a) supraventricular tachycardia with aberrant conduction, and (b) ventricular tachycardia. We performed an electrophysiological study to clarify the mechanism of the tachycardia. Atrial pacing easily induced a regular tachycardia with right bundle branch block and a superior axis (Figure B). The S‐ICD tracing during the electrophysiological study showed that the tracing of the induced tachycardia (Figure C) was exactly the same as that of the clinically observed tachyarrhythmia. The tachycardia exhibited atrio‐ventricular dissociation and was easily induced by pacing from both the atrium and ventricle. We diagnosed it as a verapamil‐sensitive idiopathic left ventricular tachycardia (ILVT) because 2.5 mg of verapamil prolonged the tachycardia cycle length. Ablation at the mid septum of the left ventricle where a Purkinje potential was recorded immediately terminated and eliminated the tachycardia. Since the ILVT did not lead to a hemodynamic breakdown, this shock therapy from the S‐ICD was an inappropriate delivery. To the best of our knowledge, this is the first case in whom verapamil‐sensitive ILVT coexisted with idiopathic VF.

graphic file with name JOA3-35-4-g046.jpg

AP19‐00840

Analysis of myocardial scar characteristics by cardiac MRI and its correlation with arrhythmic events on follow‐up in ischemic cardiomyopathy (ICMP) patients implanted with Automatic implantable cardioverter defibrillator (AICD)

Hiren Kevadiya, Narayanan Namboodiri K.K., Krishna Kumar M, Ajitkumar V.K.

U.N.Mehta Institute of Cardiology and Research Center, India

Introduction:

Ischemic cardiomyopathy (ICMP) patients remain at increased risk of SCD. Characterization of sudden cardiac death risk remains a challenge in the application of ICD therapy. As the majority of patients remains free from ICD therapy, a further refinement of criteria is needed. Evaluation of pathophysiological substrates related to electrical instability like scar burden and scar characteristics by MGE‐CMR might yield complementary prognostic information.

Methods:

We performed retrospective, single centre Observational study to identify arrhythmic risk predictors and to evaluate the association between the extent and distribution of myocardial scar, quantified using LGE‐CMR, and the burden of ventricular arrhythmias in ICMP patients having AICD. All consecutive ICMP patients implanted with AICD who had undergone CMR for myocardial scar assessment between 2013 and 2018 were included. Non ICMP patients were excluded. Scar was characterized in terms of No. of segments with any scar, transmural scar, Subendocardial scar, dense/non heterogenous scar, heterogenous scar. The end points were Appropriate ICD therapy

Result:

39 patients (mean age, 58.2 years; male sex 38) were included. Mean Ejection fraction by 2D ECHO was 35.4% (SD = 10.7). Mean amiodarone dose was 115 mg (0‐400 mg). Mean LVEF by ECHO was 35.4% in comparison to mean LVEF by MRI was 28.9%. Mean follow‐up duration was 28.8 months (3‐66 months). 17 (43.6%) out of 39 patients were noted to have VT/VF episodes, Twelve (30.8%) out of 39 patients were noted to have appropriate AICD shocks and fifteen (38.5%) were noted to have appropriate AICD therapy in form of shocks/ATP on follow‐up. Baseline characteristics, scar characteristics assessed by CMR were compared between two groups of patients having AICD events and not having events on follow‐up. There was no statistically significant difference in baseline characteristics between both the groups. There was no statistically significant difference in volumetric parameters and scar characteristics assess by cardiac MRI like number of segments with any scar or transmural scar or subendocardial scar or dense‐non heterogeneous scar or heterogenous scar between both the groups. 7.6 segments (mean) (45.2% of total) were noted to have any scar on 17 segments analysis in group of patient having AICD events on follow‐up compared to 8.4 segments (mean) (49.9%) in patients without any AICD events.

Conclusion:

In our study myocardial scar characteristics assessed by LGE cardiac MRI was not associated with AICD events/arrhythmic events on short term follow‐up in ischemic CMP who had AICD/CRT‐D implantation. LVEF by 2D ECHO or cardiac MRI has correlated with scar burden but not with arrhythmic event on follow‐up.

Keywords: Ischemic cardiomyopathy, Automatic implantable cardioverter defibrillator, Myocardial scar, Sudden cardiac death, cardiac magnetic resonance imaging (CMR)

TABLE 2 Baseline cardiac MRI characteristics (n = 39)

Mean	Min	Max	SD
LVEDV (mL)	193.9	120	314	61.2
LVESV (mL)	142.1	49	273	59.7
MRI LVEF (%)	28.9	10	62	11.7
RVEDV (mL)	73.5	25	141	29.1
RVESV (mL)	39.7	11	105	21.3
MRI RVEF (%)	46.7	21	72	13.2
No. of segments with any scar	8.1	3	12	2.5
Any scar (% of LV)	48.1	17.7	70.8	15.1
No. of segments with transmural scar	6.1	0	11	2.4
Transmural scar (% of LV)	36.4	.0	64.9	14.4
No. of segments with subendocardial scar	1.9	0	6	1.6
Subendocardial scar (% of LV)	11.6	.0	35.4	9.9
No. of segments with dense/non heterogenous scar	4.1	0	8	1.8
Dense/non heterogenous scar (% of LV)	24.5	.0	47.2	10.7
No. of segments with heterogenous scar	4.0	1	8	1.8
Heterogenous scar (% of LV)	23.6	5.9	47.2	10.7
Dense/Non heterogenous scar (% of total scar)	51.3	.0	80.0	17.1
Heterogenous scar (% of total scar)	48.6	20.0	100.0	17.1
N = 39	No. of patients		% of total
MRI LVEF (less than 35%)	30		76.9
RV scar	1		2.6

Open in a new tab

TABLE 3 Follow‐up data (n = 39)

Mean	Min	Max	SD
Follow‐up duration (months—post Device implantation)	28.8	3	66	20.4
Follow‐up duration (months after first documented VT)	38.1	3	156	30.2
Appropriate AICD shocks	1.4	0	24	4.1
No. of ATP responsive VT/VF episodes	0.8	0	13	2.4
No. of VT/VF episodes before device implantation	1.4	0	10	1.8
No. of VT/VF episodes after device implantation	2.6	0	24	5.1
Total no. of VT/VF episodes	4.0	0	27	5.6
Heart failure hospitalization (no. of admissions)	0.3	0	5	0.8
	No. of patients (N = 39)		% of total
No of patients having VT/VF episodes after device implantation	17		43.6
No of patients having Appropriate AICD shocks	12		30.8
No of patients having Appropriate AICD therapy (shock/ATP)	15		38.5

Open in a new tab

TABLE 4 Patients with AICD events vs No events

	Patients having AICD events (shocks/ATPs)
	No AICD events (n = 24 patients)		AICD events (n = 15 patients)		P value
Mean	SD	Mean	SD
Age (years)	58.1	10.6	58.2	11.3	NS
BMI (kg/m²)	24.4	2.5	24.2	2.2	NS
Prior MI (Years before device implantation)	8.9	7.3	13.1	6.5	0.07
QRS duration (milliseconds)	128.2	30.5	138.0	37.8	NS
GFR (mL/min/m²)	59.8	13.0	57.9	17.3	NS
ECHO LVEF (%)	34.4	11.5	37.0	9.3	NS
Amiodarone daily dose (mg)	112.5	107.5	120.0	94.1	NS
LVEDV (mL)	193.8	58.2	194.0	68.3	NS
LVESV (mL)	143.8	62.6	139.2	56.6	NS
MRI LVEF (%)	28.6	13.2	29.2	9.2	NS
RVEDV (mL)	75.5	30.6	70.0	27.1	NS
RVESV (mL)	41.3	24.2	37.0	15.6	NS
MRI RVEF (%)	46.2	14.7	47.6	10.4	NS
No. of segments with any scar	8.4	2.1	7.6	3.0	NS
Any scar (% of LV)	49.9	12.9	45.2	18.2	NS
No. of segments with transmural scar	6.2	2.0	6.1	3.0	NS
Transmural scar (% of LV)	36.6	12.2	36.1	17.8	NS
No. of segments with subendocardial scar	2.2	1.7	1.5	1.5	NS
Subendocardial scar (% of LV)	13.2	10.1	9.0	9.4	NS
No. of segments with dense/non heterogenous scar	4.2	1.5	4.0	2.2	NS
Dense/non heterogenous scar (% of LV)	25.0	9.4	23.6	13.0	NS
No. of segments with heterogenous scar	4.2	1.8	3.6	1.8	NS
Heterogenous scar (% of LV)	24.8	10.7	21.6	10.8	NS
Dense/Non heterogenous scar (% of total scar)	51.3	15.5	51.3	20.0	NS
Heterogenous scar (% of total scar)	48.6	15.5	48.6	20.0	NS
Follow‐up duration (months—post Device implantation)	23.8	20.5	36.8	18.1	0.04
Follow‐up duration (months after first documented VT)	29.0	23.2	52.8	34.9	0.01
No. of Appropriate AICD shocks	—	—	3.7	6.1	—
No. of ATP responsive VT/VF episodes	—	—	2.2	3.6	—
No. of VT/VF episodes before device implantation	1.4	2.2	1.3	1.1	NS
No. of VT/VF episodes after device implantation	0.3	1.3	6.2	6.7	‐
Heart failure hospitalization (no. of admissions)	0.1	0.3	0.6	1.2	0.09

Open in a new tab

AP19‐00844

Differential diagnosis between LQT1 and LQT2 by QT/RR relationships using 24‐hour Holter Monitoring

Kenji Yodogawa, Takeshi Aiba, Naokata Sumitomo, Wataru Shimizu

Nippon Medical School, Japan

Introduction:

The clinical course and the treatment consideration in the congenital long QT syndrome (LQTS) are genotype specific. However, accurate diagnosis is often challenging with standard 12‐lead ECG. We aimed to evaluate the utility of QT/RR slope by 24‐hour Holter monitoring for differential diagnosis between LQT1 and LQT2.

Methods:

Genetically identified 29 LQT1 patients and 25 LQT2 patients (mean age 23.4 + /‐14.9 years, 7 males) were enrolled. Consecutive sinus beats during each 15‐second period were averaged, and the linear regression slopes of the QT interval, measured to the apex and to the end of the T wave plotted against RR intervals (QTa/RR and QTe/RR slopes, respectively) were calculated from entire 24‐hour Holter recordings and separately during day and night periods.

Result:

Average QTe was significantly higher, and QTe/RR and QTa/RR slopes from entire 24‐hour Holter recordings were significantly steeper in the LQT2 patients in contrary to LQT1 patients (472.0 ± 40.6 vs 447.1 ± 44.8 milliseconds, P = .037; 0.262 ± 0.063 vs 0.204 ± 0.055, P = .0007; 0.233 ± 0.052 vs 0.181 ± 0.040, P = .0002, respectively). QTe/RR and QTa/RR slopes from daytime Holter recordings in the LQT2 patients were also significantly steeper than those in the LQT1 patients (0.197 ± 0.057 vs 0.158 ± 0.066, P = .024; 0.190 ± 0.048 vs 0.153 ± 0.050, P = .008, respectively). There were no significant differences in the other parameters. The receiver operating characteristic (ROC) curve analysis showed an optimal cutoff point of 0.211 of QTa/RR slope from entire 24‐hour Holter recordings, with 80.0% sensitivity, 75.0% specificity and area under the curve of 0.804 (95% confidence interval, 0.68‐0.93).

Conclusion:

QT/RR relationships using 24‐hour Holter monitoring may be useful for differential diagnosis between LQT1 and LQT2.

AP19‐00880

Patent foramen ovale with atrial septum aneurysm presenting with amaurosis fugax

Grace Lukito, Antonia Lukito, Ingrid Pardede

Pelita Harapan University, Indonesia

Introduction:

A patent foramen ovale (PFO) is an embryological remnant found in more than 25% of adults and more than half with concurrent atrial septal aneurysm (ASA). Although PFO are asymptomatic, this can result in clinical thromboembolic manifestations, including amaurosis fugax. Amaurosis fugax is a transient monocular vision loss which usually occurs in men aged over 50 yo who have vascular risk factors which placing them at higher risk of cerebral stroke.

Methods:

A 54‐yo male was referred from opthalmologist with sudden and transient right eye vision loss. He has poor controlled dyslipidemia and family history of stroke. The appropriate investigations were carried out include the laboratory studies, echocardiogram, and brain MRI. The laboratory results showed total cholesterol of 217 mg/dL and LDL‐C 171 mg/dL. The brain MRI was unremarkable, the TTE showed good LV function and mild dilated RV, the coronary CT which previously done in other hospital showed mild coronary lesion, over the re‐expertise, revealed dilated right ventricle and small‐ narrowed channel like of intraatrial septum. The TEE was then carried out using agitated saline‐bubble contrast, revealed the bubbles across the septum from right atrium to left atrium. The PFO with concurrent ASA was confirmed.

graphic file with name JOA3-35-4-g047.jpg

Result:

Patients with PFO associated with ASA are at higher risk of thromboembolic events. In this case, The patient has amaurosis fugax as an initial presentation, which may associated with the risk of future ischemic stroke. There has been ongoing debate about the role of percutaneous closure of PFO compared to medical therapy with antiplatelets or anticoagulants. Since this patient is younger than 60‐yo, no evidence of aortic arteriosclerosis disease nor hypercoagulable disorders, no vascular risk factor other than dyslipidemia, no evidence of atrial fibrillation and no terminal illness, this patient has meet the criteria for PFO Closure. Furthermore, the co‐existence of ASA, may enhanced the reason for PFO closure.

Conclusion:

Based on the evidence‐based algorithm for PFO closure by Mojadidi MK, et al, this patient presenting with amaurosis fugax and PFO with concurrent ASA is eligible to have a PFO closure. The detailed and thorough investigation should be carried out in patients with amaurosis fugax to reveal all possible causes and implement the appropriate management accordingly. The relative safety and simplicity of PFO closure and the proven protection against stroke open an avenue of further indications for PFO closure, such as in the presence of other potential causes of stroke or even as primary prevention of stroke in high‐risk persons.

AP19‐00884

Ionizing radiation exposure trends in the cardiac electrophysiology laboratory: A single centre experience

Muzaffar Ali, Deepak Padmanabhan, Bharatraj Banavalikar, Sinam Inaoton Singha, Milan Kumar Ghadei, Sanjai Pattu Valappil, Jayaprakash Shenthar

SJICR, Bangalore, India

Introduction:

Most of the procedures done in a cardiac electrophysiology laboratory are done under fluoroscopic guidance. Over the years the number and the complexity of the electrophysiological procedures have increased which also means increased ionizing radiation exposure and in turn increased risk of radiation injury to the patient, operators and other staff in the lab. One of the ways to reduce the ionizing radiation risk includes recording radiation exposure parameters and awareness of the same by the physicians delivering those exposures. Comparison of those exposures with the established norms also remains an integral part of the process.

Methods:

The aims of this study were: (a) to quantify ionizing radiation exposure in cardiac implantable electronic device (CIED) implantation and catheter ablation (CA) procedures in a large series of patients and (b) to analyze the radiation exposure trend over the time.

Result:

From September 2015 to December 2018, 3364 procedures were included in the analysis: 1616 procedures were device implantation procedures and 1748 were catheter ablation procedures. Single (pacemakers: 975; ICDs: 106) and dual chamber (pacemakers:439; ICDs:4) device implantation procedures and catheter ablation procedures without electroanatomic mapping (EAM) (n = 1490; AVNRT: 967; AP ablations: 483; AT: 21) showed a significant decrease in the radiation exposure parameters as well as the procedure time over the study period. Cardiac resynchronization therapy (CRT) device implantation procedures (n = 92) and catheter ablation procedures with EAM (n = 258) showed a significant decrease in radiation exposure parameters over the study period except for Effective Dose in ablations with EAM. Procedure time did not change significantly in CRT implantation procedures but decreased significantly in catheter ablation procedures with EAM.

Conclusion:

In this observational study we have been able to demonstrate that it is possible to significantly decrease radiation exposure in an electrophysiology lab by sticking to the standard practice of limiting radiation exposure as low as possible. As the number and the complexity of procedures done in an electrophysiology lab increases, it is imperative to employ methods that will decrease radiation exposure to the patients, operators and the support staff in the lab. We have demonstrated that using fluoroscopy routinely at 3.75 fps is feasible as well as significantly decreases radiation exposure.

TABLE 1 Radiation exposure data of all the procedures

Single chamber devices (n = 1081)	Dual chamber devices (n = 443)	CRT (n = 92)	Ablations without EAM (n = 1490)	Ablations with EAM (n = 258)
Procedure time (min)	75 (40‐270)	86 (45‐203)	152 (100‐235)	65 (30‐295)	172 (45‐360)
Fluoroscopy time (min)	8 (1‐84)	10 (2‐41)	26 (8‐62)	15 (3‐104)	29 (1‐95)
DAP (cGy.cm2)	836 (22‐13600)	1242 (71‐10046)	7275 (668‐42782)	1203 (57‐23168)	3066 (110‐33146)
ED (mSv)	2.0 (0.04‐27.2)	3.0 (0.1‐45.7)	16.2 (1.8‐85.6)	2.9 (0.1‐46.3)	7.1 (0.2‐91.5)
LAR, %	0.02 (0.0004‐0.272)	0.03 (0.001‐0.46)	0.16 (0.02‐0.86)	0.03 (0.001‐0.46)	0.07 (0.002‐0.9)

Open in a new tab

TABLE 2 CIED implantation procedures other than CRT devices

Mean age (yrs)	Male, %	Procedure time (min)	Fluoroscopy time (min)	DAP (cGycm2)	ED (mSv)	LAR, %
VVI (n=958)	64.3 (±15)	56	75 (40‐270)	8 (1‐84)	866 (37‐13600)	2.1(0.07‐27.2)	0.02 (0.0007‐0.27)
Single chamber ICD (n = 106)	55.7 (±14)	85	71 (40‐130)	6 (1‐23)	602 (22‐2911)	1.3 (0.04‐5.8)	0.01 (0.0004‐0.06)
AAI (n = 17)	58.7 (±10)	41	75 (45‐130)	6 (1‐14)	634(64‐1307)	1.5 (0.18‐3.24)	0.01 (0.002‐0.03)
DDD (n=439)	57.7 (±16)	64	86 (45‐203)	10 (2‐41)	1245 (71‐10046)	3.0(0.14‐45.7)	0.03 (0.0014‐0.46)
Dual chamber ICD (n=4)	60.8 (±10)	50	84 (45‐110)	12 (5‐16)	885 (373‐1850)	2.3 (0.75‐5.1)	0.02(0.007‐0.051)

Open in a new tab

TABLE 3 Catheter ablation procedures without EAM

Mean age (years)	Male, %	Procedure time (min)	Fluoroscopy time (min)	DAP (cGycm2)	ED (mSv)	LAR, %
AVNRT (n = 967)	47.8(±14)	43	58 (30‐170)	13 (3‐69)	846 (57‐13978)	2.1 (0.1‐28)	0.02 (0.001‐0.28)
AP (n = 483)	38.6(±14)	63	78 (30‐295)	20 (3‐104)	1879 (84‐23168)	4.6 (0.4‐46.3)	0.05 (0.004‐0.46)
AT (n = 21)	53.4(±15)	62	75 (35‐145)	20 (5‐48)	1789 (285‐9610)	4.4 (0.6‐26.5)	0.04 (0.006‐0.27)
AFL (n = 7)	53.6(±14)	86	118 (50‐285)	23 (8‐74)	2395 (454‐5057)	5.3 (0.9‐12)	0.05 (0.009‐0.12)
VA (n = 12)	45.8(±15)	67	71 (40‐165)	12 (5‐26)	1054 (328‐1851)	2.4 (0.7‐5.1)	0.02 (0.007‐0.05)

Open in a new tab

TABLE 4 Catheter ablation procedures with EAM

Mean age (years)	Male, %	Procedure time (min)	Fluoroscopy time (min)	DAP (cGycm2)	ED (mSv)	LAR, %
VA (127)	40.3(±16)	75	159 (50‐360)	25 (1‐78)	2531 (110‐31 737)	6.1 (0.2‐87.6)	0.06 (0.002‐0.88)
AFL (n = 75)	50.7(±14)	73	176 (60‐355)	33 (9‐95)	3539 (273‐33 146)	8.1 (0.8‐91.5)	0.08 (0.008‐0.92)
AT (n = 33)	46(±18)	45	171 (45‐310)	24 (6‐50)	2236 (323‐7005)	5.4 (0.6‐19.3)	0.05 (0.006‐0.19)
AF (n = 23)	52.5(±12)	74	237 (150‐330)	41 (13‐73)	5668 (502‐17 125)	12.4 (1.4‐34.3)	0.12 (0.01‐0.34)

Open in a new tab

graphic file with name JOA3-35-4-g048.jpg

AP19‐00890

Delayed association of particulate matter 2.5 air pollution exposure with loss of complexity in cardiac rhythm dynamics: Insight from detrended fluctuation analysis

Tsungying Tsai, Li‐Wei Lo, Shin‐Huei Liu, Wen‐Han Cheng, Yu‐Hui Chou, Wei‐Lun Lin, Yenn‐Jiang Lin, Shih‐Lin Chang, Yu‐Feng Hu, Fa‐Po Chung, Jo‐Nan Liao, Tze‐Fan Chao, Men‐Tzung Lo, Hui‐Wen Yang, Shih‐Ann Chen

Taipei Veterans General Hospital, Taiwan

Introduction:

PM2.5 (Ambient particulate matter <2.5 μm in aerodynamic diameter) exposure was associated with increased cardiovascular mortality and arrhythmia admissions. There was a delayed correlation between previous PM 2.5 exposure (lag 1‐2 days) and cardiovascular events, but the underlying mechanism remained unclear. We aimed to investigate the association between acute and delayed PM 2.5 exposure and cardiac autonomics through linear and non‐linear heart rate variability (HRV) analyses.

Methods:

Among 6912 patients who had received 24‐hour Holter ECG recordings between 1 October 2015 to 31 October 2016, 56 patients (31 males, 70.3 ± 12.7 years old) were enrolled with confirmation of living in the environment with reported PM 2.5 level. We classified the patients as high (>35.4 μg/m³), or low (<35.4 μg/m³) PM 2.5 groups according to their PM2.5 exposures on the day of the Holter recordings (day 0) and on lag 1‐2 days. The linear and non‐linear HRV parameters (Detrended fluctuation analysis [DFA] slope 1 and 2) were compared between groups.

Result:

Baseline characteristics including comorbidities and medications were similar between high and low exposure groups on all days. The linear and non‐linear HRV parameters were similar between the high and low exposure groups on day 0 and lag 1 day, respectively. However, the DFA slope 1 was significantly lower in higher exposure group on lag 2 days (0.784 ± 0.201 vs 0.964 ± 0.274, P = .021). Specifically, the DFA slope 1 of higher exposure group was significantly lower on daytime periods (9 am to 9 pm, 8 am to 4 pm and 4 pm to 12 pm) but not on nighttime periods.

Conclusion:

Our study demonstrated that previous PM2.5 exposure (lag 2 days) had a significant association with low DFA slope 1 and that the association is diurnal. Our results showed that air pollution may have a delayed impact on cardiovascular event risk through autonomic modulation.

Key word: Arrhythmia, Autonomic, Delayed effect, Nonlinear heart rate variability, PM

TABLE 1 HRV parameters between low and high PM2.5 exposure group on lag 2 day

HRV parameters	PM2.5 high (n = 16)	PM2.5 low (n = 40)	P value
Mean RR interval (ms)	828.14 ± 160.80	844.26±136.57	.706
SDNN	122.71±44.75	119.36±45.85	.562
LF	1029.68±2771.58	2548.12±12940.68	.814
HF	246.59±174.88	2812.25±16033.39	.211
LF/HF ratio	5.18±15.10	2.10±1.50	.217
DFA slope 1	0.78±0.20	0.96±0.27	.021
DFA slope 2	1.13±0.05	1.12±0.08	.858

Open in a new tab

DFA slope1, detrended fluctuation analysis slope 1; DFA slope2, detrended fluctuation analysis slope 2; HF, high‐frequency powers of the HRV; LF, low‐ frequency powers of the HRV; LF/HF ratio, low frequency/high frequency ratio; SDNN, standard deviation of the NN intervals; SDANN, standard deviation of sequential 5‐min R‐R interval; PM2.5, particulate matter <2.5 μm in aerodynamic diameter.

TABLE 2 Non‐linear HRV parameters between low and high PM2.5 exposure group on lag 2 day

Time periods	Parameters	PM2.5 high (n = 16)	PM2.5 low (n = 40)	P value
24 hours	DFA slope 1	0.78±0.20	0.96±0.27	.021
DFA slope 2	1.13±0.05	1.12±0.08	.858
9 am to 9 pm	DFA slope 1	0.77±0.22	0.99±0.29	.009
DFA slope 2	1.15±0.06	1.14±0.08	.744
9 pm to 9 am	DFA slope 1	0.80±0.21	0.94±0.28	.103
DFA slope 2	1.11±0.08	1.11±0.08	.986
8 am to 4 pm	DFA slope 1	0.77±0.21	0.98±0.31	.013
DFA slope 2	1.15±0.06	1.14±0.09	.404
4 pm to 12 pm	DFA slope 1	0.78±0.26	0.97±0.27	.027
4 pm to 12 pm	DFA slope 2	1.13±0.07	1.11±0.10	.663
12 pm to 8 am	DFA slope 1	0.80±0.20	0.93±0.30	.092
12 pm to 8 am	DFA slope 2	1.11±0.09	1.11±0.09	.957

Open in a new tab

DFA slope1, detrended fluctuation analysis slope 1; DFA slope2, detrended fluctuation analysis slope 2; HRV, heart rate variability; PM2.5, particulate matter <2.5 μm in aerodynamic diameter.

AP19‐00896

Myocardial fibrosis and clinical outcome in apical and non‐apical hypertrophic cardiomyopathy

Sanjai Pattu Valappil, Deepak Padmanabhan, Bharatraj Banavalikar, Milan Kumar Ghadei, Sinam Inaotan Singha, Muzaffar Ali, Jayaprakash Shenthar

Sri Jaydeva Institute of Cardiovascular Sciences, India

Introduction:

Transvenous pacing in patients with complex congenital heart disease (CHD) is challenging. Ventricular lead position in anterior wall or apex can lead to ventricular dysfunction. This study is to assess the utility of intraprocedural angiography as an aid in guiding septal placement of ventricular leads during transvenous permanent pacemaker implantation in patients with CHD.

Methods:

The study group consisted of patients with CHD and Class I or Class IIa indication for permanent pacemaker implantation and no contraindication for intravenous contrast agents. Angiography was performed through a pigtail catheter placed in the venous atrium /ventricle in the AP, LAO 40 degrees, and RAO 30 degrees using non‐ionic contrast agent. Angiography was done to define the intracardiac anatomy and to guide to placement of ventricular lead in the mid/anterior septum. Procedural success was defined as successful placement of the ventricular lead at the septal location that was validated by computed tomography (CT).

graphic file with name JOA3-35-4-g053.jpg

Result:

We used angiography for septal lead placement in 26 patients with CHD from January 2006 and July 2018. The study cohort included seven post‐surgical patients with repaired complex congenital heart disease and 19 patients with uncorrected congenital heart disease. The indication for permanent pacing was symptomatic AV block in 23 patients and sick sinus syndrome in three patients. The mean age was 19 + 8 years with male to female ratio of 16:10. The most common underlying CHD was corrected transposition of great arteries (ccTGA). Cardiac CT was performed in 24/26 patients and the ventricular lead was in the anterior septum in 19 and mid‐septum in seven patients. The mean paced QRS duration measured by electronic calipers was 132 + 10 milliseconds. The mean contrast used during the pacemaker implantation was 100 + 20 mL with average fluoroscopy time of 10 + 3 minutes. The acute procedural success was 100%. All patients tolerated the procedure well and there were no complications associated with the implantation procedure. There were no lead dislodgements or device related issues on follow up. The average duration of follow up was 44 + 18 months.

Conclusion:

Venous angiography assists the implanter to gain real time knowledge of the complex anatomy and serves as a useful aid for septal lead placement in patients with complex CHD. Angiography is safe and can be considered as an additional imaging technique during pacemaker implantation in complex CHD.

AP19‐00967

Correlation of QRS amplitude with left ventricle geometry and body size in non‐ischemic cardiomyopathy with left bundle branch block

Maki Ono, Niraj Varma

Cleveland Clinic, USA

Introduction:

QRS amplitude in electrocardiogram has been evaluated in normal population based on ethnicity and age and in cardiac hypertrophy, but not in heart failure patients in whom left ventricle (LV) mass may increase. Moreover, ECG voltage, body size and LV size may modulate result of cardiac resynchronization therapy (CRT). Hence, we evaluated the correlation of QRS amplitude with LV geometry and body size in heart failure population with left bundle branch block (LBBB).

graphic file with name JOA3-35-4-g054.jpg

Methods:

Preoperative QRS amplitudes in 12 leads were retrospectively analyzed in CRT patients with NYHA III/IV, non‐ischemic cardiomyopathy, and ‘true’ LBBB defined by Strauss criteria.

Result:

12 lead ECGs were recorded in 184 patients (age 61 ± 12 years; male 45%; LVEF 19 ± 7%; QRS duration 165 ± 20 milliseconds). QRS voltage in each lead had no correlation with LV mass or end‐systolic volume. In aVR, there was negative correlation with end‐diastolic diameter (P = .03, r = −.185) and end‐ systolic diameter (P = .001, r = −.273) and positive correlation with relative wall thickness (P = .002, r = .261). QRS voltage in lead I and aVL had negative correlation with height (P = .04, r = −.171, P = .04, r = −.173). With body mass index, lead I had positive correlation (P = .003, r = .245) and V3‐V6 had negative correlation (V3; P = .03, r = −.176, V4; P = .01, r = −.215, V5; P = .01, r = −.211, V6; P = .005, r = −.235).

Conclusion:

QRS amplitude did not correlate with left ventricle mass or volume, but showed significant though weak correlation with diameter and body size in some leads. ECG voltage may describe qualities of electrical substrate rather than simply LV or body size. This may be important for CRT.

AP19‐00992

Abnormal cardiac electrical remodelling in POTS: Mechanistic insights on potential autonomic dysregulation

Varun Malik, Anand Thiyagarajah Thiyagarajah, Dian Andien Munawar, Adrian Elliott, Dominik Linz, Ricardo Mishima, Mehrdad Emami, Rajiv Mahajan, Prashanthan Sanders, Dennis Lau

Royal Adelaide Hospital, Australia

Introduction:

Postural Orthostatic Tachycardia Syndrome (POTS) is a syndrome characterized by dysautonomia. It remains unknown if POTS individuals have abnormal cardiac electrical changes. To assess electrocardiographic markers of inter‐ atrial and ventricular conduction delay in POTS compared to patients with a history of vasovagal syncope (VVS).

Methods:

Patients who met diagnostic criteria for POTS by tilt table test and free of other autonomic or structural heart disease were compared to VVS patients. 12 lead ECGs taken pre‐ treatment were digitized (minimum 8 good quality signals) and analyzed by a cardiologist blinded to treatment. P wave and RT dispersion (PWD, RTD) were calculated (maximum–minimum P wave/RT interval duration). Peak of T‐ to‐ end of T wave (TpTe), a marker of transmural dispersion of ventricular repolarization, also sensitive to sympathetic stimulation, was measured in lead II.

Result:

11 POTS patients were compared to 9 age and sex ‐ matched VVS patients. Mean age was similar. Atrial volumes and left ventricular ejection fraction (LVEF) were normal in all patients. There was no difference in LVEF. POTS was associated with abnormal PWD (normal cut‐off 38 milliseconds) and higher RTD; taken pre‐treatment, despite lower left atrial volume. Baseline TpTe did not differ (Table 1).

Conclusion:

Compared to VVS, POTS is associated with both longer PWD (above described normal limits) and increased RTD, whilst TpTe did not differ, despite systemic sympathetic predominance in POTS. Further clinical studies are warranted to assess the relative role of subclinical cardiac structural remodeling and/or impaired cardiac autonomic nervous system for these ECG findings.

TABLE 1

POTS (n = 11)	VVS (n = 9)	P value
Baseline characteristics
Age	25	27	0.6
Females, n (%)	9 (82%)	7 (78%)	0.99
Left atrial volume; indexed to body surface area (mL/m2)	19 ± 1	24 ± 1	0.01
LVEF (%)	61	61	0.9
Heart rate (bpm)	79 ± 3	66 ± 3	0.007*
Electrical (ECG) markers
P wave Dispersion (ms)	48 ± 5	31 ± 4	0.02*
RT Dispersion (ms)	66 ± 7	46 ± 6	0.04*
TpTe (ms)	79 ± 5	80 ± 3	0.9

Open in a new tab

Continuous variables: Students t‐test. Categorical variables; Fishers exact test. Statistical significance defined as P < .05 (*).

AP19‐00994

Preexcitation and myocardial infarction: A case ith pre‐ and post percutaneous coronary intervention and pre‐ and postablation

Chye‐Gen Chin, Weita Chen, Ming‐Hsiung Hsieh

Taipei Municipal Wan Fang Hospital, Taiwan

Introduction:

The electrocardiographic (ECG) diagnosis of myocardial infarction (MI) in patients with Wolff‐Parkinson‐white (WPW) syndrome is often difficult (1,2). The abnormal activation sequence in WPW syndrome may mask the characteristic ECG findings of MI. The presence or absence of Q waves is often confusing in patients with preexcitation and possible infarction. Besides from delta wave, some reports also attributed the apparent T‐wave changes in pre‐excited patients to the clinical manifestations of acute ischemic injury (3,4). This report describes an occurrence of myocardial infarction in a patient WPW syndrome.

Methods:

Case presentation A 60‐year‐old male patient presented as chest pain during exercise. His past medical history was unremarkable except for a 20 years history of smoking. The initial ECG showed sinus rhythm with positive delta waves in the precordial leads, lead I and lead aVL, and negative delta waves in the inferior leads (Figure 1). Physical examination was unremarkable and the laboratory data revealed normal serum level of troponin I, maximum creatine kinase(CK), and creatine kinase ‐MB (0.01 [ng/mL], 68 (U/L), and 1.7 (ng/ML), respectively). Most of the discomfort was resolved after taking nitroglycerin. The follow up laboratory data after 12 hours were significant for a CK–MB of 12.7 (U/L) and troponin I of 1.19 (ng/mL) coexisting with isoelectric ST‐segments in the lead aVL and precordial leads (Figure 2). Cardiac catheterization was performed on the next day which revealed significant stenosis of the proximal left anterior descending artery (LAD). Percutaneous coronary intervention was performed, and a stent was deployed into the proximal to middle LAD. The ECG at two days later showed negative T waves in leads V3‐V6 (Figure 3). One month later, ECG showed persistent preexcitation with resolution of repolarization abnormalities (Figure 4). This patient then underwent an invasive electrophysiologic study which demonstrated a ventricular bypass tract with inducible orthodromic atrioventricular reciprocating tachycardia. Radiofrequency ablation for the right posterior septal wall accessory pathway was done successfully. The 12‐lead ECG demonstrating the memory T wave after ablation is presented in Figure 5. One week after his ablation, ECG showed a normal PR interval and the disappearance of preexcitation (Figure 6).

Result:

Discussion Only a few cases in the literature reported a clear diagnosis of myocardial infarction in pre‐excited patient by other techniques and validated ECG data, which were masked by pre‐ excitation or ST‐T change.(1,5). This case provides a unique opportunity for continuous electrocardiographic observation of myocardial infarction and after radiofrequency ablation.

Conclusion:

Acute myocardial infarction and pre‐excitation can occur simultaneously. Clinicians should be aware of this ECG pitfall to avoid misdiagnosis

FIGURE 1 This ECG, demonstrates sinus rhythm and preexcitation. There is positive delta wave in precordial lead lead I and lead aVL, negative delta wave in inferior lead. The ST‐segment is mild concave elevation in leads V1–V6 an t wave inversion in aVL

graphic file with name JOA3-35-4-g055.jpg

FIGURE 2 After 12 hours coexisting with cardiac enzyme release. Secondary ST depression with negative T waves is not present in the precordial leads. On the contrary, the ST‐segment is became isoelectric in leads V1‐V6 and avL

graphic file with name JOA3-35-4-g056.jpg

FIGURE 3 An ECG 2 days after admission shows newly emerged negative T waves in leads V3‐V6

graphic file with name JOA3-35-4-g057.jpg

FIGURE 4 A ECG was taken 1 months later after hospital discharge. It demonstrates persistent preexcitation, with resolution of repolarization abnormalities

graphic file with name JOA3-35-4-g058.jpg

FIGURE 5 Following ablation, the ECG demonstrates sinus rhythm with a normal PR interval and disappearance of preexcitation. There is a ST elevation and tall T waves in precordial lead, ST depression in inferior lead suggestive memory t wave

graphic file with name JOA3-35-4-g059.jpg

FIGURE 6 One week after ablation, the ECG demonstrates sinus rhythm without preexcitation and ST‐T change was disappear

graphic file with name JOA3-35-4-g060.jpg

graphic file with name JOA3-35-4-g061.jpg

AP19‐01001

Prevalence and factors associated with early repolarization electrocardiographic patterns among adults in the Philippines

Joseph Marc Seguban

Philippine Heart Center, Philippines

Introduction:

Early repolarization electrocardiographic pattern has been implicated in syndrome of ventricular tachyarrhythmias but the local prevalence is unknown and there is limited knowledge on associated factors.

Methods:

National Nutrition Health Survey (NNHeS) was a cross‐sectional nationwide survey performed in 2003 to determine atherosclerosis‐related diseases and risk factors using a stratified multistage sampling design covering all the regions and provinces in the Philippines. Electrocardiograms (ECG) were performed in adult subjects surveyed. This is a cross‐sectional analytical study involving the retrospective review of the 4340 ECG recordings and NNHeS database to determine the prevalence of ERP including its types and associated risk factors. Risk factors for ERP were evaluated using binary logistic regression analysis.

Result:

The overall prevalence of ERP in was 8.46%, higher in males than females (6.05% vs 2.4%), and decreasing with increasing age. Percentages of the different types of ERP, Type 1 was 21.6%, Type 2 was 78% and Type 3 was 0.28%. Binary logistic regression demonstrated that independent factors for ERP were age OR = 0.99 (CI: 0.9843‐0.9957, P < .001), male sex OR = 3.0297 (CI: 2.3856‐3.8477, P < .001), without hypertension OR = 0.5630 (CI: 0.4136‐0.7664, P < .001) and Living in region 7 OR = 1.4891 (1.0417‐2.1287, P = 0.029).

Conclusion:

ERP is common among Filipinos occurring in 8 per 100 of the population. Younger age, males, no hypertension and those living in region 7 in the Philippines are the independent factors of having early repolarization pattern.

TABLE 1 Demographic and clinical profile

Total (n=4206)	With ERP (n=356, 8.46%)	Without ERP (n=3850, 91.54%)	P‐value
Frequency (%); Mean + SD			P‐value
Age	52.56 + 18.75	49.28 + 18.50	52.85 + 18.74	<.001
Less than 20	23 (0.55)	4 (1.12)	19 (0.49)	.01
20 to 29	635 (15.10)	64 (17.98)	571 (14.83)
30 to 39	629 (14.95)	66 (18.54)	563 (14.62)
40 to 49	517 (12.29)	49 (13.76)	468 (12.16)
50 to 59	319 (7.58)	18 (5.06)	301 (7.82)
60 to 69	1260 (29.96)	99 (27.81)	1161 (30.16)
More than 69	823 (19.57)	56 (15.73)	767 (19.92)
Sex	<.001
Male	2005 (47.67)	255 (71.63)	1750 (45.45)
Female	2201 (52.33)	101 (28.37)	2100 (54.55)
Diabetes mellitus	133 (3.16)	7 (1.97)	126 (3.27)	.178
Hypertensive	916 (21.78)	50 (14.04)	866 (22.49)	<.001

Open in a new tab

TABLE 2.1 Regional profile

Total (n=4206)	With ERP (n=356, 8.46%)	Without ERP (n=3850, 91.54%)	P‐value
Frequency (%)			P‐value
Region 1	228 (5.42)	20 (5.62)	208 (5.40)	.807
Region 2	288 (6.85)	25 (7.02)	263 (6.83)	.913
Region 3	427 (10.15)	30 (10.96)	388 (10.08) 0.582
Region 4	486 (11.55)	44 (12.36)	442 (11.48) 0.604
Region 5	327 (7.77)	30 (8.43)	297 (7.71)	.605
Region 6	222 (5.28)	21 (5.90)	201 (5.22)	.537
Region 7	324 (7.70)	38 (10.67)	286 (7.43)	.037
Region 8	194 (4.61)	3 (0.84)	191 (4.96)	<.001
Region 9	147 (3.50)	8 (2.25)	139 (3.61)	.226
Region 10	208 (4.95)	12 (3.37)	196 (5.09)	.200
Region 11	183 (4.35)	17 (4.78)	166 (4.31)	.683
Region 12	153 (3.64)	13 (3.65)	140 (3.64)	1.000
Region 13	173 (4.11)	7 (1.97)	166 (4.31)	.035
Region 14	349 (8.30)	23 (6.46)	326 (8.47)	.227
Region 15	176 (4.18)	20 (5.62)	156 (4.05)	.165
Region 16	107 (2.54)	11 (3.09)	96 (2.49)	.480
Region 17	214 (5.09)	25 (7.02)	189 (4.91)	.100

Open in a new tab

TABLE 2.2 Types of ERP per region

With ERP (n=356, 8.20%)	Type 1 (n=77, 21.63%)	Type 2 (n=278, 78.09%)	Type 3 (n=1, 0.28%)
Frequency (%)			Type 3 (n=1, 0.28%)
Age	49.28 + 18.50	39.84 + 16.11	52 + 18.23	21
Less than 20	4 (1.12)	1 (25)	3 (75)	0
20 to 29	64 (17.98)	21 (32.81)	42 (65.63)	1 (1.56)
30 to 39	66 (18.54)	26 (39.39)	40 (60.61)	0
40 to 49	49 (13.76)	10 (20.41)	39 (79.59)	0
50 to 59	18 (5.06)	4 (22.22)	14 (77.78)	0
60 to 69	99 (27.81)	10 (10.10)	89 (89.90)	0
More than 69	56 (15.73)	5 (8.93)	51 (91.07)	0
Sex
Male	255 (71.63)	65 (25.49)	189 (74.12)	1 (0.39)
Female	101 (28.37)	12 (11.88)	89 (88.12)	0
Diabetes mellitus	7 (1.97)	1 (14.29)	6 (85.71)	0
Hypertensive	50 (14.04)	4 (8)	46 (92)	0

Open in a new tab

TABLE 2.3 Types of ERP per demographic profile

With ERP (n=356, 8.20%)	Type 1 (n=77, 21.63%)	Type 2 (n=278, 78.09%)	Type 3 (n=1, 0.28%)
Frequency (%)
Region 1	20 (5.62)	3 (15)	17 (85)	0
Region 2	25 (7.02)	3 (12)	22 (88)	0
Region 3	39 (10.96)	9 (23.08)	30 (76.92)	0
Region 4	44 (12.36)	7 (15.91)	36 (81.82)	1 (2.27)
Region 5	30 (8.43)	6 (20)	24 (80)	0
Region 6	21 (5.90)	6 (28.57)	15 (71.43)	0
Region 7	38 (10.67)	5 (13.16)	33 (86.84)	0
Region 8	3 (0.84)	0	3 (100) 0
Region 9	8 (2.25)	1 (12.50)	7 (87.50)	0
Region 10	12 (3.37)	3 (25)	9 (75)	0
Region 11	17 (4.78)	4 (23.53)	13 (76.47)	0
Region 12	13 (3.65)	3 (23.08)	10 (76.92)	0
Region 13	7 (1.97)	4 (57.14)	3 (42.86)	0
Region 14	23 (6.46)	9 (39.13)	14 (60.87)	0
Region 15	20 (5.62)	4 (20)	16 (80)	0
Region 16	11 (3.09)	4 (36.36)	7 (63.64)	0
Region 17	25 (7.02)	6 (24)	19 (76)	0

Open in a new tab

TABLE 3 Factors of ERP

Variables	Odds ratio	95% CI	P‐value
Age	0.9900	0.9843 to 0.9957	.001
Male patients	3.0297	2.3856 to 3.8477	<.001
Hypertensive	0.5630	0.4136 to 0.7664	<.001
Region 7	1.4891	1.0417 to 2.1287	.029
Region 8	0.1628	0.0518 to 0.5120	.002
Region 13	0.4451	0.2073 to 0.9558	.038

Open in a new tab

AP19‐01002

Clinical outcome of typical atrial flutter after radiofrequency catheter ablation

Kiyung Boo, Jong‐Il Choi, Yun Young Choi, Ha Young Choi, Do Young Kim, Yun Gi Kim, Kwang‐No Lee, Jaemin Shim, Jin Seok Kim, Young‐Hoon Kim

Korea University Medical Center, South Korea

Introduction:

In the current guideline, treatment and stroke prevention strategies are known to be similar with AF, however, there is a lack of data on coexistence of AF and evaluation of thromboembolic risk and clinical event in patients with AFL.

Methods:

We retrospectively evaluated patients who underwent RFCA for typical atrial flutter at in a tertiary center. The presence of AF before and after CTI ablation was assessed, and compared the clinical and echocardiographic parameters between two groups.

Result:

A total of 138 consecutive patients were successfully treated with CTI ablation (79% male; 52 ± 16 years). Eleven patients (8%) had AF before the ablation and 40 patients (31%) were newly diagnosed with AF after the procedure (total 51 patients were AF [37%]). LA diameter was significantly larger in patients with AF compare to those without AF (42.7 ± 7.1 mm vs 39.8 ± 7.5 mm, P = .048). However, there was no event of thromboembolism in both group, and only two noncardiac deaths were observed in patients without AF.

Conclusion:

This study demonstrated that atrial flutter showed a progression from AF up to 31%, and there was significantly larger in LA diameter in those patients. Although atrial flutter is limited to assess thromboembolic risk, it is suggested that anticoagulation may be performed by evaluating the possibility of AF based on remodeling of LA.

AP19‐01019

My first experience in EP lab: Serial cases of Parahisian accessory pathway in young adult

Ulzim Fajar, Hauda El Rasyid

Medical Faculty of Andalas University, Padang, Sumatera Barat, Indonesia

Introduction:

DR M Djamil General Hospital is one of referral center hospital in Sumatera Barat, Indonesia. We have new electrophysiology study lab that perform our very first arrhythmia patient which was diagnostic as parahisian accessory pathways. Radiofrequency catheter ablation of parahisian accessory pathways is a challenging task, due to the extremely high risk of complete atrioventricular block. In this brief report we describe the serial case of young adult persons a 17 year‐old man and 33 year‐old woman presenting a parahisian accessory pathway, who has not been followed to radiofrequency ablation. Radiofrequency catheter ablation using low‐power radiofrequency current is considered to be the most appropriate method of ablation in adult patients, and plan to be performed in tertiary hospital

Methods:

A 17‐year‐old young man presented with episodes of recurring tachycardia since 1 years. The episodes recurred up to five times per month, lasted up to 30 minutes, and were accompanied by dizziness. The patient is a high school student. He underwent a first EP study in 12 January 2019. Ventricular overdrive pacing from the right ventricular (RV) apex is used to establish the mechanism of supraventricular tachycardia (SVT) and showed earliest A activation in His, with RV ERP 200 milliseconds and AVN ERP retro 260 milliseconds. Pacing from HRA showed Parahisian pacing was compatible with the presence of an accessory pathway (AP) with AVN antegrade 260 milliseconds and AERP 230 milliseconds. The ablation procedures was canceled due to this parahisian accessory pathway. Second case, was a 33‐year‐old woman presented with episodes of recurring tachycardia since 4 years. The episodes recurred up to three times per month, lasted up to 30 minutes, and were accompanied by dizziness intermittently. The patient is a housewife. She underwent a EP study in the same day. Parahisian pacing was compatible with the presence of an accessory pathway as well, and the ablation procedures were canceled.

Result:

The ablation of accessory pathways is the recommended treatment in patients who present with episodes of supraventricular tachycardias, when an EPS proves the relatively short anterograde refractory period of the accessory pathway.¹⁰ Accessory pathway ablation has a 95%‐99% success rate with a recurrence of 5%‐10%.^10–14 A severe complication is the complete AV block resulting in the need for permanent pacemaker implantation. In order to reduce the risk of complications, ablation using lower energy levels can be performed⁶, based on cryothermia‐based mapping¹⁵ or magnetic navigation.¹⁶ In both case that reported here, neither of them underwent ablation of accessory pathways, for avoiding a complete AV block.

Conclusion:

We reported serial cases of young adult patient which was diagnosis as parahisian accessory pathway. Radiofrequency of catheter ablation at this site is a challenging task to do in district hospital.

Keywords: Parahisian accessory pathway, accessory pathway, young adult palpitation, ep study

AP19‐01022

What are we missing in teaching our medical students ECG interpretation?

Palapun Waitayangkoon, Thiratest Leesutipornchai, Sittinun Thangjui, Thanaporn Ratchataswan, Sowitchaya Panthong, Aekarach Ariyachaipanich

Chulalongkorn, Thailand

Introduction:

Studies showed that medical students had a good level of competency in interpreting basic ECG parameters but failed to recognize common ECG emergencies. Our study aims to determine ECG interpretation skill competencies among medical students in Thailand.

Methods:

We retrospectively studied ECG exam results of 4th‐year medical students who enrolled in a 6‐year MD program at Chulalongkorn university between 2014‐2018. All students were taught to interpret ECG by a mandatory lecture and bedside teachings, and were tested at the end of their medicine rotation. Each rotation was randomly assigned to interpret ECG with a different diagnosis of common ECG emergencies. Answers for basic parameters and primary diagnosis were scored as either correct or incorrect. Data were presented as percentages of the correct answers, which were considered low if the values were less than 50%.

Result:

A total of 10 ECG tracings with 4 common ECG emergencies, atrial fibrillation (AF), atrial flutter, supraventricular tachycardia (SVT) and acute myocardial infarction (MI), were interpreted by 480 students. Competency in interpreting basic ECG parameters was 83%, 85% and 60% for electrical axis, heart rate, and heart rhythm, respectively. Among the common ECG emergencies, atrial flutter was the most correctly interpreted (78%), whereas AF was the least correctly interpreted (16%). Only 34% were able to correctly interpret SVT. The overall accuracy of acute MI interpretation was 69%. Of these, inferior MI was the most correctly identified (71%). Anterior, lateral and septal MIs were correctly identified in 57%, 22% and 14% of students.

Conclusion:

The majority of students were proficient in interpreting basic ECG parameters and some common ECG emergencies such as atrial flutter, inferior MI, and anterior MI, but lack the capability of recognizing AF, septal MI, and lateral MI. This highlights the necessity to improve our medical students’ ECG interpretation competency.

AP19‐01025

A rare three‐dementional mapping in partial atrial standstill

Jun Hirokami, Yohei Sadohara, Kei Yamamoto, Rei Kuji, Kengo Kohrai, Junji Morita, Masato Fukunaga, Michio Nagashima, Kenichi Hiroshima, Kenji Ando

Kokura Memorial Hospital, Japan

Introduction:

Atrial standstill (AS) is characterized by the loss of electric and mechanical activity. Moreover, AS has been reported in families with autosomal dominant Brugada syndrome with the alpha subunit of the cardiac Na+ channel (SCN5A) mutations. We present a case that three‐dimensional (3D) mapping system showed partial left atrial AS and recovery of the electric activity using isoproterenol infusion.

Methods:

A 41–year‐old female was referred to our cardiology department with paroxysmal palpitation and short of breathness. She denied any syncope, dizziness, and chest pain. As a past medical history, she experienced cardiogenic stroke due to paroxysmal atrial fibrillation (AF), revealed by insertable cardiac monitoring system. She took apixaban 10 mg/d. Her father had advanced atrioventricular block, underwent pacemaker implantation and her son was diagnosed as Brugada syndrome. They also had SCN5A mutations.

Result:

An electrocardiogram showed atrial bigeminy at a rate of 67 beat per minutes and was otherwise normal. A chest X‐ray showed cardiomegaly without pulmonary congestion. The echocardiogram revealed normal ventricular systolic function and no left atrial dilation. She underwent catheter ablation for AF using the Abbott Ensite Precision Cardiac Mapping SystemTM with AdvisorTM HD Grid Mapping Catheter, Sensor Enabled. During the procedure, no electrical activity was recorded in the almost whole left atrium, whereas right atrium was normal. After bilateral pulmonary vein isolations, it recovered by isoproterenol infusion to check the dormant conductions and dissipated rapidly with time. Isoproterenol also improved mechanical activity of left atrium and auricular appendage in postoperative transesophageal echocardiography.

graphic file with name JOA3-35-4-g062.jpg

Conclusion:

This is the first case report about transformation of atrial viability; unique response to isoproterenol infusion in AS, visualized by 3D mapping system. Isoproterenol has been shown to be effective in electrical and mechanical recovery of AS by increasing sodium current due to beta‐receptor activation. We provide AS with SCN5A mutations is essentially a matter of sodium channel dysfunction.

AP19‐01034

Wide QRS waveform thought to be caused by hypoglycemia

Rie Akagawa, Yukio Hosaka, Osamu Saito, Kazuyoshi Takahashi, Keiichi Tsuchida, Komei Tanaka, Yuta Sakaguchi, Kenji Nakano, Norihito Oyanagi, Shinya Fujisaki, Yuka Sekiya, Masaomi Chinushi, Hirotaka Oda

Niigata City General Hospital, Japan

Introduction:

Electrolyte abnormalities are known to cause wide QRS waveforms and ventricular arrhythmias (VAs). However, hypoglycemia is not thought to induce VAs. We report a case with hypertrophic cardiomyopathy, a wide QRS waveform, and VAs that improved by correcting hypoglycemia.

Methods:

N/A.

Result:

An 86‐year‐old women with hypertrophic cardiomyopathy and chronic kidney disease had been treated for chronic heart failure. She was referred to our hospital for dyspnea caused by acute exacerbation of her chronic heart failure. On admission, her electrocardiogram showed a heart rate of 84 bpm with a QRS waveform (140 msec). She was administered diuretics intravenously, but she was unable to urinate. Her consciousness and respiratory condition gradually had become worse. Her blood tests revealed hypoglycemia (29 mg/dL) and hyperkalemia (6.6 mmol/L). The monitored electrocardiogram exhibited a heart rate of 90 bpm with a wide QRS waveform (200 msec). After a blood sugar correction, the QRS width improved rapidly to 130 msec. As the QRS width improved rapidly to a narrow QRS due to the blood glucose correction, hypoglycemia was suspected as the cause of the wide QRS waveform. We examined the relationship between the hypoglycemia and VAs. We performed a perfusion of a porcine myocardial section and examinations were performed using three different conditions of the perfusion solution. The first solution had a control glucose level (100 mg/dL) and control potassium level (4.0 mmol/L). The second solution had a low glucose level (30 mg/dL) and control potassium level. The third solution had a low glucose level and high potassium level (8.0 mmol/L). We analyzed the inducibility of the VAs with programed electrical stimulation. Under the condition of a low glucose level and control potassium level, the VAs were likely to be induced and sustained. On the other hand, under the condition of a control glucose level and high potassium level, the VAs were likely to be decreased.

Conclusion:

Clinically, as the QRS width improved rapidly to a narrow QRS due to a corrected blood glucose level, hypoglycemia was suspected as the cause of the wide QRS waveform. Further, experimentally, it was suggested that there is a relationship between hypoglycemia and VAs. Therefore, it is suggested that hypoglycemia should be suspected as a possible cause of a wide QRS waveform.

AP19‐01062

Circadian index as a predictor of high premature ventricular contraction burden: Padang ectopic beat (PEcBEAT) registry

Deri Arara, Hauda El Rasyid, Tommy Daindes

M. Djamil Hospital, Indonesia

Introduction:

Circadian Index (CI) was known as an indicator of stable organization of heart circadian rhythm and greatly influenced by an autonomic nervous system. Apart from, a premature ventricular contraction (PVC) also associated with the changes of sympathetic nerve regulation. This study aimed to identify the power of CI in predicting PVC burden and set an optimal cut‐off value.

Methods:

The subjects of this study were 337 consecutive patients referred for 24‐hour ECG monitoring for palpitations, dizziness, or syncope. Circadian index (CI) was calculated as the ratio of the average heart rate during day time (beat per minute) to average night time. High premature ventricular contraction (PVC) burden was defined as ≥10.000 PVC/24 hours.

Result:

In this study, 222 subjects were women (66%), with the mean age was 46.6 ± 16.5 years. Using MedCalc software version 17.9, the correlation coefficient between circadian index and PVC burden was −0.26 (P < .0001; 95% CI −0.36 to −0.16). On the other words, there was a negative correlation between both variables, a lower CI was associated with higher PVC burden. Area under Curve (AUC) value was 0.814, an excellent prediction power. We also found an optimal cut‐off value of CI was ≤1.18 (93.3% sensitivity and 56.3% specificity) in predicting high PVC burden.

graphic file with name JOA3-35-4-g063.jpg

graphic file with name JOA3-35-4-g080.jpg

graphic file with name JOA3-35-4-g081.jpg

Conclusion:

Circadian index has an powerful sensitivity in screening a high PVC burden.

graphic file with name JOA3-35-4-g064.jpg

AP19‐01094

Complete heart block in pregnancy: When to pacing?

Hendyono Lim, , ANTONIA Anna Lukito

Siloam Hospital Lippo Village, Indonesia

Jin Hee Choi, Ki Won Hwang, Hyun Myung Cho, Soon Myung Jung, Soo Yong Lee, Min Ku Chon, Sang Hyun Lee, Jeong Su Kim, Yong Hyun Park, June Hong Kim, Kook Jin Chon

Pusan National University Yangsan Hospital, South Korea

Introduction:

There was little known about renal function changes over time and transient worsening of renal function in patients with atrial fibrillation (AF) undergoing non‐vitamin K‐dependent antagonist oral anticoagulants (NOAC). The purpose of this study is to evaluate the incidence of acute kidney injury (AKI) and efficacy and safety of NOAC in AF patients with AKI.

Methods:

Patients with nonvalvular AF who started taking a NOAC from 2015 to 2017 were identified. Between 2015 and 2017, data were analyzed 279 patients with treatment NOAC, who underwent two or more serial creatinine measurements.. AKI was defined as (a) an increase in serum creatinine (sCr) of ≥0.3 mg/dL; (b) an increase in sCr to ≥150% of baseline. We defined major adverse cardiovascular events (MACEs) as the composite of all‐cause mortality, myocardial infarction, or stroke; and cardiovascular hospitalization, and clinically significant major bleeding. The risk of MACEs, cardiovascular hospitalization, and major bleeding was analyzed with Cox proportional hazard models.

Result:

Among 279 patients included in the analysis, the median age was 71 years and 49.5% of patients were male. AKI was observed in 59 patients (21.1%) and was associated with older age, DM, and heart failure. The risk of MACE and major bleeding was not significant associated with AKI (HR, 1.251; 95% CI, 0.246‐6.367 for MACE; and HR, 1.895; 95% CI, 0.339‐10.605 for major bleeding). Only cardiovascular hospitalization was significantly higher in patients with AKI (HR, 2.789; 95% CI, 1.182‐6.58

Conclusion:

AKI is more common in patients with older age, DM, and heart failure in AF patients with NOAC. The patients with AKI had a higher risk of cardiovascular hospitalization than the patients without AKI. Our results suggest that identification of renal function is essential to reduce the risk of cardiovascular hospitalization.

	Total (n = 279)	AKI (n = 59)	No AKI (n = 220)	P value
Outcome
MACE	8 (2.9%)	2 (3.4%)	6 (2.7%)	.678
All cause mortality	3 (1.1%)	1 (1.7%)	2 (0.9%)	.511
SEE	2 (0.7%)	1 (1.7%)	1 (0.5%)	.379
Myocardial infarction	3 (1.1%)	0 (0.0%)	3 (1.4%)	1.000
Major bleeding	6 (2.2%)	2 (3.4%)	4 (1.8%)	.610
Cerebral hemorrhage	3 (1.1%)	0 (0.0%)	3 (1.4%)	1.000
GI bleeding	3 (1.1%)	2 (3.4%)	1 (0.5%)	.114
Cardiovascular hospitalization	25 (9.0%)	10 (16.9%)	15 (6.8%)	.016

Open in a new tab

AP19‐01126

New onset left bundle branch block after TAVR: EP study guided pacemaker implantation

Arijit Chanda

Mary Washington Hospital, United States

Introduction:

Transcatheter Aortic Valve Replacement (TAVR) has now become the dominant method of aortic valve replacement in the United States, with excellent outcomes. New onset LBBB (NLBBB) is seen in up to 20% of patients post TAVR. There has not been a broad consensus about protocols regarding permanent pacemaker (PPM) placement in these cases, though the death and urgent pacemaker placement in this group is about 23%. The question remains, how do we evaluate the need for PPM placement in these patients. We developed an EP study guided protocol with administration of procainamide. PPM was implanted if the baseline HV interval is ≥ 80 ms during the EP study, if not, then patients were administered 1000 mg of procainamide over 10 minutes infusion, if the HV interval prolonged to 80 ms or greater then PPM was implanted. Here we report our findings

Methods:

Retrospective data was collected about patients with new onset LBBB post TAVR between 2017 and 2019. Baseline characteristics, including valve type, age, gender, ECG findings, EF, HV interval pre and post procainamide infusion was recorded. Outcomes assessed were, need for future pacemaker placement, survival and follow up Ejection Fraction (EF).

Result:

Total of 81 patients underwent TAVR during this time period, 11 patients had NLBBB (13.6%). Baseline QRS duration was 99 ± 11 ms. Post TAVR QRS duration was 141 ± 12, HV interval was 61.9 ± 9 ms, HV interval post procainamide was 66.8 ± 14 ms. PPM was placed in 9% of the patients. Follow up was 11.8 ± 7 months. There were no deaths, no additional or urgent need for PPM, EF remained steady at 60 ± 9.7%.

Conclusion:

Our study shows that EP study guided PPM placement in NLBBB leads to lower rate of PPM placement post TAVR (9% compared to 23% in the standard published literature) and also has excellent long‐term outcome, with no death or additional need for PPM placement. Data collected in larger group of patients and/or randomized study is needed to solidify these findings.

Total number of patients	81
New onset LBBB after TAVR	11 (13.6%)
Age	60.4 ± 10.3
Follow up in months	11.8 ± 7.2
Valves used	Edward Sapien S3 in mm: 23‐2, 26‐5, 29‐2 Medtronic Evolut 29 mm‐2
TAVR	Pre TAVR	Post TAVR
PR interval in milliseconds (ms)	185.9±21	202.4±39
QRS duration (ms)	99±11.2	141.3±12
EP Study , HV interval in milliseconds	Baseline 61.9±8.6	After Procanamide 66.9±14
Pacemaker implanted		1 (9%)
HV interval of PPM patient	74 ms	94 ms
Ejection Fraction (EF)remained unchanged	60 ±9.8%	60±9.8%
Emergent PPM implant or death at follow up	N/A	None

Open in a new tab

AP19‐01130

The impact of metabolic syndrome and obesity on ragmented QRS in twelve lead ECG in East Asian population

HungKai Huang, ChingPei Chen

Changhua Christian Hospital, Taiwan

Introduction:

Several papers have found that both patients with obesity and with metabolic abnormalities have increased insulin resistance. Fragmented QRS (fQRS) in 12 lead ECG can predict poor prognosis in patients with variable cardiac diseases or systemic diseases. We aimed to establish the relationship of patients with obesity and metabolic abnormalities to predict the fQRS ECG.

Methods:

This retrospective, observational study was based on the “Registry of health examination at Chang‐Hua Christian Hospital” database. The study group included 3136 consecutive patients with age more than 18 years old who received health examination between 1 January 2010 and 31 December 2014 in Chang‐Hua Christian Hospital in middle Taiwan. Metabolic syndrome was defined as ATP III definition. Obesity was defined as BMI ≥27.5 kg/m² in WHO Asian BMI cut points. Based on ATP III definition and Asian BMI cutoff level, the patients were divided into four groups, including healthy subjects, obese subjects, non‐obese patients with metabolic abnormalities, and obese patients with metabolic abnormality. The baseline data and risk factor of patients were compared among groups. The percentage of fQRS in 12 lead ECG in each patient group were compared among groups. Conditional logistic regression analysis was used to examine the association between obesity and metabolic abnormalities and fQRS in ECG. The effects of obesity and metabolic abnormalities on the risk of fQRS in ECG are presented as aORs and 95% CIs.

Result:

Among 1,940 healthy subjects, 197 obese subjects, 580 non‐obese patients with metabolic abnormality, and 419 obese patients with metabolic abnormality in the study, the baseline characteristics of each groups is listed and compared in table 1. The percentage of fQRS in 12 lead ECG in each group was shown in Figure1, and there are 31.89%, 39.34%, 62.71% and 56% of fQRS observed in l2 lead ECG, respectively. The table 2 demonstrated the multivariate logistic regression analysis of obese or metabolic syndrome of our population in prediction of fQRS. While the age and gender matching data are used, non‐obese or obese patients with metabolic syndrome were susceptible to fQRS (P < .001, odd ratio [OR]: 3.00, 95% confidence interval [CI]: 1.70‐5.31; P < .001, odd ratio [OR]: 2.28, 95% confidence interval [CI]: 1.65‐3.15). The table 3 demonstrated the multivariate logistic regression analysis of number of diagnosis criteria for metabolic content or obesity in prediction of fQRS. While the age and gender matching data are used, patients with components of diagnosis criteria for metabolic syndrome were susceptible to fQRS. The risk of fQRS increased when the patients had increased components of diagnosis criteria for metabolic syndrome.

Conclusion:

The study revealed that both patients with metabolic abnormality and obesity are associated with increased fQRS ECG than healthy subjects in East Asians.

TABLE 1 Baseline characteristics

Healthy	Obesity	MS (not obese)	Obesity MS	P‐value
Number	1940	197	580	419
Gender, Male	879 (45.31%)	63 (31.98%)	217 (37.41%)	141 (33.65%)	<.001	Chi‐square test
Female	1061 (54.69%)	134 (68.02%)	363 (62.59%)	278 (66.35%)	<.001	Chi‐square test
Age	49 (40,58)	50 (39,58)	55 (49,62)	53 (45,61)	<.001	Kruskal‐Wallis One‐way ANOVA test
SBP	120 (110,132)	127 (118,134)	129 (120,141)	132 (123,145)	<.001
DBP	77 (71,84)	79 (74,87)	82 (78,88)	85 (80,92)	<.001
Height	163.4 (157.4,169.3)	165.8 (158,170.7)	164.3 (158.25,170.55)	164.2 (156.4,170.5)	.091
Weight	60.5 (53.65,67.2)	78.8 (72.4,84.1)	66.75 (60.6,72.7)	78.6 (71.6,85.3)	<.001
Waist Circumference	78 (72,83.25)	91 (87,96)	86 (82,90)	94 (90,99.5)	<.001
BMI	22.72 (20.86,24.45)	28.24 (27.45,29.85)	24.93 (23.62,25.94)	28.93 (27.81,30.67)	<.001
Triglyceride	80 (58,112)	97 (77,129)	166 (107,223.5)	161 (112,216)	<.001
Total Cholesterol	195 (172,219)	205 (184,224)	199.5 (174,228)	199 (173,224)	.002
LDL‐C	121 (101,142.8)	135 (114,153)	123.4 (101,150)	124 (102,147)	<.001
HDL‐C	51 (43,61)	46 (41,55)	39 (34,45)	39 (34,46)	<.001
AC sugar	92 (86,97)	93 (88,98)	103 (96,116)	103 (94,118)	<.001
HBA1C	5.5 (5.2,5.7)	5.6 (5.3,5.8)	5.8 (5.5,6.2)	5.9 (5.6,6.4)	<.001
Homocysteine	8.71 (7.05,10.48)	9.45 (7.93,11.13)	9.34 (7.56,11.21)	9.53 (7.9,11.34)	<.001
Hemoglobin	14.1 (13,15.2)	14.7 (13.5,15.6)	14.5 (13.5,15.5)	14.7 (13.7,15.6)	<.001
Uric Acid	5.4 (4.5,6.4)	6.5 (5.6,7.3)	6.2 (5.2,7.2)	6.7 (5.5,7.5)	<.001
Creatinine	0.78 (0.63,0.93)	0.855 (0.67,0.98)	0.815 (0.67,0.95)	0.84 (0.68,0.98)	<.001
Hypertension	839 (43.25%)	101 (51.27%)	496 (85.52%)	367 (87.59%)	<.001	Chi‐square test
DM	355 (18.3%)	23 (11.68%)	403 (69.48%)	270 (64.44%)	<.001	Chi‐square test

Open in a new tab

TABLE 2

Variables	Crude OR (95% CI)	P‐value	Adjusted OR† (95% CI)	P‐value
Healthy	1.000	1.000
Metabolically healthy but obese	1.38 (1.06,1.81)	.018	1.22 (0.92,1.61)	.172
Metabolically abnormal but not obese	3.59 (2.06,6.25)	<.001	3.00 (1.70,5.31)	<.001
Metabolically abnormal obese	2.72 (1.99,3.72)	<.001	2.28 (1.65,3.15)	<.001

Open in a new tab

†adjusted for age, gender.

TABLE 3

Met‐S total and obesity	Crude OR (95% CI)	P‐value	Adjusted OR† (95% CI)	p‐value
Met‐S total
0	1.000	1.000
1	2.54 (1.86,3.46)	<.001	2.36 (1.72,3.24)	<.001
2	3.16 (2.04,4.9)	<.001	2.9 (1.86,4.52)	<.001
3	5.15 (3.41,7.75)	<.001	4.65 (3.05,7.1)	<.001
≥4	3.45 (2.24,5.32)	<.001	3.14 (2.00,4.93)	<.001
BMI≥24	1.6 (1.27,2)	<.001	0.84 (0.63,1.11)	.217

Open in a new tab

†adjusted for age, gender.

graphic file with name JOA3-35-4-g082.jpg

AP19‐01134

Characterization of the TU‐wave complex of Andersen‐Tawil syndrome with KCNJ2 mutations using high‐frequency ECG data

Hitoshi Horigome, Yasuhiro Ishikawa, Norito Kokubun, Masao Yoshinaga, Naokata Sumitomo, Lisheng Lin, Yoshiaki Kato, Yuri Tanabe‐Kameda, Seiko Ohno, Masami Nagashima, Minoru Horie

University of Tsukuba, Japan

Introduction:

Andersen‐Tawil syndrome (ATS) is characterized by ventricular arrhythmias, periodic paralysis, and dysmorphic facial and skeletal features. Electrocardiograms (ECGs) of ATS are characterized by large U waves, a prolonged repolarization process, frequent premature ventricular contractions (PVCs), and polymorphic/bidirectional ventricular tachycardia. However, the exact differences between the U‐waves of ATS and those of healthy individuals remain to be investigated. We tried to characterize the TU‐wave complex of ATS using high‐frequency ECG data.

graphic file with name JOA3-35-4-g066.jpg

Methods:

ECGs were recorded as time series data with a 2 kHz frequency ECG amplifier in 10 patients with ATS type 1 (positive for KCNJ2 mutation, ATS1 group) and age‐matched healthy individuals (control group). Conventional temporal parameters (corrected by √RR) were measured, and independent component analysis (ICA) was applied to TU‐wave complex on raw tracings. Data obtained were compared between the 2 groups.

Result:

Although QUc and QUp (Q to U peak) were longer in the ATS1 group than the control group, QTc and QTp (Q to T peak) were comparable between the groups. Time from T end to U end (TeUe), time from T peak to U peak (TpUp), time from bottom to U peak (BUp), and time from bottom to U end (BUe), where bottom is the lowest point between T and U waves, were all significantly longer in the ATS1 group than the control group (P < .0001). ROC curve analysis revealed that AUC values of U wave‐ related parameters (QUc, TeUe, TpUp, BUp, and BUe) were > 0.9 (indicating high accuracy). Particularly, the AUC of BUe was 1.0. Multivariate logistic regression analysis revealed that BUe could completely differentiate the 2 groups with no overlaps. More importantly, ICA extracted one or two U wave‐specific independent components (ICs) that exclusively comprise the U wave in ATS1, whereas U waves in the control group were composed of some ICs that also comprised T waves. Figure is an example of the results of ICA in a patient with ATS1, showing that one U‐wave specific IC (IC6) is extracted.

Conclusion:

This study indicates that U waves in patients with ATS1 can be differentiated from those in healthy individuals by several U wave‐related temporal parameters, particularly BUe. Furthermore, the existence of U wave‐specific ICs, extracted in the ICA, is useful for differentiation of U waves in ATS1 from those in healthy individuals, although the mechanisms of independency of the ICs from T wave remain to be clarified.

AP19‐01172

Long QT in the patient with myocardial bridging: Is it harmful?

Wendy Wiharja

Universitas Pelita Harapan, Indonesia

Introduction:

The Myocardia Bridging (MB) is an anomaly characterized by an intra‐myocardial route of a segment of one of the major coronary arteries. Functional myocardial bridging is less commonly observed on angiography (0.5%‐16%) and can range from 4 to 80 mm in length. Long QT is one of arrhythmias which might occur in the patient with MB. This case is about Long QT in the patient with MB and its implication.

Methods:

Case description: A 66 years old female presented to ER with typical angina CCS 3 gradually increased since 1 week ago. Associated symptoms were dyspnea and dyspepsia. On physical examination, BP(110/70 mm Hg), Pulse(86times/minute), RR(26 times/minute), Temperature (36.4°C), SaO2 (97%). Cardio‐pulmonary examination was unremarkable. ECG showed Long QT interval, T‐ inverted on V1‐V4, cardio enzymes ware not increased, Chest X‐ray showed cardiomegaly, Echocardiography showed LVH with normal LVEF. Nitrate, Clopidogrel, and Aspilet were given in ER, and the patient transferred to cath‐lab. CT‐Angiography showed MB in mid LAD, catheterization was done and the patient was given bisoprolol for maintenance drugs. After few days, the Long QT was resolved spontaneously, and the patient was discharged

graphic file with name JOA3-35-4-g067.jpg

graphic file with name JOA3-35-4-g068.jpg

graphic file with name JOA3-35-4-g069.jpg

Result:

Case discussion: Patients with MB are often asymptomatic but this anomaly may be associated with ACS, arrhythmias, or even sudden cardiac death. Although MB can be found in any epicardial artery, 67‐98% occurs in the LAD. The typical angiographic feature of a myocardial bridge is systolic narrowing of an epicardial artery, which is often completely resolved during the diastolic phase of the cardiac cycle. The hemodynamic impact of MB depends on the thickness and length of the bridge, orientation of the bridge relative to myocardial fibers and presence of loose connective or adipose tissue around the bridged segment. Long QT might be a sign of impairing rhythm in ventricular and might be suggested as early sign of the presence of critical stenosis in the bridged segment, and it should be alerted physician about the deadly complication of ventricular arrhythmia and sudden cardiac death. In our patient, the MB appear to be symptomatic, so to normalize flow and abolish symptoms, catheterization was done and to control symptoms beta blocker was gives as maintenance drugs

Conclusion:

Myocardial Bridging, if presented symptomatically, especially as ACS, may be lethal. Long QT may indicate as early sign of ventricular arrhythmia, which should be monitored regularly. Flow normalization and symptoms controlling in such manner are best achieved by PCI and Beta‐blocker

AP19‐01176

Assessment of management ability based on electrocardiographic findings in medical students whom had just finished cardiovascular system module

Audrey Hadisurya

Rekha Nova Iyos, Mohammad Iqbal, Giky Karwiky, Astri Astuti, Januar Wibawa Martha, Mohammad Rizki Akbar

Hasan Sadikin Hospital, Padjadjaran University, Indonesia

Introduction:

Arrhythmogenic Right Ventricular Dysplasia/Cardiomyopathy (ARVD/C) is a rare form of cardiomyopathy resulting, most frequently, from desmosomal gene mutations that encode cell‐to‐ cell adhesion. These mutations cause progressive replacement of Right Ventricular (RV) myocardium into fibrofatty tissue, disrupting electrical conduction and function. Malignant Arrhythmias and even sudden cardiac death may manifest before the development of any discernible structural abnormalities. Prompt diagnosis of ARVD/C is a priority in order to quickly follow up and treat these challenging cases. Multi‐Slice Computed Tomography (MSCT) cardiac may help in settings where optimal imaging modalities are limited.

Methods:

A 32‐year old female with history of palpitations from the past month was diagnosed with recurrent Ventricular Tachycardia (VT) of Right Ventricular Outflow Tract‐anteroseptal origin. Electrocardiographic (ECG) recordings show VT with Left Bundle Brach Block (LBBB) morphology, inferior axis, and inverted T waves in V1‐V4. Holter ECG reports show multiple VT episodes that lasted approximately 1.5 hours. She planned to undergo catheter ablation with RV pacing and isoproterenol infusion based on pace mapping, but did not induced. She had normal RV dimensions and function based on echocardiography. An MSCT cardiac (128 slices, single source) reconstructed at 75% of R‐R intervals, showed a mildly dilated RV with thinning of the RV free wall and fat infiltration at the RV Free wall apex. A diagnosis of ARVD/C was made. The Dose length product (DLP) was 1025.6 mGy.cm and considered acceptable.

graphic file with name JOA3-35-4-g070.jpg

Result:

Cardiac CT Scan is not currently included in the diagnostic ARVD Task Force Criteria. It quite unpopular due to high radiation exposure, and therefore Cardiac Magnetic Resonance (CMR) is the chosen modality for RV analysis in suspected ARVD/C cases. However, Cardiac CT may provide some benefits compared to CMR by being faster, easier to perform, and providing a more reliable image quality. It is also more accessible and less expensive, which make it selected in areas with limited resources.

Conclusion:

Cardiac CT might have a significant role in the diagnosis of ARVD/C in lieu of MRI. It might be suitable and appropriate in the evaluation of patients with a high degree of suspicion towards ARVD/C as an initial screening, with acceptable radiation exposure.

AP19‐01232

Association of deep terminal negativity of P wave in V1 with severity of rheumatic mitral stenosis and risk of mortality

Karlina Alferinda, Carol Natasha, Joey Martinus Sidarta, Elizabeth Marcella, Jansen Malikin, Vito Anggarino Damay

Pelita Harapan University, Indonesia

Introduction:

Myocardial bridge (MB) is a congenital anomaly in which a segment of a coronary artery takes a “tunneled” intramuscular course under a “bridge” of overlying myocardium. The pathogenesis occurred primarily at diastolic because systolic contraction obstructs the flow of coronary artery, particularly to sub‐endocardium part. Medication is the main choice for preventing myocardial ischemic complication. This case report explains a patient with myocardial bridging with STEMI anterolateral on ECG and ventricular extrasystole (VES).

Methods:

A 62‐year‐old man came to the Siloam hospital emergency room with complaints of seizures. Initially, the patient complained of the abdominal pain continuously felt throughout the abdomen, sore and twisting sensation. The next day the patient got seizure and came to hospital with sudden spasm throughout the body, the hands and feet moved vertically, unconsciously, and was difficult for answering questions. The patient's shortness of breath condition was difficult to be analyzed. Physical examination was normal. The vital signs were BP: 170/100 mm Hg; HR: 110x /m; RR: 24x/m; BT: 37.10°C. The ECG showed anterolateral STEMI and VES, trivial heart valve insufficiency with left ventricle systolic function was in good condition. There was increased in CKMB level (34.8) and normal level of troponin T (8,8). The CAG was done and the result was myocardial bridging vein was found in Left anterior Descending (LAD) without coronary artery stenosis.

Result:

Myocardial bridge is categorized as normal anatomy variance of coronary artery. The previous study showed the clinical course of MB is generally benign with a five‐year survival rate of 97.5%, but a problem was found in this patient in which this case showed a patient in whom myocardial bridging is potentially pathologic. He came in seizure and abdominal pain condition only without any other symptoms of myocardial ischemic or heart attack, but the ECG showed anterolateral STEMI with VES arrhythmia, which reinforces a suspicion of ACS, therefore CAG was done. The CAG result showed a systolic compression (milking) in LAD which confirmed the presence of MB. The patient was treated with amiodarone IV until the ECG returned to normal.

Conclusion:

Myocardial bridges have traditionally been considered as benign condition, but this case is a proof that MB can possibly induce arrhythmia, and warrant the recent studies that the clinical complications of MB can be dangerous (acute coronary syndrome, arrhythmia, transient ventricular dysfunction, and sudden death). The prognosis of patients with MB, therefore, is not as benign as it was believed to be in the past. This case report is an example of the clinical effects of myocardial bridge. It is therefore interesting not only because of the rarity of the case, but also because it brings the attention of cardiologists to an anomaly that is often neglected.

Picture 1 ECG result on (7/12/2018‐12/12/2018)

graphic file with name JOA3-35-4-g074.jpg

Picture 2 X‐ray cor in normal range (CTR<50%) with aorta elongation and mark of tuberculosis

graphic file with name JOA3-35-4-g075.jpg

Picture 3 CAG showed MB in LAD

graphic file with name JOA3-35-4-g076.jpg

Picture 4 Echocardiography showed trivial heart valve insufficiency with left ventricle systolic function was in good condition

graphic file with name JOA3-35-4-g077.jpg

AP19‐01282

The correlation between left ventricle end diastolic pressure and P dispersion in ST‐elevation myocardial infarction patient

Monika Putri Adiningsih

Gadjah Mada University, Indonesia

Introduction:

P‐wave dispersion (Pwd) is defined as the difference between the maximum and the minimum P‐wave duration recorded from 12 ECG leads. Pwd reflects prolongation in conduction time intra and interatrial. Studies show Pwd correlates with left ventricular diastolic dysfunction (LVDD). One of the marker of LVDD is elevated left ventricular end diastolic pressure (LVEDP) and common following myocardial infarction. This study aims to analyze the association between Pwd and LVEDP in ST‐elevation myocardial infarction (STEMI) patients who underwent primary percutaneous coronary intervention (PCI).

Methods:

This is a cross sectional study on STEMI patient admitted to Sardjito Hospital since December 2018–January 2019 who underwent PCI and fulfilled the inclusion and exclusion criteria. The Pwd were measured in ECG using ImageJ program. Echocardiography examination results were performed and recorded.

Result:

Thirty seven patients were included in this study with mean age was 57.31 ± 11.07. Mean LVEDP was 9.712 ± 4.300, mean Pwd was 73.886 ± 25.184, mean EF was 43.08 ± 9.37. No‐significant positive correlation was found between Pwd and parameters of left ventricular function. Pwd and lateral (e’ lat) annulus (P = .977, R = .005), medial (e'med) annulus (P = .977, R = .005), deceleration time (P = .530, R = .107), early filling/atrial filling velocity (E/A) (P = .759, R = .052), early mitral inflow velocity (E) (P = .675, R = .71), mitral annular early diastolic velocity (P = .902, R = .021). We also found a non‐significant positive correlation between LVEDP and Pwd (P = .913; R = .019).

Conclusion:

There is no significant positive correlation between Pwd and LVEDP in patients with STEMI who underwent primary percutaneous coronary intervention.

AP19‐01283

Inhospital mortality rate analysis of patient with ST elevation myocardial infarction treated with primary percutaneous coronary intervention, does Tpeak‐Tend Interval holds a significant impact ?

Muhammad Iqbal Amin

Faculty of Medicine, Public Health, and Nursing Universitas Gadjah Mada, Indonesia

Introduction:

The interval from the peak to the end of the T wave (Tpeak – Tend), a new electrocardiographic markers of ventricular repolarization, have been recently proposed to predict ventricular arrhythmic events and sudden cardiac death. It represents an index of transmural dispersion of repolarization (TDR). The prolongation of the interval of Tpeak – Tend, of the 12‐lead electrocardiogram is a marker of ventricular arrhythmogenesis. Some researchers have shown an increase in mortality in patients with acute coronary syndrome, especially with ST‐segment elevation myocardial infarction (STEMI).

Methods:

This cross sectional study was designed in STEMI patients who were underwent primary PCI that fulfilled the inclusion and exclusion criteria. We analyze Tpeak – Tend interval in ECG which impacts the survival rate of the patient by using Kaplan‐Meier analysis

Result:

We conducted study for a total 40 patients who diagnosed as STEMI (34 males and 6 females) with mean age was 58 ± 11.04. From T‐Test analysis, there is no significant difference of Tpeak – Tend interval between survived patient and inhospital mortatility patient group (P = .07) with the mean are 104.5 and 139.2 respectively. However in mantel‐cox analysis, the Tpeak – Tend interval prolongation are significantly associated with inhospital mortality (P = .048).

Conclusion:

There is a significant impact of Tpeak – Tend interval prolongation in ECG to inhospital mortality rate in patient with ST Elevation Myocardial Infarction Treated with Primary Percutaneous Coronary Intervention

Keywords: Inhospital mortality – ST Elevation Myocardial Infarction – Tpeak – Tend – STEMI – Percutaneous coronary intervention

AP19‐01288

Death is temporary: A severe case from complication of temporary cardiac pacing

Kiagus Muhammad Andri Akbar, Dony Yugo Hermanto, Sunu Budhi Raharjo, Dicky Armein Hanafy, Yoga Yuniadi

Indonesian Heart Rhythm Association, Indonesia

Introduction:

Temporary transvenous cardiac pacing is still one of the choice in acute profound bradycardia. They were used in emergency situations especially for older patients in poor general condition who are hemodynamically unstable that suffering from severe bradyarrhythmias. Complications include local trauma, pneumothorax, arrhythmias, and cardiac perforation, and in some case death on the table can also occur. This case report is made to warn us about how our intention to saving life can make debilitating effect to the patient.

Methods:

A 78 years old woman came to emergency NCCHK hospital suffering from malaise and near syncope. She felt dizzy 7 days prior to hospital. On physical examination, her blood pressure were about 180/100 mmHg with heart rate 30‐35 bpm. there was Pansystolic murmur 3/6 in the left lateral sternal border, and profound pulmonic sound. Electrocardiogram showed total atrioventricular block with appearance “Salvatore deli's moustache” on precordial lead. The patient than took to catheterization lab for temporary pacing. Assuming the apex was scarring and not paceable, entering the RV till the base, and pace was occurred. The echocardiographic was made to evaluate the catheter and effusion was minimally shown. 3 days later, the patient was found arrest, and ecg showed asystole, chest decompression was delivered, about 30 minute later the patient was ROSC, the echocardiographic showed effusion markedly elevated, and we assessed as cardiac tamponade. The patient than took to the cath lab for pericardiocentesis. Fluoroscopy was made and found that the bipolar catheter was outside form cardiac silhouettes, assume cardiac was perforated, open thoracostomy was arranged. The operation was successful but unfortunately the patient passed away at the ICU because of blood loss.

Result:

Major serious complication of temporary cardiac pacing are not uncommon (22% of all patients), and can range from femoral hematoma to cardiac tamponade and even death (6%). There were some approaches to make sure the position of bipolar catheter has entering and on the apex of the right ventricle. Location of pacing impulse from the electrocardiogram in the daily basis, can evaluate the position of bipolar catheter. Another method requiring echocardiography to find the tip of catheter in apex of RV. In this patient we found the tip was in the basal‐apex, but we cannot know the rest of catheter whereabouts from echocardiography, the last resort was with fluoroscopy

Conclusion:

We reporting a case of temporary cardiac pacing complication that leads the patient death. The patient suffering from total atrioventricular block due to digitalis intoxication, with differential diagnosis due to sinus node dysfunction. Closed monitoring has to be made for cases with problems intra procedure. ECG and Echocardiographic monitoring is a must to assess the position of bipolar catheter at right place

FIGURE 1 Flourosave on TPM attempt

graphic file with name JOA3-35-4-g078.jpg

Conclusion:

A process improvement initiative conducted at centers across South Asia significantly increased both the diagnosis of SND and subsequent treatment with guideline indicated pacemaker therapy. Diagnosis of SND and pacemaker implantation improved overtime despite similar insurance and cost constraints.

Keywords (predefined): Sinus Node Disease, Bradycardia, Pacemaker therapy

PERMALINK

General Electrophysiology

AP19‐­00005

A retrospective comparative study of 12 lead electrocardiogram and 2D—Echocardiography derived left ventricular ejection fraction among patients of Fatima University Medical Center

AP19‐­00007

Shortcut in our future

AP19‐­00011

Electrocardiographic characteristics for prediction of irreversible fulminant hepatitis in patients with acute hepatic failure

AP19‐­00012

Impact of alfa‐­ and beta‐­blocker, carvedilol on the long‐­term clinical outcomes in benign prostatic hypertrophy patients with palpitation

AP19‐­00015

Too much for a single heart: Case report

AP19‐­00016

Evaluation of the accuracy of a single lead adhesive ECG patch monitoring device (S‐­Patch) in patients post myocardial infarction

AP19‐­00021

Early repolarization pattern characterized by right precordial T‐­wave inversion in a healthy African‐­Japanese athlete

AP19‐­00045

Impact of oxidative stress on the long‐­term heart rate variability: Linear vs nonlinear heart rate dynamics

AP19‐­00061

Diagnostic value of QTc dispersion and QT dispersion ratio changes in treadmill training test for detecting coronary lesion in stable angina pectoris patients

AP19‐­00141

Initial genetic results for Brugada syndrome and hypertrophic cardiomyopathy patients in Brunei Darussalam

AP19‐­00169

Electrophysiologic study in the developed new conduction abnormality in post TAVI patients Ramathibodi hospital, Thailand

AP19‐­00170

QT interval in right ventricular pacing: how to define “normal” or “prolonged”

AP19‐­00172

Diagnostic performance of ST‐­segment elevation in lead aVR during exercise stress test for the prediction of severe coronary artery disease: A meta‐­analysis

AP19‐­00188

Near Zero X‐­Ray mapping approach with a novel ablation technology in SVT procedures: Preliminary experience from the CHARISMA registry

AP19‐­00219

A case of mitral regurgitation deterioration via right ventricular apex constant pacing caused by pilsicainide hydrochloride induced impaired atrioventricular conduction

AP19‐­00222

Fasciculoventricular accessory pathway unmasked by a pseudo gap phenomenon

AP19‐­00234

Radiation exposure reduction during catheter ablation by changing the setting of fluoroscopic system

AP19‐­00255

When Wellens’ syndrome meets Brugada phenocopy

AP19‐­00271

Epicardial ablation of accessory pathways: Single centre experience

AP19‐­00286

Outcome of failed index and redo procedures in catheter ablation for arrhythmias—A single centre experience

AP19‐­00305

Ventricular late potentials measured by signal‐­averaged electrocardiogram in young Korean professional soccer players

AP19‐­00317

The spatio‐­temporal differences of the precordial electrocardiographic amplitude after flecainide provocative test: The novel predictor of fatal arrythmia in Brugada syndrome

AP19‐­00331

Anatomic distribution and electrophysiological characteristics of ventricular arrhythmias originating in aortic coronary cusps

AP19‐­00375

AVRT with QRS alternans refractory to medical treatment: A challenging case from Pahang, Malaysia

AP19‐­00390

A case of complete heart block mimicking 2‐­to‐­1 atrioventricular block: A diagnostic challenge

AP19‐­00392

Postprandial electronegative very‐­low‐­density lipoprotein is positively associated with atrial dilatation in metabolic syndrome

AP19‐­00415

The confirm Rx™ SMART registry: Early safety and clinical outcomes

AP19‐­00417

Retrospective analysis of confirm Rx™ SharpSense™ technology using real‐­world data from the SMART registry

AP19‐­00431

A meta‐­analysis on the use of intracardiac echocardiography in percutaneous catheter ablation: Impact on efficiency, effectiveness, and safety outcomes

AP19‐­00436

Development of premature ventricular contraction (PVC) detection system from the paper electrocardiograph (ECG) records

AP19‐­00448

Optimal contact force to minimize edema volume during radiofrequency ablation

AP19‐­00453

Anatomical and clinical features in patients underwent atypical coronary sinus cannulation

AP19‐­00466

Clinical significance of cardiac arrhythmias on readmission and cardiac death in hospitalized patients with heart failure

AP19‐­00472

Automated localization of accessory pathway by deep neural network interpretation of surface electrocardiography

AP19‐­00477

Incidental findings discovered at computed tomography scan for noninvasive 3D cardiac mapping using the cardioInsight system

AP19‐­00478

Imaging technique, radiation dose and image noise: CT acquisition for noninvasive 3D cardiac mapping using the cardioinsight system

AP19‐­00539

Total AV block in hyperthyroid

AP19‐­00550

Recurrent ventricular arrhythmia from left ventricular summit after ablation, what should we do next for ablation strategy?

AP19‐­00553

Electrocardiographic changes after TAVI: experience from a tertiary care centre in North India

AP19‐00005

AP19‐00007

AP19‐00011

AP19‐00012

Impact of alfa‐ and beta‐blocker, carvedilol on the long‐term clinical outcomes in benign prostatic hypertrophy patients with palpitation

AP19‐00015

AP19‐00016

Evaluation of the accuracy of a single lead adhesive ECG patch monitoring device (S‐Patch) in patients post myocardial infarction

AP19‐00021

Early repolarization pattern characterized by right precordial T‐wave inversion in a healthy African‐Japanese athlete

AP19‐00045

Impact of oxidative stress on the long‐term heart rate variability: Linear vs nonlinear heart rate dynamics

AP19‐00061

AP19‐00141

AP19‐00169

AP19‐00170

AP19‐00172

Diagnostic performance of ST‐segment elevation in lead aVR during exercise stress test for the prediction of severe coronary artery disease: A meta‐analysis

AP19‐00188

Near Zero X‐Ray mapping approach with a novel ablation technology in SVT procedures: Preliminary experience from the CHARISMA registry

AP19‐00219

AP19‐00222

AP19‐00234

AP19‐00255

AP19‐00271

AP19‐00286

AP19‐00305

Ventricular late potentials measured by signal‐averaged electrocardiogram in young Korean professional soccer players

AP19‐00317

The spatio‐temporal differences of the precordial electrocardiographic amplitude after flecainide provocative test: The novel predictor of fatal arrythmia in Brugada syndrome

AP19‐00331

AP19‐00375

AP19‐00390

A case of complete heart block mimicking 2‐to‐1 atrioventricular block: A diagnostic challenge

AP19‐00392

Postprandial electronegative very‐low‐density lipoprotein is positively associated with atrial dilatation in metabolic syndrome

AP19‐00415

AP19‐00417

Retrospective analysis of confirm Rx™ SharpSense™ technology using real‐world data from the SMART registry

AP19‐00431

A meta‐analysis on the use of intracardiac echocardiography in percutaneous catheter ablation: Impact on efficiency, effectiveness, and safety outcomes

AP19‐00436

AP19‐00448

AP19‐00453

AP19‐00466

AP19‐00472

AP19‐00477

AP19‐00478

AP19‐00539

AP19‐00550

AP19‐00553

AP19‐00555

Prolonged QTc due to moxifloxacin in overcoming multi‐drug resistant‐tuberculosis

AP19‐00579

AP19‐00580

AP19‐00585

AP19‐00586

AP19‐00597

AP19‐00599

AP19‐00603

AP19‐00615

AP19‐00632

Clinical utility of fluorodeoxyglucose positron emission tomography/ magnetic resonance imaging in assessment of non‐ischemic cardiomyopathy

AP19‐00636

AP19‐00646

AP19‐00662

AP19‐00682

AP19‐00683

Assessment of ischemia reperfusion injury after PCI for ST‐elevation myocardial infarction using speckle tracking echocardiography

AP19‐00684

AP19‐00712

AP19‐00722

Electrocardiographic abnormalities can predict new‐onset atrial fibrillation after cavo‐tricuspid isthmus dependent atrial flutter ablation

AP19‐00736

AP19‐00745

Electrocardiogram characteristics and arrhythmic events at fever state in patients with fever‐ induced Brugada syndrome

AP19‐00747

he V1‐V3 transition index as a novel electrocardiographic criterion for differentiating left from right ventricular outflow tract ventricular arrhythmias

AP19‐00788

Analysis of 12‐lead electrocardiogram signal based on deep learning