Abstract
Introduction
Interatrial block (IAB) is strongly associated with recurrence of atrial fibrillation (AF) in different clinical scenarios. Atrial fibrosis is considered the responsible mechanism underlying the pathogenesis of IAB. The aim of this study was to investigate whether IAB predicted AF at 12 months follow‐up in a population of patients with ST segment elevation myocardial infarction (STEMI).
Hypothesis
We aimed to investigate whether IAB predicted AF at 12 months follow up in a population of patients with STEMI.
Methods
Prospective, single center, observational study of patients presenting with ST‐segment elevation myocardial infarction (STEMI) and referred to primary percutaneous coronary intervention (P‐PCI). Surface electrocardiograms (ECG) were recorded on admission and at 6th hour post P‐PCI. Patients were screened for the occurrence of AF at a 12‐months visit.
Results
A total of 198 patients were included between September 2015 and September 2016. IAB (partial and advanced) was detected in 102 (51.5%) patients on admission. Remodeling of the P‐wave and subsequent normalization reduced the prevalence of IAB to 47 (23.7%) patients at 6th hour. AF was detected in 17.7% of study patients at 12 months. Partial IAB (p‐IAB) on admission (OR 5.10; 95% CI, 1.46‐17.8; P = 0.011) and on 6th hour (OR 4.15; 95% CI, 1.29‐13.4; P = 0.017), presence of a lesion in more than one coronary artery (OR 3.29; 95% CI, 1.32‐8.16; P = 0.010) found to be independent predictors of AF at 12 months.
Conclusion
IAB is common in patients with STEMI and along with the presence of diffuse coronary artery disease is associated with new onset of AF.
Keywords: interatrial block, ischemia, STEMI
1. INTRODUCTION
Interatrial block (IAB) is defined as a delayed or blocked electrical conduction between the right and left atrium.1 The conduction block seen in IAB occurs at the Bachmann region which is the largest and most common anatomical route for interatrial conduction.2 Atrial fibrosis is considered the major contributor to the underlying pathophysiological mechanism of IAB through altering the structural and electrical properties of cardiac myocytes.3, 4, 5 IAB can be easily diagnosed on the 12‐lead surface electrocardiogram (ECG) as a prolongation of the P‐wave duration (>120 ms). Advanced IAB (a‐IAB) presents biphasic morphology in the inferior leads (II, III, aVF) while partial IAB (p‐IAB) does not present a negative component in the inferior leads. Recently, several studies identified IAB as a reliable predictor for new onset of atrial fibrillation (AF),6, 7, 8 AF recurrences following pulmonary vein isolation9 and pharmacological cardioversion10 and increased risk of ischemic stroke.11, 12, 13, 14
Our aim in the present study was to investigate the prevalence of IAB in patients presenting with acute ST‐segment elevation myocardial infarction (STEMI), its relation with specific culprit coronary artery lesion and its ability to predict new onset AF at 12 months follow‐up.
2. METHODS
Prospective, single center, observational study including patients without prior coronary artery disease who presented to the hospital with acute STEMI between September 2015 and September 2016 and underwent successful primary percutaneous coronary intervention (P‐PCI) within 12 hours from the onset of pain. Patients with cardiogenic shock, prior atrial arrhythmias, significant valvular heart disease, valvuloplasty, valve replacement procedures, or unsuccessful P‐PCI were excluded from the study. Patients with prior AF or pacemaker rhythm on admission were also excluded from the study. The study was approved by the institutional ethical committee.
Baseline demographic characteristics, relevant medical, and clinical information of each study patient were recorded on admission.
A standard 12‐lead ECG (Schiller, Cardiovit AT‐10 plus) (filter 150 Hz, 25 mm/s, 10 mm/mV) was recorded for all patients on admission and 6 hours following P‐PCI. ECG images were amplified eight times and P‐wave duration was measured blindly by using semiautomatic digital calipers in all 12 leads to acquire the longest duration. The onset of P‐wave was determined as the point of initial up‐ or downward deflection from the baseline and the offset of P‐wave was determined as the returning point of the deflection to the initial baseline. IAB was classified according to the latest consensus paper: (1) Partial IAB (p‐IAB) as P‐wave duration longer than 120 ms without biphasic morphology in the inferior leads, (2) Advanced IAB (a‐IAB) as P‐wave duration longer than 120 ms with biphasic morphology in the inferior leads.15
STEMI diagnosis was made according to the latest European Society of Cardiology guideline for the management of acute myocardial infarction in patients presenting with ST‐segment elevation.16 Briefly, patients with persistent chest pain suggestive of ischemia with at least two contiguous ST‐segment elevation ≥2.5 mm in men <40 years, ≥2 mm in men ≥40 years, ≥ 1.5 mm in women in leads V2 and V3 and/or ≥ 1 mm in the other leads (in the absence of left ventricular [LV] hypertrophy and left bundle branch block [LBBB]) and/or ≥ 0.5 mm in the leads V7‐V9 and/or new or presumably new LBBB were diagnosed as acute STEMI and underwent P‐PCI. Periprocedural pharmacotherapy and revascularization technique was left to the primary operator discretion. Successful P‐PCI was defined as the achievement of thrombolysis in myocardial infarction (TIMI) grade 3 flow, resolution of ischemic chest pain and ST‐segment elevation (>70% at 60 minutes).
All patients underwent two‐dimensional transthoracic echocardiographic (TTE) (Vivid 7, GE healthcare; Horten, Norway) evaluation on the third day of hospitalization by an expert on cardiovascular imaging. Left atrial antero‐posterior diameter was measured in parasternal long axis at the end‐systole. Left ventricular ejection fraction was obtained by using modified Simpson's method as specified by current guideline of chamber quantification by American Society of Echocardiography.17
Patients were routinely screened for AF in a clinical visit at 12 months. 12‐lead surface ECG was performed on each patient. In addition, our hospital's electronic database was searched for any 12‐lead ECG and 24‐h Holter monitoring records that detected AF in patients within 12 months of revascularization.
All statistical data were evaluated by using IBM SPSS version 22 (IBM SPSS). Mean and standard deviations were used for quantitative variables. Student t test was used for normally distributed variables in both groups and Mann Whitney U test was used for variables which were not normally distributed. Univariate analysis was performed for evaluating the association of the collected data. One‐way anova and independent‐sample t tests were performed for the continuous data and chi‐square tests (Pearson or Fisher’ s exact as appropriate) were performed for the categorical data. Multivariable logistic regression analysis was performed to identify the independent predictors of AF at 12 months using variables showing marginal association with it on univariate testing (P < 0.10). A P value of <0.05 was accepted as statistically significant.
3. RESULTS
From September 2015‐September 2016, a total of 262 patients presented to the hospital with a diagnosis of STEMI. Six patients had prior episodes of atrial tachyarrhythmias, 17 had prior coronary artery disease, 8 presented with AF on admission, 3 had significant valvular heart disease, valvuloplasty or valve replacement procedures, 7 had cardiogenic shock, 4 had no coronary obstruction detected during P‐PCI, and on 19 patients TIMI grade 3 flow could not be achieved. After excluding these patients, the final study population included 198 patients.
Patients' demographic and clinical characteristics according to presence of IAB on admission are shown in Table 1. IAB was detected in 102 (51.5%) (p‐IAB: 88 [44.4%] and a‐IAB: 14 [7.1%]) patients on admission. Patients with IAB on admission were significantly older compared to those without (59.4 ± 11.1 vs 54.5 ± 11.2; P < 0.01). Angiographic characteristics and periprocedural pharmacotherapy according to presence of IAB on admission are shown in Table 2. Patients with an obstruction in any part of the right coronary vasculature (63 [61.8%] vs 40 [41.7%]; P < 0.01) and in more than one coronary artery (diffuse coronary artery disease) (56 [54.9%] vs 34 [35.4%]; P < 0.01) had a greater prevalence of IAB.
Table 1.
Demographic and clinical characteristics of patients on admission
| IAB (+) (n = 102) | IAB (−) (n = 96) | P value | |
|---|---|---|---|
| Age | 59.4 ± 11.1 | 54.5 ± 11.2 | <0.01 |
| Gender (female) (%) | 15 (14.7) | 10 (10.4) | 0.36 |
| Syntax score | 11.8 6 | 12.2 6.7 | 0.73 |
| Hypertension | 43 (42.2) | 37 (38.5) | 0.60 |
| Hyperlipidemia | 17 (16.7) | 20 (20.8) | 0.45 |
| Diabetes mellitus | 28 (27.5) | 33 (34.4) | 0.29 |
| Smoking | 67 (65.7) | 65 (67.7) | 0.76 |
| Obesity | 22 (21.6) | 18 (18.8) | 0.62 |
| PAD | 4 (3.9) | 9 (9.4) | 0.12 |
| CHF | 1 (1) | 1 (1) | 0.59 |
| CVD/TIA | 3 (2.9) | 3 (3.1) | 0.94 |
| COPD | 4 (3.9) | 4 (4.2) | 0.93 |
| OSAS | 2 (2) | 6 (6.3) | 0.13 |
| Hypothyroidism | 4 (3.9) | 8 (8.3) | 0.19 |
| Previous medication | |||
| ASA | 12 (11.8) | 7 (7.3) | 0.29 |
| Clopidogrel | 1 (1) | 2 (2.1) | 0.52 |
| Beta blocker | 11 (10.8) | 7 (7.3) | 0.39 |
| ACEI/ARB | 21 (20.6) | 21 (21.9) | 0.82 |
| CCB | 7 (6.9) | 5 (5.2) | 0.63 |
| Statins | 9 (8.8) | 8 (8.3) | 0.90 |
| LA‐AP diameter (mm) | 36.7 ± 5.3 | 36 ± 4.5 | 0.66 |
| EF (%) | 48.4 ± 8.7 | 47.7 ± 10.8 | 0.14 |
Abbreviation: ACEI, angiotensin converting enzyme inhibitor; AF, atrial fibrillation; ARB, angiotensin receptor blocker; ASA, acetyl salicylic acid; CCB, calcium channel blocker; CHF, congestive heart failure; CKD, chronic kidney disease; CVD, cerebrovascular disease; COPD, chronic obstructive pulmonary disease; EF, ejection fraction; IAB, interatrial block; LA‐AP, left atrial antero‐posterior; OSAS, obstructive sleep apnea syndrome; PAD, peripheral artery disease; TIA, transient ischemic attack.
Table 2.
Baseline diagnoses, in‐hospital medications and coronary angiographic findings of patients on admission
| IAB (+) (n = 102) | IAB (−) (96) | P value | |
|---|---|---|---|
| Anterior MI (%) | 38 (37.3) | 38 (39.6) | 0.74 |
| Inferior MI (%) | 53 (52.0) | 41 (42.7) | 0.19 |
| High lateral MI (%) | 1 (1.0) | 6 (6.3) | 0.05 |
| Posterior MI (%) | 2 (2.0) | 1 (1.0) | 0.60 |
| Inferior + RV MI (%) | 4 (3.9) | 7 (7.3) | 0.30 |
| LAD px (%) | 19 (18.6) | 24 (25.0) | 0.28 |
| LAD mid/dis (%) | 20 (19.6) | 17 (17.7) | 0.73 |
| OM (%) | 2 (2.0) | 7 (7.3) | 0.07 |
| CX px (%) | 3 (2.9) | 5 (5.2) | 0.42 |
| CX mid (%) | 6 (5.9) | 3 (3.1) | 0.35 |
| CX distal (%) | 6 (5.9) | 4 (4.2) | 0.58 |
| RCA px (%) | 18 (17.6) | 12 (12.5) | 0.31 |
| RCA mid (%) | 5 (4.9) | 1 (1.0) | 0.11 |
| RCA distal (%) | 20 (19.6) | 18 (18.8) | 0.88 |
| Any part of right coronary vasculature (%) | 63 (61.8) | 40 (41.7) | <0.01 |
| Any part of left coronary vasculature (%) | 85 (83.3) | 72 (75.0) | 0.15 |
| Lesion in more than one coronary artery (%) | 56 (54.9) | 34 (35.4) | <0.01 |
| ASA | 102 (100) | 96 (100) | — |
| Clopidogrel | 35 (34.3) | 28 (29.2) | 0.44 |
| Prasugrel | 18 (17.6) | 16 (16.7) | 0.86 |
| Ticagrelor | 49 (48) | 52 (54.2) | 0.39 |
| Tirofiban | 15 (14.7) | 14 (14.6) | 0.98 |
| Beta blocker | 97 (95.1) | 91 (94.8) | 0.92 |
| ACEI/ARB | 96 (94.1) | 93 (96.9) | 0.35 |
| Statin | 102 (100) | 96 (100) | — |
Abbreviations: ACEI, angiotensin converting inhibitor, ARB, angiotensin receptor blocker; ASA, acetyl salicylic acid; CX, circumflex artery; LAD, left anterior descending artery; MI, myocardial infarction; OM, obtuse marginal artery; RCA, right coronary artery; RV, right ventricle.
After resolution of ischemia (ECG done at 6 hours post‐procedure) the prevalence of IAB decreased to 23.7% (47 patients) (p‐IAB: 38 [19.2%] and a‐IAB: 9 [4.5%]). Patients' demographics and clinical characteristics according to presence of IAB at 6th hour are depicted in Table 3. Patients with older age (60.2 ± 10.9 vs 56.1 ± 11.4; P < 0.01) and female gender (10 [21.3%] vs 15 [9.9%]; P < 0.01) were more frequently associated with IAB at 6th hours. IAB was more common in patients with RCA mid lesion (4 [8.5%] vs 2 [1.3%]; P < 0.01).
Table 3.
Demographic and clinical characteristics of patients on 6th hour
| IAB (+) (n = 47) | IAB (−) (n = 151) | P value | |
|---|---|---|---|
| Age | 60.2 ± 10.9 | 56.1 ± 11.4 | 0.03 |
| Gender (female) (%) | 10 (21.3) | 15 (9.9) | 0.04 |
| Syntax score | 12.0 ± 6.3 | 12 ± 6.4 | 0.98 |
| Hypertension | 20 (42.6) | 60 (39.7) | 0.73 |
| Hyperlipidemia | 10 (21.3) | 27 (17.9) | 0.60 |
| Diabetes mellitus | 16 (34.0) | 45 (29.8) | 0.58 |
| Smoking | 26 (55.3) | 106 (70.2) | 0.06 |
| Obesity | 14 (29.8) | 26 (17.2) | 0.06 |
| PAD | 4 (8.5) | 9 (6.0) | 0.54 |
| CHF | 1 (2.1) | 2 (1.3) | 0.68 |
| CVD/TIA | 1 (2.1) | 5 (3.3) | 0.68 |
| COPD | 2 (4.3) | 6 (4.0) | 0.93 |
| OSAS | 2 (4.3) | 6 (4.0) | 0.93 |
| Hypothyroidism | 3 (6.4) | 9 (6.0) | 0.92 |
| Previous medication | |||
| ASA | 4 (8.5) | 15 (9.9) | 0.77 |
| Clopidogrel | 1 (2.1) | 2 (1.3) | 0.69 |
| Beta blocker | 4 (8.5) | 14 (9.3) | 0.87 |
| ACEI/ARB | 11 (23.4) | 31 (20.5) | 0.67 |
| CCB | 3 (6.4) | 9 (6.0) | 0.92 |
| Statins | 5 (10.6) | 12 (7.9) | 0.57 |
| LA‐AP diameter (mm) | 36.8 ± 5.5 | 35.8 ± 4.5 | 0.12 |
| EF (%) | 47.8 ± 8.3 | 48.2 ± 10.2 | 0.35 |
Abbreviations: ACEI, angiotensin converting enzyme inhibitor; AF, atrial fibrillation; ARB, angiotensin receptor blocker; ASA, acetyl salicylic acid; CCB, calcium channel blocker; CHF, congestive heart failure; CKD, chronic kidney disease; CVD, cerebrovascular disease; COPD, chronic obstructive pulmonary disease; EF, ejection fraction; IAB, interatrial block; LA‐AP, left atrial antero‐posterior; OSAS, obstructive sleep apnea syndrome; PAD, peripheral artery disease; TIA, transient ischemic attack.
AF was detected in 17.7% of study patients at 12 months. Patients' basal characteristics according to presence of AF were shown in Table 4. Longer P‐wave duration on admission (135 ± 16.0 vs 116.8 ± 14.6; P < 0.01) and at the 6th hour (123.4 ± 11.7 vs 108.6 ± 12.2; P < 0.01), presence of a‐IAB on admission (11 [31.4%] vs 3 [1.8%]; P < 0.01) and at 6th hour (7 [20%] vs 2 [1.2%]; P < 0.01) and presence of p‐IAB at the 6th hour (15 [42.9%] vs 23 [14.1%]; P < 0.01) were associated with new onset AF at 12 months. The only angiographic data that was associated with AF was the presence of obstruction in more than one coronary artery (25 [71.4] vs 65 [39.9]; P < 0.01). After performing multivariate analysis p‐IAB on admission (OR 5.10; 95% CI, 1.46‐17.8; P = 0.011) and on 6th hour (OR 4.15; 95% CI, 1.29‐13.4; P = 0.017), presence of a lesion in more than one coronary artery (OR 3.29; 95% CI, 1.32‐8.16; P = 0.010) and P‐wave duration on admission (OR 1.09; 95% CI1.05‐1.14; P < 0.001) found to be independent predictors of AF at 12 months (Table 5).
Table 4.
Demographic and clinical characteristics of patients according to detection of AF at 12 months
| AF (+) at 12 months (n = 35) | AF (−) at 12 months (n = 163) | P value | |
|---|---|---|---|
| Age | 58.9 ±11.5 | 56.6 ±11.3 | 0.28 |
| Gender (female) (%) | 6 (17.1) | 19 (11.7) | 0.38 |
| Syntax score | 11.7 ± 6.4 | 12.1 ± 6.3 | 0.78 |
| Hypertension | 18 (51.4) | 62 (38.0) | 0.14 |
| Hyperlipidemia | 10 (28.6) | 27 (16.6) | 0.09 |
| Diabetes mellitus | 15 (42.9) | 46 (28.2) | 0.09 |
| Smoking | 19 (54.3) | 113 (69.3) | 0.09 |
| Obesity | 11 (31.4) | 29 (17.8) | 0.07 |
| PAD | 2 (5.7) | 11 (6.7) | 0.82 |
| CHF | 1 (2.9) | 3 (1.8) | 0.43 |
| CVD/TIA | 2 (5.7) | 4 (2.5) | 0.31 |
| COPD | 3 (8.6) | 5 (3.1) | 0.13 |
| OSAS | 3 (8.6) | 5 (3.1) | 0.13 |
| Hypothyroidism | 2 (5.7) | 10 (6.1) | 0.93 |
| Previous medication | |||
| ASA | 3 (8.6) | 16 (9.8) | 0.82 |
| Clopidogrel | 1 (2.9) | 2 (1.2) | 0.47 |
| Beta blocker | 4 (11.4) | 14 (8.6) | 0.60 |
| ACEI/ARB | 10 (28.6) | 32 (19.6) | 0.24 |
| CCB | 1 (2.9) | 11 (6.7) | 0.38 |
| Statins | 5 (14.3) | 12 (7.4) | 0.18 |
| LA‐AP diameter (mm) | 36.7 ± 3.7 | 36.0 ± 5.0 | 0.50 |
| EF (%) | 50.6 ± 8.0 | 47.5 ± 10 | 0.12 |
| P‐wave duration (on admission) | 135 ± 16.0 | 116.8 ± 14.6 | <0.01 |
| p‐IAB (on admission) | 20 (57.1) | 68 (41.7) | 0.10 |
| a‐IAB (on admission) | 11 (31.4) | 3 (1.8) | <0.01 |
| P‐wave duration (6th h) | 123.4 ± 11.7 | 108.6 ±12.2 | <0.01 |
| p‐IAB (6th h) | 15 (42.9) | 23 (14.1) | <0.01 |
| a‐IAB (6th h) | 7 (20) | 2 (1.2) | <0.01 |
Abbreviations: a‐IAB, advanced interatrial block; ACEI, angiotensin converting enzyme inhibitor; AF, atrial fibrillation; ARB, angiotensin receptor blocker; ASA, acetyl salicylic acid; CCB, calcium channel blocker; CHF, congestive heart failure; CKD, chronic kidney disease; CVD, cerebrovascular disease; COPD, chronic obstructive pulmonary disease; EF, ejection fraction; LA‐AP, left atrial antero‐posterior; OSAS, obstructive sleep apnea syndrome; p‐IAB, partial interatrial block; PAD, peripheral artery disease; TIA, transient ischemic attack.
Table 5.
Independent predictors of AF at 12 months
| Univariate OR (95% CI) | P value | Multivariate OR (95% CI) | P value | |
|---|---|---|---|---|
| p‐IAB (on admission) | 1.86 (0.89‐3.89) | 0.099 | 5.10 (1.46‐17.8) | 0.011 |
| p‐IAB (6th h) | 4.57 (2.05‐10.2) | <0.001 | 4.15 (1.29‐13.4) | 0.017 |
| Lesion in more than one coronary artery | 3.77 (1.70‐8.37) | <0.001 | 3.29 (1.32‐8.16) | 0.010 |
| P‐wave duration (on admission) | 1.08 (1.05‐1.12) | <0.001 | 1.09 (1.05‐1.14) | <0.001 |
Abbreviation: p‐IAB, partial interatrial block.
4. DISCUSSION
IAB was found in more than half of the patients presenting with STEMI that were successfully revascularized with P‐PCI. Patients with stenosis in any part of the right coronary vasculature or with diffuse coronary artery disease were more likely to have IAB at presentation. At the 6th hour following P‐PCI, following resolution of ischemia and reverse electrical remodeling, the prevalence of IAB decreased to one quarter and no angiographic data were identified to be associated with IAB. At 12 months follow‐up, AF was detected in 17.7% of patient. Predictors of new onset AF were p‐IAB on admission and on 6th hour, diffuse coronary artery disease and P‐wave duration on admission.
Atrial fibrosis is the electrical substrate that promotes AF. Atrial fibrosis involves complex interrelated neurohormonal and cellular mediators including the renin‐angiotensin system, TGF‐β, and oxidative stress pathways. Dense and disorganized accumulation of collagen fibrils separate functioning myocytes and create barriers for electrical propagation.18 These ultrastructural alterations lead to impairment in interatrial conduction and conduction heterogeneity which is considered the underlying mechanism for the development of AF.
Several studies have reported that IAB is associated with advanced atherosclerosis and atrial ischemia. Alexander et al analyzed patients with non STEMI (NSTEMI).19 The presence of diffuse coronary artery disease was associated with IAB. No correlation was found between any coronary artery lesion localization and the presence of IAB. Ariyajarah et al investigated patients with IAB at rest who underwent coronary angiography after a positive exercise tolerance test.20 Proximal or middle right coronary was more likely to be involved in patients with IAB as compared to those without. In addition, IAB was associated with diffuse coronary artery disease although it failed to reach statistical significance at that sample size. Recently, Alvarez‐Garcia et al demonstrated that iatrogenic atrial branch occlusion during elective percutaneous coronary intervention to the right or circumflex coronary artery was significantly associated with the development of IAB.21 Our findings are concordant with previous studies showing that diffuse myocardial ischemia is a major contributor for the occurrence of IAB. In our population, the right coronary artery was more frequently involved in patients with IAB on admission. Inconsistent results for the association of IAB with specific coronary artery localization can be explained by the fact that the main arterial supply of Bachmann region is a branch that arises from sinoatrial nodal artery which is originated from either right or circumflex coronary arteries in 55% and 45% of cases, respectively.22, 23
In the present study, the prevalence of IAB decreased from 51.5% to 23.7% after revascularization. Although it is widely accepted that IAB is the result of atrial fibrosis, reversed electrical remodeling was observed in patients with obstructive sleep apnea syndrome24 and advanced heart failure after cardiac resynchronization therapy.25 We can speculate that successful revascularization ameliorated the devastating effects of myocardial ischemia on conduction properties of the atrium. In addition, hyperadrenergic state and increased left atrial filling pressures that are encountered during the acute phase of STEMI could contribute to the conduction heterogeneity in the atrial myocardium and caused development of IAB.26
There is solid evidence that IAB is a strong predictor for new onset AF including symptomatic6 and asymptomatic episodes detected by cardiac implantable electronic devices.7 IAB was evaluated in many different clinical situations previously and AF was detected in 9%‐15% of included patients in those studies.11, 19, 27 Recent BAYES' syndrome‐ HF registry revealed that AF was detected in almost half of patients during follow‐up.11 In our study 17.7% of patients developed new onset AF. It is reasonable to conclude that a higher prevalence of IAB, hypertension, and obesity could contribute to high rate of AF occurrence. Diffuse coronary artery disease, again, was found to be a predictor of AF. This finding is consistent with the previous study by Alexander on the NSTEMI population.19 Although with the present data we can't give any precise explanation for the effect of revascularization on IAB, it can be assumed that presence of IAB at the beginning and 6th hour following STEMI can reliably predict new onset AF. The ongoing BAYES registry will provide more data for further understanding the pathophysiological mechanisms of IAB and its clinical implications.28
5. LIMITATIONS
This is a single center study with limited number of patients. Although, we excluded patients with prior atrial arrhythmias, silent episodes could be unrecognized. At the 12 months visit, we screened patients for AF by using ECG and hospital electronic database system. However, longer rhythm monitoring could detect more episodes of symptomatic and asymptomatic AF. The number of patients with a‐IAB was limited; thus, we did not include them in multivariate analysis. In the present study we did not include other P‐wave indices in the literature that were associated with new onset AF.
6. CONCLUSION
IAB is highly prevalent in patients presenting with STEMI. Diffuse coronary artery disease was associated with the presence of IAB. IAB in patients presenting with STEMI reliably predicted new onset AF at 1 year.
Conflict of interest
The authors declare no potential conflict of interests.
Çinier G, Tekkeşin Ahmet İlker, Genç D, et al. Interatrial block as a predictor of atrial fibrillation in patients with ST‐segment elevation myocardial infarction. Clin Cardiol. 2018;41:1232–1237. 10.1002/clc.23029
REFERENCES
- 1. de Luna AB, Bonnin O, Ferriz J, et al. Trastorno de conducción intraauricular con conducción retrógrada auricular izquierda. Estudio electrocardiológico y clínico a propósito de 24 casos. Rev Esp Cardiol. 1978;31:173‐178. [PubMed] [Google Scholar]
- 2. Platonov PG, Mitrofanova L, Ivanov V, Ho SY. Substrates for intra‐atrial and interatrial conduction in the atrial septum: anatomical study on 84 human hearts. Heart Rhythm. 2008;5(8):1189‐1195. [DOI] [PubMed] [Google Scholar]
- 3. Ariyarajah V, Kranis M, Apiyasawat S, Spodick DH. Potential factors that affect electrocardiographic progression of interatrial block. Ann Noninvasive Electrocardiol. 2007;12(1):21‐26. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 4. Pang H, Ronderos R, Pérez‐Riera AR, Femenía F, Baranchuk A. Reverse atrial electrical remodeling: a systematic review. Cardiol J. 2011;18(6):625‐631. [DOI] [PubMed] [Google Scholar]
- 5. Conde D, Baranchuk A. Bayes de Luna a. Advanced interatrial block as a substrate of supraventricular tachyarrhythmias: a well recognized syndrome. J Electrocardiol. 2015;48(2):135‐140. [DOI] [PubMed] [Google Scholar]
- 6. Agarwal YK, Aronow WS, Levy JA, Spodick DH. Association of interatrial block with development of atrial fibrillation. Am J Cardiol. 2003;91(7):882. [DOI] [PubMed] [Google Scholar]
- 7. Tekkesin AI, Çinier G, Cakilli Y, Hayıroğlu Mİ, Alper AT. Interatrial block predicts atrial high rate episodes detected by cardiac implantable electronic devices. J Electrocardiol. 2017;50(2):234‐237. [DOI] [PubMed] [Google Scholar]
- 8. Tse G, Wong CW, Gong M, et al. Predictive value of inter‐atrial block for new onset or recurrent atrial fibrillation: a systematic review and meta‐analysis. Int J Cardiol. 2018;250:152‐156. [DOI] [PubMed] [Google Scholar]
- 9. Caldwell J, Koppikar S, Barake W, et al. Prolonged P‐wave duration is associated with atrial fibrillation recurrence after successful pulmonary vein isolation for paroxysmal atrial fibrillation. J Interv Card Electrophysiol. 2014;39(2):131‐138. [DOI] [PubMed] [Google Scholar]
- 10. Enriquez A, Conde D, Hopman W, et al. Advanced interatrial block is associated with recurrence of atrial fibrillation post pharmacological cardioversion. Cardiovasc Ther. 2014;32(2):52‐56. [DOI] [PubMed] [Google Scholar]
- 11. Escobar‐Robledo LA, Bayés‐de‐Luna A, Lupón J, et al. Advanced interatrial block predicts new‐onset atrial fibrillation and ischemic stroke in patients with heart failure: the “Bayes' syndrome‐HF” study. Int J Cardiol. 2018. [DOI] [PubMed] [Google Scholar]
- 12. Ariyarajah V, Apiyasawat S, Najjar H, Mercado K, Puri P, Spodick DH. Frequency of interatrial block in patients with sinus rhythm hospitalized for stroke and comparison to those without interatrial block. Am J Cardiol. 2007;99(1):49‐52. [DOI] [PubMed] [Google Scholar]
- 13. Chhabra L, Gowdar S. Interatrial block to guide the thromboembolic prevention strategy: should it be the next step? Am J Cardiol. 2016;120(3):e7. [DOI] [PubMed] [Google Scholar]
- 14. O'Neal WT, Kamel H, Zhang Z‐M, Chen LY, Alonso A, Soliman EZ. Advanced interatrial block and ischemic stroke the atherosclerosis risk in communities study. Neurology. 2016;87(4):352‐356. [DOI] [PMC free article] [PubMed] [Google Scholar]
- 15. Bayes de Luna A, Platonov P, Cosio FG, et al. Interatrial blocks. A separate entity from left atrial enlargement: a consensus report. J Electrocardiol. 2012;45(5):445‐451. [DOI] [PubMed] [Google Scholar]
- 16. Ibanez B, James S, Agewall S, et al. 2017 ESC guidelines for the management of acute myocardial infarction in patients presenting with ST‐segment elevation: the task force for the management of acute myocardial infarction in patients presenting with ST‐segment elevation of the European Society of Cardiology (ESC). Eur Heart J. 2017;39(2):119‐177. [DOI] [PubMed] [Google Scholar]
- 17. Lang RM, Badano LP, Mor‐Avi V, et al. Recommendations for cardiac chamber quantification by echocardiography in adults: an update from the American Society of Echocardiography and the European Association of Cardiovascular Imaging. Eur Heart J Cardiovascu Imaging. 2015;16(3):233‐271. [DOI] [PubMed] [Google Scholar]
- 18. Burstein B, Nattel S. Atrial fibrosis: mechanisms and clinical relevance in atrial fibrillation. J Am Coll Cardiol. 2008;51(8):802‐809. [DOI] [PubMed] [Google Scholar]
- 19. Alexander B, MacHaalany J, Lam B, et al. Comparison of the extent of coronary artery disease in patients with versus without interatrial block and implications for new‐onset atrial fibrillation. Am J Cardiol. 2017;119(8):1162‐1165. [DOI] [PubMed] [Google Scholar]
- 20. Ariyarajah V, Fernandes J, Apiyasawat S, Spodick DH. Angiographic localization of potential culprit coronary arteries in patients with interatrial block following a positive exercise tolerance test. Am J Cardiol. 2007;99(1):58‐61. [DOI] [PubMed] [Google Scholar]
- 21. Alvarez‐Garcia J, Vives‐Borras M, Gomis P, et al. Electrophysiological effects of selective atrial coronary artery occlusion in humans. Circulation. 2016;133(23):2235‐2242. [DOI] [PubMed] [Google Scholar]
- 22. DiDio L, Lopes A, Caetano A, Prates J. Variations of the origin of the artery of the sinoatrial node in normal human hearts. Surg Radiol Anat. 1995;17(1):19‐26. [DOI] [PubMed] [Google Scholar]
- 23. Busquet J, Fontan F, Anderson RH, Ho SY, Davies MJ. The surgical significance of the atrial branches of the coronary arteries. Int J Cardiol. 1984;6(2):223‐234. [DOI] [PubMed] [Google Scholar]
- 24. Baranchuk A, Parfrey B, Lim L, et al. Interatrial block in patients with obstructive sleep apnea. Cardiol J. 2011;18(2):171‐175. [PubMed] [Google Scholar]
- 25. Alexander B, Sadiq F, Azimi K, et al. Reverse atrial electrical remodeling induced by cardiac resynchronization therapy. J Electrocardiol. 2017;50(5):610‐614. [DOI] [PubMed] [Google Scholar]
- 26. Desanctis RW, Block P, Hutter AM. Tachyarrhythmias in myocardial infarction. Circulation. 1972;45(3):681‐702. [DOI] [PubMed] [Google Scholar]
- 27. Bernal E, Bayés‐Genís A, Ariza‐Solé A, et al. Interatrial block, frailty and prognosis in elderly patients with myocardial infarction. J Electrocardiol. 2018;51(1):1‐7. [DOI] [PubMed] [Google Scholar]
- 28. Martínez‐Sellés M, Baranchuk A, Elosua R, Luna AB. Rationale and design of the BAYES (interatrial block and yearly events) registry. Clin Cardiol. 2017;40(4):196‐199. [DOI] [PMC free article] [PubMed] [Google Scholar]