Abstract
A male in his mid 50s, chronic smoker and hypertensive for 10 years presented with history suggestive of typical angina, electrocardiographic evidence of pre-excitation and serial elevation of cardiac biomarkers. Serial electrocardiograms showed subtle changes (axis shift, horizontal ST-segment changes) that could be presumptive of an anterior wall myocardial infarction. Speckle tracking echocardiography revealed territorial reduction of longitudinal strain corresponding to the left anterior descending artery with coronary angiography corroborating the same and underwent successful revascularisation. Exercise stress testing showed abrupt and complete disappearance of delta wave and normalisation of PR interval which indicates that the patient has low risk of developing malignant arrhythmias and sudden cardiac death.
Keywords: interventional cardiology, ischaemic heart disease, pacing and electrophysiology
Background
The diagnosis of acute ST-segment elevation myocardial infarction in a patient with chronic manifest pre-excitation based on an surface electrocardiogram is technically challenging because the underlying secondary repolarisation abnormalities could mask infarction changes. Deformation techniques using speckle tracking echocardiography could assist in diagnosing myocardial infarction in patients with asymptomatic manifest pre-excitation with its inherent limitations due to the abnormal premature ventricular activation through the accessory pathway. A well-structured clinical history, supplemented by serial electrocardiograms and cardiac biomarkers, comprehensive echocardiogram and risk assessment using exercise stress testing could help in appropriate management.
Case presentation
A male in his mid 50s presented to the emergency department with constricting type of central chest pain for a duration of 30 min associated with sweating and radiation to the left shoulder. He had no history of dyspnoea, orthopnoea, fatigue, palpitation or weakness of limbs. He had history of dyspnoea on exertion for the past that subsided after taking rest for 10 min. He is a chronic smoker(10 pack years) and a hypertensive for the past 8 years on tablet amlodipine 5 mg once daily. There was no family history of coronary artery disease or sudden cardiac arrest. On initial evaluation in the emergency department, his blood pressure was 130/80 mm of mercury, pulse rate was 94 beats per minute and oxygen saturation was 98% at room air. His jugular venous pressures were normal and auscultation revealed a fourth heart sound and no murmur was present. Other systems examination were unremarkable.
Investigations
His laboratory investigations (complete blood count, renal and liver function tests, serum electrolytes) were unremarkable. He tested positive for highly sensitive troponin-I quantitative analysis of 0.32 (control: 0.12 IU/L) with serial elevation to 0.62 IU/L and Creatine Kinase MB isoenzyme (CKMB) was elevated to 110 IU/L (control: 0–24 IU/L).
Electrocardiogram
12-lead electrocardiogram (figure 1A) taken at the time of admission showed normal sinus rhythm at a rate of 90 /minute, normal P wave axis, QRS axis of 0→−30°, QTc of 343 ms. Additionally pre-excitation was observed in all leads (figure 1) with a positive delta wave in leads V1–V6, I and aVL with secondary repolarisation changes (downsloping ST depression with T inversion), negative delta wave in leads II, III and aVF suggestive of a possible left postero-septal accessory pathway. An ECG repeated after 30 min (figure 1B) showed QRS axis shift from initial 0→−30° to 0→90° associated with horizontal ST-segment depression with T wave inversion in leads V2–V5 (figure 2). Serial ECG showed significant QRS axis shift from intial 0→−30°̊ to 90→120°̊ associated with upright T wave in V1, subtle ST-segment elevation in V3, V4 and horizontal ST-segment depression in V5 and V6 (figure 3) which could indicate primary repolaristion abnormalities due to myocardial ischaemia.
Figure 1.
(A) 12-lead ECG at the time of admission showing sinus rhythm at a rate of 90/min, normal P wave axis and QRS axis of 0→−30°̊, QTc of 343 milliseconds. Pre-excitation observed in all leads with a positive delta wave in leads V1–V6, I and aVL, negative delta wave in leads II, III and aVF with secondary repolarisation changes (zoomed inset (c) showing downsloping ST depression with asymmetrical T inversion).(B) ECG repeated after 30 min showed an axis shift of 0→90°̊ associated with horizontal ST-segment depression with T wave inversion in leads V2–V5 (zoomed inset (d) showing horizontal ST depression with symmetrical T inversion).
Figure 2.
Serial ECG showing a significant QRS axis shift of 90→120° associated with upright T wave in V1, subtle ST-segment elevation in V3, V4 and horizontal ST segment depression in V5 and V6.
Figure 3.
(A) Strain curves of six left ventricular segments in apical four-chamber view using two-dimensional speckle tracking shows systolic lengthening of basal anterolateral segment (red colour-coded strain curve (highlighted in blue arrows) and post-systolic shortening (highlighted in blue arrows) with a longitudinal strain of −9%. (B) Anteroseptal segment (red colour-coded strain curve) in apical long axis view shows post-systolic shortening with a longitudinal strain of −12% (highlighted with white arrow). (C) Basal and mid anterior (red and blue colour-coded strain curve) segments in the apical two-chamber view shows systolic lengthening (highlighted with blue arrows) with longitudinal strain of −3% and −4%, respectively.
Transthoracic echocardiogram
Two-dimensional transthoracic echocardiogram (PLAX and PSAX views, video 1) showed concentric left ventricular hypertrophy and no wall motion abnormalities with a visually assessed ejection fraction of 65%. Apical five-chamber view did not show any outflow tract gradients and all valves were normal (videos 2 and 3). Analysis of strain curves of apical four-chamber (figure 3A) view using two-dimensional speckle tracking showed systolic lengthening of basal anterolateral segment (red colour-coded strain curve, highlighted in blue arrows) and post-systolic shortening (highlighted in blue arrows) with a longitudinal strain of −9%. Strain curve of the basal-anteroseptal segment (red colour-coded strain curve) in apical long axis view (figure 3B) showed post-systolic shortening with a longitudinal strain of −12%. Basal and mid anterior (red and blue colour-coded strain curve) segments in the apical two-chamber view (figure 3C) showed systolic lengthening with longitudinal strain of −3% and −4%, respectively. The global average global longitudinal strain was −11.9%. Bull’s eye plot (figure 4) showed significantly reduced territorial strain in the mid and basal anterior, anterolateral and lateral segments corresponding to the left anterior descending artery. Basal inferior and inferolateral segments also showed significant reduction of longitudinal strain (figure 4).
Video 1. Two-dimensional transthoracic echocardiogram: parasternal long axis view and parasternal short axis view showing no regional wall motion abnormalities involving the left ventricle with concentric left ventricular hypertrophy.
Video 2. Two-dimensional transthoracic echocardiogram: apical four-chamber view and apical long axis view (2B) showing no regional wall motion abnormalities with left ventricular hypertrophy, normal mobility of the mitral and aortic valves, non-dilated left atrium, right atrium and right ventricle.
Video 3. Two-dimensional transthoracic echocardiogram: colour Doppler evaluation of apical four-chamber view and apical five-chamber view showing normal mitral, aortic, left ventricular outflow tract and tricuspid valves.
Figure 4.
Bull’s eye plot of longitudinal strain of 17 myocardial segments analysed using two-dimensional STE showing an average GLS of −11.9% with severely diminished strain in the mid and basal anterior, anterolateral and lateral segments corresponding to the left anterior descending artery.
Coronary angiogram
Patient was taken for a coronary angiogram which showed a codominant system with total occlusion of the left anterior descending artery (figure 5A, B) and a normal left circumflex artery (figure 5B, video 4). The right coronary artery was totally occluded (J-CTO score: −2) (figure 5C, video 4)with distal filling seen from heterocollaterals from the left system.
Figure 5.
(A) Coronary angiogram (RAO 30° caudal 26° view) showing total occlusion of the left anterior descending artery (highlighted in yellow arrows) and a normal left circumflex artery. (B) Total occlusion of the left anterior descending artery in LAO 20° cranial 35° view(highlighted in yellow arrows). (C) LAO cranial 45° view showing total occlusion of the right coronary artery (highlighted in yellow arrows). (D)TIMI III flow in the left anterior descending artery revascularisation with an everolimus eluting stent.
Video 4. Coronary angiogram LAO cranial view and RAO caudal view showing totally occluded left anterior descending artery disease free left circumflex artery, LAO caudal view showing chronic totally occlusion of right coronary artery and after revascularised left anterior descending artery with an everolimus eluting stent.
Differential diagnosis
The patient had a history suggestive of a typical angina associated with dynamic changes on serial electrocardiograms. Since the patient had baseline pre-excitation, the ST-segment T wave changes on the admission ECG could be due to secondary repolarisation changes inherent to pre-excitation. Serial electrocardiograms showed subtle QRS axis changes from the initial −30° °to 120°̊ associated with horizontal ST-segment changes and symmetric T inversion associated with doubling of cardiac biomarkers (highly sensitive troponin from 0.32→0.62) at an interval of 2 hours. Two-dimensional transthoracic echocardiography did not show obvious wall motion abnormalities but longitudinal strain analysed by speckle tracking echocardiography showed post-systolic shortening of mid and basal anterior and anterolateral segments with severely diminished longitudinal strain corresponding to the left anterior descending artery. Global Longitudinal Strain (GLS) was almost reduced in all myocardial segments (figure 4) with an average of low −11.9% which we presume could be due to long-standing hypertension induced microvascular damage and subclinical dysfunction. Since patient had baseline pre-excitation, abnormal deformation observed in the strain curves inherent to premature activation of ventricular myocardium could not be nullified. Since chronic pre-excitation induced left ventricular dysfunction is more common with right free wall accessory pathways, our patient was with possible left postero-septal accessory pathway and so we presume that post-systolic shortening observed in the myocardial segments corresponding to the left anterior descending artery could be due to infarction. Coronary angiogram confirmed our diagnosis of acute anterior wall myocardial infarction with total occlusion of the left anterior descending artery.
Treatment
Patient underwent primary angioplasty of the left anterior descending artery using an everolimus eluting stent (size: 3×36 mm) (figure 5D, video 4) and the procedure was uneventful. An ECG after primary angioplasty (figure 6) showed incomplete pre-excitation with disappearance of delta wave in lead III, aVF and V1 and normalisation of PR interval (160 ms) and horizontal ST-segment depression with T inversion (primary repolarisation abnormalities) were observed in leads V2-–V6.
Figure 6.
ECG taken after revascularisation shows normalisation of PR interval (160 ms) and disappearance of delta wave in lead III, aVF and V1. Horizontal ST-segment depression with T inversion (highlighted in green arrows: primary repolarisation abnormalities) were observed in leads V2–V6.
Outcome and follow-up
Exercise stress testing (tread mill) was performed a week after primary angioplasty to assess loss of pre-excitation during exercise that could indicate a low probability to develop malignant arrhythmias. At a heart rate of 120/min (shortest RR interval 400 ms) (figure 7B), there was complete loss of pre-excitation in all leads with normalisation of PR interval (160 milliseconds). Patient was started on guideline-directed medical therapy, discharged uneventfully and under regular follow-up.
Figure 7.
(A) An ECG taken in supine position before the initiation of exercise stress testing showing baseline pre-excitation at an RR interval of 680 ms, zoomed inset (C) showing short PR interval and delta wave at rest. (B) ECG taken at stage III showing disappearance of delta wave and normalisation of PR interval at an RR of 400 ms, zoomed inset(d) showing disappearance of delta wave.
Discussion
The diagnosis of ST-segment elevation in patients with underlying pre-excitation is challenging because primary repolarisation abnormalities of ST segement elevation myocardial infarction (STEMI) could be masked by secondary ST-segment and T wave changes (secondary repolarisation abnormalities) induced by pre-excitation. The amount of pre-excitation depends on the relative contribution of both AV-nodal and accessory pathway conduction leading to ventricular activation. Positive delta wave masks necrotic Q wave, whereas negative delta wave could simulate Q wave.1 Q wave–T wave concordance could help in diagnosing myocardial infarction with serial electrocardiograms.2 In the absence of dynamic changes with serial electrocardiograms, pharmacological agents like atropine or amyl nitrite and non-pharmacological manoeuvres like exercise test stress testing could be used to enhance atrio-ventricular node (AV)-nodal conduction and unmask ischaemic changes on an ECG.3 Anti-arrhythmic agents, particularly class Ia (procainamide) could selectively block conduction over the accessory pathway and enhance AV-nodal conduction.3 But pharmacological and non-pharmacolgical manoeuvres could precipitate malignant arrhythmias in patients with acute myocardial infarction. In patients with underlying pre-excitation, myocardial infarction could be diagnosed on an ECG by ST segment–T wave concordance with delta wave, horizontal ST-segment changes, symmetric T wave inversion and dynamic ST-segment T wave changes in serial electrocardiograms.4 Pre-excitation masking or mimicking an infarction depends on the location of the accessory pathway in which case an accessory pathway ipsilateral to the infarction will exaggerate the infarction changes, whereas a contralateral location masks infarction changes.5 The average time lag from symptom onset to cardiac biomarker elevation is ~3 hours for conventional non-high-sensitivity troponin and 1–3 hours for highly sensitive troponin.6 In the ischaemic cascade since echocardiographic abnormalities (diastolic dysfunction and systolic regional wall motion abnormalities) precede electrocardiographic changes and cardiac biomarker elevation, deformation imaging could hasten therapeutic decision-making.6 Additionally, in acute coronary syndromes two-dimensional speckle tracking could be used to predict the severity of occlusion and major adverse cardiovascular outcomes like malignant arrhythmias, heart failure, target lesion revascularisation and mortality.7 Due to the above limitations, it is imperative to arrive at a diagnosis based on a comprehensive clinical history, clinical examination, serial electrocardiograms, cardiac biomarkers and correlate it with regional wall motion abnormalities identified with an echocardiogram. Analysis of the strain curves in apical four-chamber view showed abnormal deformation (systolic lengthening) in the mid and basal anterolateral segments which could be due to underlying pre-excitation or infarction-induced changes. Post-systolic shortening of the basal antero-lateral and antero-septal segments are more likely to be infarction-induced changes rather than due to pre-excitation.
Anomalous accessory pathways leading to premature activation of the ventricular myocardium could produce abnormal early deformation in the systolic phase (before aortic valve closure) of the strain curve that might help in localising the accessory pathway. Chronic pre-excitation, particularly right free wall and right postero-septal pathways leads to mechanical dyssynchrony and abnormal interventricular septal8 9 motion resulting in left ventricular dysfunction,8 a mechanism similar to left ventricular dysfunction caused by chronic left bundle branch block with a QRS duration >150 ms. In addition, patients with manifest right-sided pre-excitation can have regional wall motion abnormalities due to aberrant activation of ventricular myocardium.8 There is some evidence that mechanical dyssynchrony due to pre-excitation disturbs myocardial regional workload and wall stress leading to wall motion abnormalities, myocardial perfusion defects and changes in coronary blood flow. Decreased workload and hypotrophy leads to thinning of the pre-excited myocardial segment.
Exercise test stress testing could be used in patients with pre-excitation to identify individuals at high risk for developing malignant arrhythmias and sudden cardiac death. During exercise increased sympathetic tone increases preferential conduction through the AV node and could indicate that the accessory pathway has a long antegrade effective refractory period with lower incidence of sudden arrhythmic death.6 10 For an asymptomatic individual with manifest pre-excitation who demonstrate abrupt and clear loss of manifest pre-excitation during exercise stress testing, adequate counselling regarding arrhythmic symptoms and regular follow-up would just be adequate.6 10 Our patient underwent exercise test testing a week after revascularisation, and there was complete disappearance of pre-excitation with normalisation of PR interval at a shortest RR interval of 400 ms that indicates that he has low risk for developing sudden arrhythmic death.
Patient’s perspective.
I had severe left sided chest pain that had spread to my left shoulder and arm while working in my shop. The pain lasted for more than 15 minutes and since the pain was increasing I visited a nearby health centre. An ECG was taken and I was informed by the doctor in the emergency department that the ECG had some variation and I might require a consultation from a cardiologist. I was then shifted to the critical coronary unit and an ECG was repeated. An echocardiogram was performed and blood investigations were taken. The doctors informed that my blood tested for a heart attack and there are some changes in the echocardiogram for which I might require a coronary angiogram. After discussing with my family members we consented for a coronary angiogram. After the coronary angiogram, the doctors explained me that there are two critically occluded blood vessels and one blood vessel required immediate angioplasty. The risks and benefits of the procedure was explained and I consented for the emergency procedure. After angioplasty, my chest pain reduced significantly and was kept in the coronary ICU for 48 hours. I was started on oral medications and the importance of regular exercise was explained to me at the time of discharge. The doctors advised to continue all medications regularly and come for a follow up after one week.
Learning points.
Cardiac troponin supplemented by serial electrocardiograms could help in suspecting acute coronary syndrome in patients with underlying pre-excitation.
Two-dimensional Speckle tracking echocardiography (STE) could be used to localise the accessory pathway and the culprit artery in patients presenting with myocardial infarction that would assist to plan an appropriate therapeutic strategy.
Astute knowledge of limitations of deformation techniques is imperative before diagnosing infarction with baseline pre-excitation.
Exercise stress testing could be used to risk stratify patients and identify individuals at low risk of developing malignant arrhythmias due to pre-excitation.
Footnotes
Contributors: KR was responsible for echocardiographic and electrocardiographic data interpretation and data acquisition. AT helped in critical revision of the intellectual content. MKS prepared the first draft. AS did the final proof reading.
Funding: The authors have not declared a specific grant for this research from any funding agency in the public, commercial or not-for-profit sectors.
Case reports provide a valuable learning resource for the scientific community and can indicate areas of interest for future research. They should not be used in isolation to guide treatment choices or public health policy.
Competing interests: None declared.
Provenance and peer review: Not commissioned; externally peer reviewed.
Ethics statements
Patient consent for publication
Consent obtained directly from patient(s).
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