Acute Myocardial Infarction in a Patient with Wolff-Parkinson-White Pattern ECG

Abbreviations

AMI, Acute myocardial infarction

ECG, Electrocardiogram

LCx, Left circumflex artery

PCI, Percutaneous coronary intervention

RCA, Right coronary artery

WPW, Wolff-Parkinson-White

INTRODUCTION

Wolff-Parkinson-White (WPW) syndrome is the most common form of ventricular preexcitation. Due to alterations on ventricular intramural conduction and repolarisation, electrocardiogram changes can mimic that seen in myocardial infarction, and diagnosis in the presence of both conditions can be difficult. Differentiation of WPW patterns from actual infarction could thus prove difficult. We report an interesting case where the WPW pattern on electrocardiogram (ECG) could have potentially masked the diagnosis of an acute myocardial infarction (AMI).

CASE

A 46-year-old male presented with first onset central chest pain at rest. It lasted for 30 minutes and was associated with mild dyspnea. The patient denied palpitation, diaphoresis, syncope and fever. He is an active cigarette smoker with a 20-pack-year smoking history. He has no past medical history or family history of sudden cardiac death or heart disease. In addition, a previous health screen and exercise stress test 4 years ago was unremarkable. He was not taking any medication or over the counter supplements.

On arrival to hospital, the patient was afebrile, with blood pressure of 135/88 mmHg, heart rate of 85 beats per minute, respiratory rate of 16 per minute and oxygen saturation of 98% on room air. Physical examination was unremarkable. Cardiac auscultation revealed normal first and second heart sounds with no murmurs. Initial ECG revealed sinus rhythm, short PR interval, delta wave, 1 mm ST elevation and biphasic T waves in V5-6 and inferior leads (Figure 1A). In addition, there were 1 mm ST depressions and T inversions in lead I and aVL. There was no available right sided ECG. Laboratory results revealed normal electrolytes, renal, liver panel and thyroid function. High-sensitive troponin I level on presentation was 45 ng/L and peaked at 8,274 ng/L (normal range 0-18 ng/L). Lipid panel showed elevated low density lipoprotein-cholesterol of 4.3 mmol/L, triglycerides 10 mmol/L and high density lipoprotein-cholesterol 0.9 mmol/L. Chest radiography showed no consolidation or pleural effusion. His reverse-transcription polymerase chain reaction for COVID-19 was negative.

Figure 1.

(A) Initial electrocardiogram showing sinus rhythm, short PR interval, delta wave, 1 mm ST segment elevations and biphasic T inversions in V5-6 and the II, III and aVF, 1 mm ST segment depressions in I and aVL. (B) Repeat electrocardiogram was done on day 5 of hospitalization showing sinus rhythm, delta wave and resolution of ST segment changes in V5-6, II, III, aVF, I and aVL.

Coronary angiogram showed double vessel disease with acute occlusion of the left circumflex artery (LCx) and 90% stenosis in the proximal right coronary artery (RCA) (Figure 2A, B). Primary percutaneous coronary intervention (PCI) was done with placement of a drug-eluting stent in LCx (Figure 2C). Staged PCI was performed to his RCA three days later. Transthoracic echocardiogram showed left ventricular ejection fraction of 55% with normal wall motion. Inpatient telemetry did not reveal any significant arrhythmia. A repeat ECG on day 5 of hospitalisation showed resolution of ST segment changes in the inferior leads, I and aVL (Figure 1B).

Figure 2.

(A) Coronary angiogram revealing acute occlusion of the left circumflex artery (LCx). (B) There was a 90% stenosis in the proximal right coronary artery. (C) Successful re-establishment of blood flow with implantation of a drug-eluting stent in LCx. PCI, percutaneous coronary intervention.

The electrophysiology team was consulted, and impression was that of WPW pattern ECG. The patient was subsequently discharged well on day 6 of hospitalization, and was scheduled for an outpatient exercise stress test, for further risk stratification.

DISCUSSION

The appearance of delta wave in WPW can mimic ischemia by producing pseudo-infarct Q waves in the corresponding leads. Goldberger et al. demonstrated that concordant Q/T waves were highly suggestive of primary ischemic changes.¹ This unique pattern have been described in identifying ischemia among patients with hypertrophic cardiomyopathy, left ventricular hypertrophy and paced rhythm.² AMI and WPW pattern ECG may present simultaneously and represent a lethal event.³ At times, the electrocardiographic diagnosis of myocardial infarction can only be made from normally conducted beats. In addition, presence of fragmented QRS complexes increases the specificity for infarction to 96%.^4,5

Coronary artery vasospasm and Takotsubo cardiomyopathy are key differential diagnoses to consider in this case. Thus, invasive coronary angiogram remains the gold standard in evaluating coronary anatomy. Peri-myocarditis also needs to be excluded in the setting of raised troponin, wall motion abnormalities and patent coronaries. Benign repolarization ECG pattern remains largely a diagnosis of exclusion.

Depolarization abnormalities on ECG are usually associated with repolarization changes. They include bundle branch blocks, intraventricular conduction delays and pre-excitation.⁶ Early repolarization ECG pattern has been previously reported as well.^7,8 In our case, despite the ECG changes, the combination of angina, significant cardiovascular risk factor of smoking and elevated troponins raises the suspicion of an acute myocardial infarction. This highlights the importance of identifying the ECG subtleties in the appropriate clinical situation. Identification of concordant Q/T wave changes in WPW pattern is an important but often overlooked feature. In certain cases, serial ECG and troponin evaluation may be required to aid in the diagnosis. Patient of WPW with AMI may presents with arrhythmia (may include atrial or ventricular fibrillation), necessitating early defibrillation or administration of procainamide.

Once confirmed, definitive therapy such as cardiac catheterization and if required, PCI, should be performed. In our patient, coronary catheterization revealed a 100% acute occlusion of the LCx, which is the culprit vessel contributing to his symptoms and ECG abnormalities.

The patient was reported to have an unremarkable exercise stress test a few years prior to his current event. Not uncommonly, the delta wave may "manifest" intermittently. Intermittent loss of pre-excitation on ECG and abrupt loss of pre-excitation during exercise are the best predictors of low risk WPW.⁹ The abrupt and complete loss of delta wave during symptomatic stimulations indicates that the accessory pathway is incapable of rapid antegrade conduction, and this puts the patient at a lower risk of tachyarrhythmia.¹⁰ Management of asymptomatic WPW remains debatable, and, catheter directed radiofrequency ablation is of Class IIA based on the latest guidelines.¹¹ Identification of accessory pathway based on ECG is important during ablation and aid with the eventual management.¹²

AMI is an important cause of chest pain in WPW. This case illustrates how ST segment elevation acute myocardial infarction can be masked in the presence of WPW pattern ECG. Having a high index of suspicion, along with careful and systematic interpretation of the ECG and consideration of its differentials are essential in securing an accurate diagnosis in patients with WPW pattern ECG.

LEARNING POINTS

• It is imperative to recognise the significant ECG changes in the setting of WPW.

• In the setting of acute coronary syndrome and pre-excited ECG changes, early identification is important in administration of appropriate life-saving therapy.

DECLARATION OF CONFLICT OF INTEREST

All the authors declare no conflict of interest.

AUTHORS’ CONTRIBUTIONS

SW: Drafting the manuscript, acquisition of data. SS: drafting the manuscript. JL: supervision and critical revision of manuscript.

FUNDING

None.