Refractory Angina Confounded by Preexcitation Syndrome.

Abstract

Scenario: This 12-lead electrocardiogram (ECG) was obtained on a 48-year-old man who came to the emergency department with progressively worsening left lateral crushing chest pain and dyspnea of 3 hours’ duration. The patient drinks 9 beers daily, is an active smoker, and is treated for hypertension and hypercholesterolemia. His initial vital signs during prehospital transport showed a heart rate of ~110/minute and blood pressure of 151/100 mm Hg. Paramedics administered aspirin and sublingual nitroglycerin during ambulance transport, and this ECG was obtained upon arrival in the emergency department.Sinus rhythm with Wolff-Parkinson-White (WPW) syndrome type A.In the normal electrical conduction system, the atrioventricular (AV) node serves as a gatekeeper to regulate the propagation of signals from the atria into the ventricles. When an accessory pathway exists, ventricular activation occurs through both the AV node and the extra anatomical pathway, yielding a shorter PR interval and a slurred upstroke of the QRS complex (ie, delta wave). When the accessory pathway connects to the left ventricle, the preexcitation starts in the left ventricle first before it proceeds normally through the bundle of His and bundle branches (called WPW type A). This syndrome manifests as a wide QRS complex with pseudo right bundle branch block pattern (ie, tall R wave in right precordial leads). Because of the temporal heterogeneity in ventricular activation, repolarization abnormalities (or non-specific ST-segment and T-wave changes) are common, including early repolarization pattern (eg, J-point elevation best seen in lead V3 in this example). Such dispersion in ventricular depolarization and repolarization might lead to back propagation of the signal to the atria either through the bundle of His or through the accessory pathway. This back propagation may create an atrioventricular reentry circuit and sustained tachycardia. Although WPW syndrome is usually benign, curative catheter ablation is considered in symptomatic or hemodynamically unstable patients.Although secondary repolarization changes are common in WPW syndrome, the ST-segment elevation in the anterior wall that is accompanied with reciprocal changes in the inferolateral walls, coupled with the highly suspicious presenting symptoms and history, are worrisome for acute myocardial infarction. In this specific patient, the initial cardiac workup was negative, and the patient was admitted to the telemetry unit for serial ECGs and troponin assays. Owing to persistent refractory angina, the patient was referred for cardiac angiography the following morning, which revealed normal left ventricular function and mild atherosclerotic disease in the right coronary artery at 20% to 30% occlusion. The patient was discharged home on oral anti-ischemic therapy (eg, aspirin, nitroglycerin) with a referral to cardiac electrophysiology for further management of the underlying WPW syndrome. Long-term ambulatory monitoring (eg, Holter ECG) is warranted to rule out reentry tachyarrhythmias.