Wellens’ syndrome over the past three decades


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The 12-lead ECG plays a central role in the evaluation of patients with chest pain in the emergency department as it is rapid, reliable, noninvasive and inexpensive, 1–3 and identifies cases that need early intervention. 1,4 Although most physicians are well trained in recognizing STEMI in an ECG, other ominous signs such as Wellens’ syndrome are not well recognized. 4 We present a review of the literature over the past three decades since the seminal publication 5 characterizing these changes, with an illustrative case.An 87-year-old man without known coronary disease but with a past history of abdominal aortic aneurysm measuring 4.1 cm and tobacco abuse presented with episodes of angina for the past 3 days. On presentation his blood pressure was 126/64 mmHg and his heart rate 72 beats/min; the physical exam was unremarkable. His initial 12-lead ECG showed biphasic T-wave inversions in leads V2–V4 (Fig. 1). Initial troponin was mildly elevated at 0.043 ng/ml. He received aspirin, β-blocker, statin and heparin drip and underwent a left heart catheterization that revealed 95% occlusion of the distal left main (Fig. 2). The patient underwent coronary artery bypass grafting and made an uneventful recovery.DiscussionGerson et al. 6 in 1979, initially described ECG findings of exercise-induced inverted terminal T waves in the precordial leads in patients with proximal left anterior descending (LAD) ischemia. In 1980, Gerson et al. again described these ECG changes at rest, in patients with LAD or left main ischemia in 89% of described cases. 7 In 1982, de Zwaan et al. 5 described a clinical syndrome consisting of angina with a pattern of characteristic ECG changes associated with critical stenosis of the proximal LAD. Clinical and electrocardiographic criteria of Wellens’ syndrome are as follows: A history of angina with the following ECG changes:(a)Biphasic or deeply inverted T waves in leads V2 and V3, and occasionally in leads V1, V4, V5 and V6.(b)No or minimal ST-segment elevation (<1 mm).(c)No loss of precordial R-wave progression.(d)No pathological precordial Q wave.(e)No or minimal elevation of cardiac enzymes. Other ECG characteristics associated with Wellens’ type T-wave abnormalities: 8,9 (a)Isoelectric or minimally elevated (<1 mm) ST segment with a straight or convex morphology.(b)Sharp down-slope of the T wave.(c)Prolonged QT interval. The ECG changes can be further classified based on pattern of T-wave changes into two types 5 that are as follows: Type 1: seen in 75% of cases, T waves are deeply (≥5 mm) and symmetrically inverted in leads V2–V4.Type 2: 25% of cases, the T wave has a positive–negative biphasic morphology in leads V2–V4.de Zwaan et al. 5 showed that 75% of patients who developed these ECG changes and who were treated medically without coronary angiography developed an extensive anterior wall myocardial infarction within a mean of 8.5 days. Also, the more proximal the LAD stenosis, the more widespread precordial T-wave abnormalities were found. 5 In our patient distal left main stenosis caused typical ECG changes with a more widespread precordial lead involvement. Similar involvement of distal left main stenosis with precordial ECG changes has been described in other case reports. 10 In a follow-up study of patients with unstable angina, 180 patients (14%) who had this characteristic T-wave pattern had stenosis of 50% or more in the proximal left anterior descending artery, and 18% had complete occlusion of the left anterior descending artery.

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