The clinical scenario now widely known as Wellens syndrome refers to the presence of characteristic precordial lead ST-segment and T-wave changes in patients with rest angina, signifying critical stenosis in the proximal LAD with risk of anterior myocardial infarction.1 A follow-up publication by de Zwaan et al2 documented reversible anterior regional wall motion abnormalities in the majority of these patients, reflecting ischemic myocardial stunning.
Wellens ECG changes occur in 2 distinctive patterns: type A (24% of cases) is characterized by biphasic T waves with initial positivity followed by negativity most commonly in leads V2 and V3 but occasionally in leads V1 through V6, whereas type B (76% of cases) is characterized by deep T-wave inversion in the precordial leads, most commonly in leads V1 through V4 but occasionally extending to leads V5 through V6.2 In the current patient, the initial ECG was consistent with a Wellens type A pattern evolving to a type B pattern the next morning, a process described in previous literature on Wellens syndrome.3 Ordinarily, the characteristic ECG abnormalities are present when the patient is pain free and troponin level is normal or mildly elevated.