The first ECG (Figure, A) showed what at first glance would appear to be normal STE in anterior precordial leads (almost 1 mm), but normal STE in leads V2 through V4 is never accompanied by STD in leads V5 through V6 and also never by STD in leads II, III, and/or aVF. This feature suggests LAD occlusion or near occlusion as the cause of that STE.1
The biphasic T-wave inversion on the second ECG (Figure, B), along with the resolution of chest pain, are manifestations of subtle Wellens syndrome pattern A,2 which is a clinical syndrome of resolved typical chest pain and characteristic precordial T-wave inversions. The hidden cause of the syndrome is acute LAD occlusion that goes unrecorded by any ECG, followed by spontaneous reperfusion and resulting Wellens T waves. Reperfusion T waves can be biphasic (Wellens pattern A; positive in the early and negative in the late stretch) or symmetric negative (Wellens pattern B), constituting 25% and 75% of cases, respectively. Thus, Wellens syndrome is a transient STEMI, in which the STEMI was not recorded.3 In this case, the LAD occlusion is indeed recorded but is subtle because the STE does not meet STEMI criteria. Transient STEMI can be managed with a next-day angiogram and percutaneous coronary intervention, but many will reocclude in the middle of the night, rendering delayed intervention a high risk.4