Case: STEMI equivalent without classic ECG changes – what can we learn?

A man in his 60s was admitted to hospital around 4 p.m. with chest pain. The pain subsided after administration of 5 mg morphine and nitroglycerin. The admission ECG (ECG 1) was described as normal. Initial troponin T was 36 ng/L, rising to 66 ng/L one hour later. The patient was diagnosed with NSTEMI. He was started on clopidogrel in addition to aspirin, which had been given prehospital. He was then transferred to the ward with a plan for coronary angiography the following day.

Around 2 a.m. the same night, the patient experienced recurrent chest pain. A new ECG (ECG 2) was taken, and he again received morphine and nitroglycerin. Troponin T had further increased to 495 ng/L. Despite this, no further measures were initiated at that time. Coronary angiography the next day revealed an occluded LAD, and PCI was performed with restored flow. Post-PCI ECG (ECG 3) showed T-wave inversions and Q-wave development in the precordial leads. Echocardiography demonstrated infarction sequelae in the anterior wall. Troponin T had then risen to 3545 ng/L.

This represents an acute LAD occlusion (a STEMI equivalent) that occurred around 2 a.m. but was not treated as an acute revascularization emergency. Earlier angiography might have significantly reduced myocardial damage.

ECG interpretation

ECG 1: Shows subtle but likely pathological hyperacute T-waves in V2 and V3. These may be difficult to interpret, especially without a baseline for comparison.

ECG 2: Shows mild ST elevations, pronounced hyperacute T-waves in V2 and V3, and R-wave loss in V2 – a serious finding indicating ongoing transmural ischemia.

ECG 3: Shows T-wave inversions and further R-wave loss in the precordial leads consistent with reperfusion and established myocardial injury.

Hyperacute T-waves are typically broad and tall, representing viable but ischemic myocardium. They often appear during the pain phase. In younger individuals, large T-waves can be a normal variant, particularly in the precordial leads, but when accompanied by R-wave loss, this strongly suggests pathology.

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 Learning points

• In patients with NSTEMI and persistent or recurrent chest pain, there is a high likelihood of reduced or intermittent coronary flow. Acute coronary syndrome often involves a dynamic thrombotic process with repeated occlusion and spontaneous recanalization – a so-called “on-off phenomenon.”

• Measuring troponin T during new episodes of chest pain has limited clinical value in the acute phase, as rises are delayed and rarely influence immediate management.

• When in doubt about further management, consult a cardiologist or experienced physician early. Clinical suspicion of occlusion should be given high weight, even in the absence of classic STEMI ECG changes.

• An occluded coronary artery does not always produce ST elevation on ECG. STEMI criteria have high specificity but low sensitivity for detecting all patients with transmural ischemia. This highlights the importance of recognizing STEMI equivalents and atypical ECG presentations.

Conclusion

This case illustrates that acute coronary occlusion can occur without classic STEMI changes on ECG. In patients with recurrent chest pain and dynamic ECG findings, strong clinical suspicion should prompt consideration of early revascularization to limit myocardial injury.