From culprit artery reperfusion to non-culprit revascularization: Will ECG play a bigger role in the evolving STEMI care?

Abstract

STEMI evolves rapidly after culprit artery occlusion, causing acute infarct zone contractile dysfunction. With worse infarct zone contractility, greater “work stress” follows on the non-infarct zone with compensatory hyperkinesis to maintain stroke volume, and on the whole heart with compensatory (reflex) tachycardia to maintain cardiac output. This “stress test” tests the ability of the non-culprit arteries to supply the non-infarct zone during this special time of increased demand. The scale of this “stress test” is the extent of acute contractile dysfunction — the larger the incoming STEMI, the greater the stress on the non-infarct zone.