Case #004

Exertional chest pain with sweating and nausea is acute coronary syndrome until an ECG says otherwise, and here the ECG settles it. Three millimetres of ST elevation across V2 to V4 is a contiguous anterior territory rather than the diffuse saddle-shaped elevation of pericarditis, and the reciprocal ST depression in the inferior leads is what separates a true infarct from the mimics that also elevate ST segments; the absent friction rub argues the same way. Those leads also localise the culprit before angiography does, since V2 to V4 is left anterior descending territory. The troponin is the trap. Forty minutes in, mildly elevated is exactly right, since the rise lags the occlusion by hours, and a normal value would have excluded nothing. Nobody waits for it. Muscle downstream of the proximal LAD is dying now, so the only question left is which method reopens the artery soonest. That is primary PCI wherever it can be reached in time: mechanical reopening with a stent, target under 90 minutes from first contact. Past about 120, transfer delay costs more than the drug does, so a fibrinolytic (tenecteplase, alteplase) is given and the patient sent for angiography afterwards regardless. It is a fallback rather than an equal, reopening roughly half of arteries against over ninety per cent, with a bleeding risk PCI lacks. Either way aspirin and a P2Y12 inhibitor such as ticagrelor start immediately, since the clot is platelet-rich and an opened vessel re-occludes without them.