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BySteven Lome, MD

Pathophysiology of STEMI

BySteven Lome, MD

Pathophysiology – CAD - STEMI

Some atherosclerotic plaques have a stable fibrous cap; others, with a thin cap, are considered “vulnerable.” Unfortunately, only a few research centers have access to the techniques and expertise required to assess plaque morphology in living patients in the catheterization laboratory.

The “vulnerable” plaque responsible for acute coronary syndromes and, ultimately, coronary artery thrombosis, has a thin cap and a necrotic core; see Atherosclerosis Topic Review. There are conditions that mimic STEMI, and distinguishing these can be difficult; these are described in Diagnosis. Tissue factor, a key protein component of the clotting cascade, is located, among many other places, within the necrotic core of atherosclerotic plaques.

With “plaque rupture” or “plaque erosion,” the thin fibrous cap covering the plaque is disrupted or ulcerated. This exposes the blood flow to tissue factor, activates the clotting cascade and leads to intravascular thrombosis. Plaque rupture and thrombosis frequently occurs at plaques that cause only modest coronary stenosis (< 50% luminal narrowing).

STEMI most often results from coronary thrombosis after plaque rupture rather than fixed obstruction. Unstable angina has a lower incidence of coronary thrombosis compared with non-STEMI or STEMI and is more often associated with fixed atherosclerotic stenosis (with critically low flow).

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