A clinical myocardial infarction almost never arises from a "smooth" thick-capped plaque at the moment of an exam narrative. It arises from a complicated lesion. In the teaching morphological ladder this is the third stage after spots and fibrous plaques: atheromatosis, ulceration, haemorrhage into the plaque, mural thrombus. In the Stary 1995 classification this is type VI: fissure, haematoma, thrombus.
Let us go through the words that are confused on a specimen.
Atheromatosis is the breakdown of the lipid-necrotic core into a gruel-like mass (atheromatous debris) with cholesterol crystals. The core becomes soft, the cap becomes a lid over a cavity.
Ulceration (atheromatous ulcer) is a defect of the cap through which the debris communicates with the lumen. Cholesterol crystals and fragments fall into the lumen — the source of cholesterol emboli. On the aorta the ulcer looks like a crater with undermined edges and a yellow floor; a thrombus easily settles on such a floor.
Haemorrhage into the plaque comes from neovessels or through a fissure communicating with the lumen. It sharply increases the volume of the plaque and can bring a stenosis to occlusion even without a large thrombus.
Mural thrombus — clots on the damaged surface. In a coronary artery, a thrombus occluding the lumen is the morphological substrate of ST-elevation myocardial infarction. A non-occlusive thrombus on a damaged plaque is the substrate of non-ST-elevation myocardial infarction and unstable angina. ESC CCS 2024 describes a clinical continuum: a person with chronic coronary syndrome can move into ACS and return to "a stabilised phase after ACS, percutaneous coronary intervention (PCI) — angioplasty and/or stenting of a coronary artery — or coronary artery bypass grafting (CABG) — bypassing the stenosis with a graft". The morphological bridge of this transition is the complicated plaque.
Why the cap ruptures. A thin cap, rich in macrophages and poor in collagen, especially at the shoulder of the plaque; a large soft core; intraplaque haemorrhage. The working concept of the "thin-cap fibroatheroma" came from the morphology of sudden coronary death (the line of work by Virmani et al., Arterioscler Thromb Vasc Biol., 2000s) and is used in imaging. In the teaching ladder it is enough to be able to say: a complication is the destruction of plaque integrity with thrombosis and/or embolisation of debris.
Atherothrombosis as a clinical language. European documents speak of ASCVD — atherosclerotic cardiovascular disease. A thrombus on a plaque is the mechanism of an acute event in the coronary, cerebral and peripheral territories. Cholesterol embolism after manipulations on the aorta is a separate syndrome (renal ischaemia, livedo, eosinophilia); its detailed discussion lies beyond the boundaries of the course, but the source of the emboli — an ulcerated aortic plaque — belongs to this stage.
The boundary of the lesson. Not every acute coronary syndrome equals "plaque rupture": there is cap erosion with a thrombus on a relatively preserved surface, and there is a purely vasospastic mechanism. ESC CCS 2024 includes vasospasm in the spectrum. On a pathological specimen of the aorta, the teaching stage "complicated lesion" is still assigned by ulcer, atheromatosis and thrombus, not by spasm, which cannot be seen on a fixed specimen.