When extracellular lipid merges into a lipid-necrotic core and a layer of connective tissue forms over it, the lesion becomes a fibrous plaque. In the Stary classification this is type IV (atheroma: a core is present, fibrosis does not yet dominate) and type V (fibroatheroma: thick layers of fibrous tissue). The teaching macroscopic stage "fibrous plaques" combines both.
Macroscopy. Dense, whitish-yellow elevations of the intima, often confluent. On section: a gruel-like yellow core and a white cap. In the aorta the plaques deform the inner surface; in the coronary and cerebral arteries they also narrow the lumen.
The microscopy you need to be able to label on a specimen.
- Lipid-necrotic core: amorphous debris, cholesterol crystals, foam cells at the periphery.
- Fibrous cap: collagen, smooth muscle cells, proteoglycans. The thickness and cellularity of the cap determine how resistant the plaque is to rupture.
- Cellular inflammatory infiltrate: macrophages, T lymphocytes — especially at the shoulder of the plaque, where the cap is thinner.
- Newly formed vessels from the adventitia (plaque neoangiogenesis): the source of intraplaque haemorrhage.
- Preserved or thinned media beneath the plaque.
Haemodynamic meaning. As long as the plaque grows outward (positive remodelling according to Glagov), the lumen can remain adequate for a long time — hence "silent" coronary disease with an already large atherosclerotic burden. When the remodelling reserve is exhausted, stenosis appears. ESC CCS 2024 specifically emphasises: ischaemia can be caused not only by a fixed focal stenosis, but also by diffuse atherosclerosis without "critical" narrowing, as well as by vasospasm and microvascular dysfunction. For the pathologist looking at an aortic specimen, this refinement does not cancel the stage "fibrous plaque"; for the clinician it forbids reducing all angina to a percentage of stenosis.
A stable fibrous plaque with a thick cap more often causes chronic ischaemia (stable angina, intermittent claudication, chronic cerebral ischaemia) than sudden thrombosis. This is a statistical tendency of morphology, not a guarantee: any plaque can become complicated.
The boundary of the lesson. The percentage of stenosis on angiography is not the same as the morphological stage. Angiography sees the lumen, not the core. CT angiography and intravascular ultrasound are closer to morphology but also do not replace histology. At a pathological anatomy exam "70% stenosis" is not the name of a stage; the name of the stage is fibrous plaque (or complicated, if there is thrombus, ulcer or haemorrhage).
The link to the next lesson. It is at the stage of the fibrous plaque that it is decided whether the disease will follow the path of slow stenosis or the path of a complicated lesion — cap rupture, atheromatous ulcer, thrombosis.