Coronary artery disease is driven by atherosclerosis — an active, constantly changing process involving the deposition of lipids, fibrous tissue, smooth muscle cells, and calcium in the intimal layer of the coronary arteries.
This plaque buildup can produce two distinct clinical patterns:
- Progressive luminal narrowing (stenosis) that restricts blood flow — the substrate for stable angina and ischemia
- Sudden rupture or erosion with intraluminal thrombosis — the substrate for acute coronary syndromes and myocardial infarction
Worth keeping front of mind: the anatomic size of a plaque is not always directly related to the degree of luminal narrowing it causes. Positive remodeling (the Glagov effect) lets the outer vessel wall expand to maintain the lumen even as plaque accumulates — which is why a large, dangerous plaque can hide on conventional angiography until it ruptures.
The articles that follow break this down: starting with the normal vessel, then plaque composition, how stenosis is graded, and the features that make a non-stenotic plaque dangerous.