Vulnerable Plaque

Generally an Atheroma becomes vulnerable if it grows more rapidly and has a thin cover separating it from the bloodstream inside the arterial Lumen . Tearing of the cover is called ''plaque rupture''.

Upon rupture, tissue debris spill into the blood stream; these debris are often too large (over 5 micrometers) to pass on through the Capillaries downstream. In this, the usual situation, the debris obstruct smaller downstream branches of the artery resulting in temporary to permanent end artery/capillary closure with loss of blood supply to, and death of the previously supplied tissues. During angioplasty, a severe case of this, enough to be visible on the basis of slow clearance of injected contrast down the artery lumen, the situation is often termed non-reflow.

Additionally, Atheroma rupture may allow bleeding from the Lumen into the inner tissue of the Atheroma making the Atheroma size suddenly increase and protrude into the Lumen of the artery producing Lumen Narrowing or even total obstruction.

Blood Clotting on top of the site of the ruptured plaque may become so large as to largely or completely block the Lumen of the Artery , thereby stopping blood flow to the tissues the Artery supplies.

Medical research since the early to mid-1990s, using IVUS , Thermography , careful clinical follow-up and other methods, have indicated that these lesions are the ones which produce most heart attacks. Unfortunately, vulnerable plaques are not revealed by either cardiac stress testing or coronary angiography, the heart tests most commonly performed clinically with the goal of testing suspectibility to future heart attack.

Repeated Atheroma rupture and healing is one of the mechanisms, perhaps the dominant one, which creates Artery Stenosis .

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Vulnerable Plaque