The Vulnerable Plaque
The Vulnerable Plaque
For many years now, we have recognized that the abrupt damage of an atheromatous plaque in a coronary artery could cause acute myocardial ischemia and infarction. In the late 1940s, the ischemic condition that was just short of infarction was called preliminary infarction and later on, it was labeled pre-infarction angina. More elegant injection studies of the coronary arteries taught us that slow narrowing of the coronary artery stimulated the development of collateral coronary arterioles that seemed to prevent infarction even when total obstruction of the artery occurred.
Fifty years ago, we believed that a nonobstructing atheromatous plaque became acutely obstructive when there was hemorrhage under the plaque. More recently, we have been taught that the nonobstructive plaque with a large amount of lipid core (> 40%) would likely rupture and obstruct the artery.
Maseri and Fuster have pointed out recently that this view of the cause of acute obstruction of a previously nonobstructive plaque is too simplistic. They emphasize that a blood factor, chronic and acute coronary inflammation, and coronary plaque fissures and erosions play a role in the final obstructing event.
For many years now, we have recognized that the abrupt damage of an atheromatous plaque in a coronary artery could cause acute myocardial ischemia and infarction. In the late 1940s, the ischemic condition that was just short of infarction was called preliminary infarction and later on, it was labeled pre-infarction angina. More elegant injection studies of the coronary arteries taught us that slow narrowing of the coronary artery stimulated the development of collateral coronary arterioles that seemed to prevent infarction even when total obstruction of the artery occurred.
Fifty years ago, we believed that a nonobstructing atheromatous plaque became acutely obstructive when there was hemorrhage under the plaque. More recently, we have been taught that the nonobstructive plaque with a large amount of lipid core (> 40%) would likely rupture and obstruct the artery.
Maseri and Fuster have pointed out recently that this view of the cause of acute obstruction of a previously nonobstructive plaque is too simplistic. They emphasize that a blood factor, chronic and acute coronary inflammation, and coronary plaque fissures and erosions play a role in the final obstructing event.