Correction Appended

Most people have of a clear image of how atherosclerosis, popularly known as hardening of the arteries, causes a heart attack — fatty deposits called plaque build up in a coronary artery until the day the blood flow that sustains the heart is blocked.

If only they were right. In reality, severe coronary artery blockages almost always cause chest pain known as angina and other symptoms as they form. But among those who suffer heart attacks, half of the men and two-thirds of the women report never experiencing a warning symptom. And autopsies of such victims frequently show blood clots jammed into arteries that have been only modestly narrowed.

Standard atherosclerosis therapies include bypass surgery to route blood around blockages, angioplasty and stenting to clear blockages from inside the artery, and drugs like statins that reduce cholesterol levels to slow the formation of plaque. But they have not been enough to prevent 200,000 to 500,000 American deaths annually from what doctors refer to as coronary artery disease.

As a result, many researchers have turned their attention from atherosclerosis in general to the tendency of some patients to develop a form of plaque prone to inflammation and rupture, which can spill a stew of cells into the bloodstream that can incite rapid clotting. Such plaques have been called “vulnerable” plaque.