Like the rest of the muscles in your body, the heart requires a steady supply of oxygenated blood in order to function. But heart muscle cells cannot extract oxygen directly from the blood that passes through the heart’s chambers. Instead, the heart must pump blood to itself via the right coronary artery and left main coronary artery and their branches, which nourish every portion of the heart with oxygen and nutrients.
Atherosclerosis refers to the buildup of fatty deposits called plaques within the lining of arteries. These plaques—largely made up of cholesterol, fibrous tissue, and calcium—develop beneath the innermost layer of an artery and slowly reduce the artery lumen (the space through which blood passes).
If blood flow through one of these vital arteries is obstructed by plaque, the heart muscle cells supplied by that artery may not receive enough blood during periods of exertion, resulting in ischemia (oxygen deprivation to cells). In most cases, rest or medications can restore sufficient blood flow to the area.
Some plaques, however, are unstable and highly susceptible to rupturing. A blood clot may then form on the exterior of the ruptured plaque. A heart attack most commonly occurs when a portion of the clot breaks loose and lodges in a narrow section of the artery, blocking the flow of blood. A blood clot can also block blood flow to the heart at the site of the ruptured plaque, as illustrated above.
In either case, unless the blood supply is restored within minutes, heart muscle cells will die from lack of oxygen. This is called a myocardial infarction—the medical term for a heart attack. The extent of permanent damage depends on the location of the blockage, the availability of alternative arteries to supply blood to the deprived area and the promptness of treatment.