1. Plaque forms on the inner wall of an artery

Arterial plaque forms on the wall of an artery due to stress on the internal lining of the artery from:

• high blood pressure
• high lipids in the blood
• diabetes
• smoking
• genetic factors

Plaque is a deposit of a fat-like substance that is hard on the outside and soft on the inside. If the cap of a plaque deposit ruptures, it exposes the blood to a lipid-rich layer inside.

2. The hard surface of the plaque tears, exposing the soft inside

Plaque is disrupted or the inner lining of the artery overlying the plaque is eroded away. The plaque can eventually burst or tear. This creates a "snag" where a clot forms.

3. Platelets arrive to form a blood clot. The clot restricts blood flow.

Platelets and other components (fibrin) in the blood immediately react to the newly exposed layer and a clot begins to form. Depending on the size of the rupture, blood flow can begin to diminish beyond the site. This reduces the oxygen delivery to the myocardium. At some point the oxygen supply is reduced enough to cause chest pain or other symptoms.

At the same time, the body begins trying to break up the clot with its own clot-busting agents. Clot dissolving (fibrinolytic) enzymes attempt to remove the clot and open the blood vessel. This is a dynamic and rapidly changing process. It explains why many patients can have short and recurring periods of symptoms.

If the thrombus completely blocks the artery, the area of oxygen-starved tissue dies. If the body is able to reduce the size of the thrombus to allow oxygen delivery beyond the site, the patient most likely will develop angina. When angina is unstable or increasing a patient is at severe risk for a complete myocardial infarction.

Atherosclerosis is another process that causes myocardial ischemia but does not involve actual disruption of an unstable plaque deposit. A stable plaque deposit can increase in size and diminish blood flow past its location.

In this case, the reduced oxygen delivery can meet the myocardial demand while the patient is at rest, but can fall short with exertion. The patient can then develop chest pain as with angina. This chest pain should resolve with either decreasing the workload, stopping exertion and resting, or by increasing the blood flow past the stable plaque by taking nitroglycerin, which causes the artery to dilate.

A less common cause of a heart attack is a severe spasm (tightening) of the coronary artery that cuts off blood flow to the myocardium. These spasms can occur in persons with or without coronary artery disease. Vasospasms can be caused by drugs such as cocaine and cigarette smoking.

In Prinzmetal's angina, atherosclerosis is not the underlying cause. Rather there is a spasm of the artery that acutely reduces or stops blood flow through the artery.