Understanding Heart Attack
By Arthur E. Fass, MD
The last decades have ushered in a new era in the treatment of heart attacks. Gone are the days of passive convalescence. No longer are doctors relegated to the role of concerned observers, powerless to alter the natural course of the illness. Today, heart attack victims are given a range of the most modern and aggressive treatments available in cardiology. Heart attack patients arriving in the hospital now have a greater than 90% chance of surviving the event. Most will go on to lead fully productive and active lives.
What causes a heart attack?
The crucial breakthrough in improving treatment was a superior understanding of the cause of heart attacks. Utilizing anatomic and angiographic studies, it is now known that heart attacks are usually caused by blood clots that block the flow of blood in a coronary artery. The clotting occurs when an underlying atherosclerotic plaque tears or erodes, exposing cholesterol and other clot-promoting substances to the bloodstream.
We do not know what specifically causes a coronary plaque to rupture and trigger a heart attack. Many plaques remain stable for years and never lead to a major clinical event. A great deal of research effort is now directed at attempting to identify vulnerable plaque and preventing it from causing trouble.
The role of risk factors
While a specific inciting cause in plaque rupture is often unknown, there is general agreement that certain risk factors predispose to coronary events. These include hypertension, cholesterol abnormalities, cigarette smoking, diabetes, obesity, and sedentary lifestyle. High levels of mental stress or anger may play a contributory role.
Rarely do risk factors occur in isolation. They are interrelated and tend to bunch together. For example, a sedentary life style is often associated with obesity and diabetes. One aspect common to all risk factors may be the inflammatory response. Inflammation is a complicated series of biochemical reactions mounted by the body in response to a variety of insults such as injury and infection. In a sense, the known coronary risk factors represent forms of physical or biochemical injury to blood vessels resulting in an inflammatory response. Inflammation, in turn, renders atherosclerotic plaques more vulnerable to rupture. It follows that by avoiding or minimizing these risk factors, one will lower the risk of heart attacks. It is tempting to think that by improving the biologic conditions in the coronary circulation that coronary plaques can be stabilized and not cause clinical problems.
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