DOCTOR'S VIEW ARCHIVE
(December 26, 1997) - The way a heart attack (myocardial infarction) comes about is clear. It involves the death of part of the heart muscle (myocardium) due to blockage of a coronary artery delivering nutrients and oxygen to the myocardium. Blockage of the coronary artery is commonly caused by a clot that forms on the inner wall of the artery at the site of damage by atherosclerosis, the accumulation of cholesterol deposits on the walls of the artery. These cholesterol deposits cause hardening and thickening of artery walls and narrowing of their interior diameter.
Some of the risk factors for atherosclerosis and heart attacks are also quite well known. They include a high blood cholesterol (especially, an elevated level of the "bad" LDL cholesterol), high blood pressure (hypertension), diabetes mellitus, cigarette smoking, and a family history of coronary artery disease. There is considerable evidence that an elevated blood level of the amino acid homocysteine may be a risk factor, too.
Not infrequently, however, advanced atherosclerosis is found in the coronary arteries of people with no known added risk factor. Given the absence of a obvious culprit, scientists are examining some new suspects. One of these is infection.
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The concept is that certain chronic (long-term) infections may trigger atherosclerosis -- or they may at the least aggravate it -- and lead to heart attacks. In this regard, Drs. Sandeep Gupta and John Camm from St George's Hospital Medical School in London have weighed the available scientific data associating infections with the development of atherosclerosis and coronary heart disease. Their comprehensive review was published in the periodical Clinical Cardiology (vol. 20, pages 829-836,1997).
In the laboratory, for example, chickens infected with a strain of herpes virus were discovered to have aggressive atherosclerosis in their coronary arteries. Prior vaccination against the virus protected against much of the coronary atherosclerosis.
From epidemiology, it is known that there is a higher incidence of heart attacks in the winter and spring than in the summer and autumn, possibly related to the seasonal increase of the common cold and influenza infections.
On a clinical level, in some cases, common cold or flu-like symptoms are known to have preceded the heart attack. However, common colds are by definition common and flu-like symptoms are quite common, too. Such circumstantial evidence hardly constitutes concrete proof that infections cause coronary atherosclerosis and heart attacks.
One of the more provocative clues pointing to infection as a factor in the development of coronary atherosclerosis and heart disease involves a small bacteria, Chlamydia pneumoniae (C. pneumoniae). As its name suggests, C. pneumoniae causes respiratory tract infections and, in fact, it does so very commonly. About half of middle-aged adults have had C. pneumoniae. Most initial infections with C. pneumoniae cause no symptoms or just mild flu-like symptoms. Many people with C. pneumoniae are unaware they have it.
The projected role of C. pneumoniae infection in atherosclerosis and coronary heart disease rests upon the remarkable capacity of this bacteria to cause chronic occult infection, long-lasting hidden infection that smolders below the surface. Antibodies are proteins produced by the body's immune system to fight infection. In most types of infections, the appearance of antibodies in the blood signals the eventual eradication of the infection and the development of immunity against the infectious agent However, with C. pneumoniae infection, the antibodies produced by the body against C. pneumoniae may be ineffective in
eradicating the bacteria. Therefore. finding C. pneumoniae antibodies in the blood can signify prior exposure or (more importantly) ongoing infection with C. pneumoniae.
Scientists in Europe and the U.S. have independently observed an association between elevated blood antibodies against C. pneumoniae and coronary atherosclerosis and heart attacks. Finnish researchers showed that patients with recent heart attacks had significantly elevated blood levels of antibodies against C. pneumoniae compared with healthy subjects. In Seattle, doctors measured antibodies against C. pneumoniae in patients undergoing coronary angiography, an X-ray dye study to detect narrowing of the coronary arteries due to atherosclerosis. They found a two-fold increase in coronary artery disease in patients with elevated blood antibodies against C. pneumoniae.
Among male heart attack survivors, Gupta and colleagues in London found that increased levels of blood antibodies against C. pneumoniae were associated with an increased risk of developing another adverse cardiac event (defined as an imminent heart attack requiring urgent treatment, another non-fatal heart attack, or sudden death from a heart attack). Moreover, they found that treatment with azithromycin, a potent antibiotic against C. pneumoniae, not only decreased antibodies levels but also decreased the risk of adverse cardiac events.
How chronic infections may cause atherosclerosis and coronary heart disease is not clearly known. It may be caused by direct infectious damage to the artery walls, by disturbances in the body's cholesterol (or other lipid) metabolism, or by increasing the body's tendency to form blood clots. Further research is needed to clarify the connection (and also to validate all of the observations to date).
Atherosclerosis may therefore turn out to be caused or compounded by a chronic bacterial infection. And this is a condition that is potentially treatable and curable with antibiotics.
Lest this concept of coronary artery disease seem just wishful thinking, viewers are reminded of a similar change in concept in the causation of peptic ulcers. For many years, stress and excess acid were believed to be important causes of ulcer disease. Now, H. pylori (a bacteria causing chronic infection of the stomach lining) is believed to be the major cause of ulcer disease. Instead of antacids, current treatment of ulcer disease is with combinations of antibiotics to eradicate this bacteria.
In the years ahead, you may be given antibiotics to keep your heart in tiptop shape. Take that to heart!
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