Feb. 9, 1999 DALLAS, Feb. 9 -- A new study links an abnormality in the immune system to some forms of congestive heart failure, a finding that may have important implications for how the disease is treated, say researchers in today's Circulation: Journal of the American Heart Association.
The researchers, located in Germany, say their study is the first to show that the immune system -- the disease fighting system of the body -- in individuals with congestive heart failure produces antibodies programmed to attack heart tissue. Congestive heart failure, the fastest growing form of heart disease, is a chronic condition in which a heart muscle becomes damaged by coronary heart disease including heart attacks.
In a study of 104 patients, the researchers found that 26 percent of those with dilated cardiomyopathy -- congestive heart failure not caused by coronary heart disease -- had autoantibodies attacking a specific region of the heart called the beta-andrenergic receptors. The autoantibodies stimulated the heart to beat too rapidly.
In contrast, only 10 percent of people with the most common form of congestive heart failure, caused by heart attack and coronary heart disease, had autoantibodies.
Only one percent of the 108 healthy individuals without congestive heart failure or other diseases had the autoantibodies.
Fritz Boege, M.D., head of the department of clinical chemistry at Medizinische Poliklinik, University of Wüerzburg, and co-author of the study, says this research might explain why drugs called beta-blockers -- which act on the beta-andrenergic receptors to slow the heart's beating -- are effective in many patients with congestive heart failure.
The beta-blockers used to treat heart failure act directly on these receptors, which are sites on the cells that act as gatekeepers directing the entry or binding of other molecules to the cells
Roland Jahns, M.D., of the department of cardiology at same clinic, says, "Individuals with heart failure make extra adrenaline, a hormone that helps the heart pump faster. The binding of adrenaline to the beta-receptors makes the heart beat even faster and contract more strongly. The autoantibodies seem to prolong the active state of the receptors. They stimulate the receptor, which enhances the effect of adrenaline." Researchers found that in dilated cardiomyopathy, the hearts of those who had the autoantibodies pumped less blood compared to those who did not.
"The constant beta-receptor activity leads to a vicious cycle of overdrive wearing out the heart muscle," says Jahns.
In further support of this conclusion, test tube studies showed that adding the beta-blocker bisoprolol to the individual's blood could block the autoantibody. However, they add, it is too soon to conclude that there is a cause and effect relationship between autoantibodies and heart failure, says Jahns. And researchers do not understand yet why the autoantibodies are produced. Congestive heart failure can cause shortness of breath and extreme limitations in physical activity. With the aging population, understanding the mechanisms of the disease becomes more important every year. About 4.6 million Americans have congestive heart failure.
Co-authors are Roland Jahns, M.D.; Valerie Boivin-Jahns, Ph.D.; Christian Siegmund, M.D.; Gerhard Inselmann, M.D.; Martin J. Lohse, M.D.; and Fritz Boege, M.D.
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