DALLAS, Nov. 7 – Three studies published in today’s Circulation: Journal of the American Heart Association provide new insight into the role of infections and inflammation in heart attacks.
One study found that older people who had been infected with the herpes simplex virus type 1 (HSV-1) had twice the risk of having a heart attack or dying from heart disease as those never infected by the virus. A second study suggests that some organisms that cause lung infections might hitch a ride to the heart inside certain immune system cells. And the third study reported a link between a high white blood cell count – an indicator of infection and inflammation – and a higher risk of death following a heart attack. “Infections are of interest, in part, because of the increasing attention paid to the role of inflammation in heart disease,” says David S. Siscovick, M.D., professor of medicine and epidemiology at the University of Washington in Seattle. “The role of prior infection as a contributor to heart disease, however, remains controversial.”
Studies among middle aged people have supported the hypothesis that certain infections are associated with heart disease. However, several recent large studies have yielded conflicting results.
Siscovick and colleagues examined blood samples for evidence of prior infection by three common organisms to see if there was an association with an increased risk of heart attack or heart disease death in people age 65 and older. They looked for antibodies to HSV-1, which causes cold sores; Chlamydia pneumoniae, which causes upper and lower respiratory tract infections; and cytomegalovirus, which can cause a body-wide infection that often produces no symptoms.
The team used data from 618 participants in the Cardiovascular Health Study (CHS), pairing 213 patients who suffered a heart attack during the study with 405 participants who had not.
“We found that antibodies to HSV-1, which indicate prior infection, were associated with a two-fold increase in the risk of heart attack and death from heart disease,” explains Siscovick. No adverse association was found with cytomegalovirus, but the findings regarding the third organism were more complex.
“Overall, there was no relationship between the presence of antibodies to Chlamydia pneumoniae and the incidence of heart attack and heart disease death,” notes Siscovick. “However, in patients with very high levels of the antibodies, there was evidence of a possible association.”
Siscovick regards the findings as preliminary and says infection is not likely the sole factor in determining whether an individual will develop heart disease.
If HSV-1 and Chlamydia pneumoniae are involved in heart disease, how do they reach the heart? Chlamydia pneumoniae is normally found in the lungs. In a second study in today’s Circulation, a research team at the University of California, Davis (UCD), suggests that Chlamydia pneumoniae may travel from the lungs to the heart via immune system cells.
They examined immune system cells in the blood of 28 heart patients and 19 healthy blood donors for Chlamydia pneumoniae DNA. They found the DNA in the cells of 13 of the heart disease patients and five of the healthy donors. In 15 of the 18, the DNA was found inside white blood cells called CD3 T-cells – cells which can accumulate in the fatty artery deposits that cause heart attacks. “Because we found Chlamydia pneumoniae DNA in T-cells, it suggests this is how the infection reaches the heart vessels,” says lead author Ravi Kaul, Ph.D., an associate professor of pediatric infectious diseases at UCD.
In the third study, UC-San Francisco researchers sought to learn how inflammation affects blood flow to the heart during a heart attack and whether it is a factor in survival. The team examined data from 975 people who had suffered heart attacks during an earlier study, the Thrombolysis in Myocardial Infarction (TIMI) trial, which tested the use of a clot-busting drug to save lives. They then determined which patients had inflammation by measuring the patients’ white blood cell count at the time of treatment. “Patients with inflammation – elevation of their white blood cell count – had poorer blood flow into the heart muscle and more blood clots in the artery receiving the clot-dissolving drug than patients with low white cell counts,” says C. Michael Gibson, M.D., chief of interventional cardiology at UCSF. The higher the white blood cell count, the higher a patient’s risk of death from a heart attack or of developing congestive heart failure.
Co-authors with Siscovick are Stephen M. Schwartz, Ph.D.; Lawrence Corey, M.D.; J. Thomas Grayston, M.D.; Rhoda Ashley, Ph.D.; San-Ping Wang, Ph.D.; Bruce M. Psaty, M.D., Ph.D.; Russell P. Tracy, Ph.D.; Lewis H. Kuller, M.D., Dr.P.H.; and Richard A. Kronmal, Ph.D. Co-authors with Kaul are Janet Uphoff, M.Sc.; Jean Wiedeman, M.D., Ph.D.; Sanjay Yadlapalli, M.D.; and Wanda M. Wenman, M.D. Co-authors with Gibson are Hal V. Barron, M.D.; Christopher P. Cannon, M.D.; Sabina A. Murphy, M.P.H.; and Eugene Braunwald, M.D. Siscovick’s work was supported in part by the National Heart, Lung, and Blood Institute.
The above post is reprinted from materials provided by American Heart Association. Note: Content may be edited for style and length.
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