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Study links infections, heart disease

By ANDRé PICARD
PUBLIC HEALTH REPORTER
Tuesday, January 8, 2002 – Print Edition, Page A1
 

Evidence is growing that common bacterial and viral infections such as those that cause cold sores, ulcers and pneumonia can also contribute to cardiovascular disease.

And people with heart disease who have been infected with certain microbes are far more likely to die of cardiovascular illness than those who have not, probably because of swelling of arteries, researchers report in today's edition of Circulation, a journal published by the American Heart Association.

"We showed a significant association between the number of infections to which a patient has been exposed and the extent of atherosclerosis in the arteries of the heart, neck and legs," said Hans Rupprecht of Johannes Gutenberg University in Mainz, Germany. "The risk for death was increased by the number of infectious agents, especially in people with advanced artery disease."

In atherosclerosis, or hardening of the arteries, fat accumulates along the walls of blood vessels, gradually blocking blood flow or breaking off to cause clots.
A theory gaining acceptance is that swelling of the arteries caused by the inflammatory response to an infection narrows the blood vessel and helps trap fat and immune cells. In fact, some researchers have shown that drugs known to protect against heart disease, like aspirin and cholesterol-lowering statins, work by reducing inflammation.

Proponents of the so-called "new germ theory" go further, saying that heart disease and many other chronic illnesses are linked to infections, not just heredity and lifestyle. That notion remains controversial.

Dr. Rupprecht and his team tested 572 patients with heart disease for prior exposure to eight common microbes. They included herpes simplex virus 1 and 2, which cause cold sores and genital herpes; cytomegalovirus, which causes body-wide infection but often no symptoms; Epstein-Barr virus, which causes mononucleosis; hemophilus influenzae, a bacterium that causes ear and respiratory infections; mycoplasma pneumoniae, and helicobacter pylori, which causes most stomach ulcers.

Previous research looking individually at some of these infectious agents and others produced conflicting results. The German study is the first to look at the impact of a broad range of infectious diseases.

The Gutenberg University team found that among patients who had been exposed to six to eight of the pathogens the death rate was 15 per cent over three years. For those who showed exposure to four or five, it was 9.8 per cent, and with three or fewer it was 3.1 per cent.

Among patients with advanced atherosclerosis, the differences were equally striking. Twenty per cent of those who had had six to eight of the infections died, compared to 7 per cent of those with three exposures or fewer.

"Based on these results, we think that the number of infections to which an individual has been exposed may be involved in the development and programs of atherosclerosis," said Christine Espinola-Klein, another member of the research team. "Both bacterial and viral pathogens seem to be involved."

In an accompanying editorial in Circulation, Paul Ridker, director of the Center for Cardiovascular Disease Prevention at Brigham and Women's Hospital in Boston, said there may be an alternate explanation for the results and cautioned that "investigators must be careful not to confuse association with causation."

Dr. Ridker noted that all the people studied had heart disease, and that the infections could have come after the heart disease, or that people with artery disease are more prone to infections.

Dr. Espinola-Klein acknowledged that other factors could skew the findings, but said that, even after adjusting for age, gender, cardiovascular risk and other kinds of inflammation, the associations of infection with development of atherosclerosis remained significant. In fact, the association was strongest with the four bacterial infections, and much less so with the viral infections.

The researchers stressed that infection is certainly not the sole factor in determining whether an individual will develop heart disease. A proper diet and regular exercise are keys to heart health, but the role of infections cannot be dismissed.

Still, while a growing number of studies have linked infection and heart disease, none has shown that taking antibiotics lowers the risk of heart disease.

In Canada, cardiovascular disease is the leading cause of death. It also results in the most hospital admissions, apart from pregnancy and childbirth.

About 80,000 Canadians annually die of heart disease. According to the Canadian Heart and Stroke Foundation, cardiovascular disease costs the economy about $19.7-billion annually.

 


Copyright © 2002 Bell Globemedia Interactive Inc. All Rights Reserved.
 

"Meier et al have shown retrospectively that previous use of tetracyclines and quinolones was associated with a lower risk of acute myocardial infarction, providing indirect evidence that infection with microorganisms susceptible to tetracycline antibiotics might be involved in the aetiology of ischaemic heart disease".(10) Meier CR, Derby LE, Jick SS, el ai. Antibiotics and risk of subsequent first-time acute myocardial infarction.[AKA heart attack]  JAMA 1999;281:427-31.

"C pneumoniae is the agent with the most evidence for a causal association with atherosclerosis (provided by seroepidemiological, pathological, and animal models, and in vitro studies). Although Koch's postulates seem to be fullfilled for C pneumoniae infection and atherosclerosis, definitive proof that a particular microorganism causes atherosclerosis may not come
from this direction, but from the prevention of primary infection by vaccination or the eradication of the agent by
antimicrobials."

and "HELICOBACTER PYLORI
In an in vitro study it has been shown that polyunsaturated fatty acids
inhibit the growth of H pyloni and prevent/arrest atherosclerosis.(60) "

- J Clin Pathol 2000; 53: 647-654

S. A . Morré, W  Stooker, W K Lagrand, A J C van den Brule,
H W M
Niessen

Department of Pathology, University Hospital Vrije Universiteit
 PO Box 7057, De
Boelelaan 1117,1007 MB Amsterdam,
The
Netherlands


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