Dec 24 (Reuters Health) - People with heart disease appear to be at a slightly increased risk of life- threatening cardiovascular problems if they are infected with a common virus belonging to the herpesvirus family, according to new research.

Among more than 3,000 people with heart disease, those whose blood carried antibodies--a sign of current or past infection--to cytomegalovirus (CMV) showed a 24% increased risk of experiencing a heart attack or stroke, or of dying from cardiovascular disease within 4-1/2 years.

CMV, which belongs to the herpesvirus family, usually remains dormant in the bodies of healthy people and causes no symptoms, although it can be harmful to fetuses and to people with weak immune systems. As many as 90% of the US population may carry CMV. Researchers have speculated that the virus might contribute to heart disease by increasing inflammation in the body.

Antibodies to other pathogens, such as one that infects the lungs, the ulcer- causing bug Helicobacter pylori or the hepatitis A virus, appeared to have no link to an increased risk of any of the events seen in connection to CMV, the authors report.

People who carry antibodies to hepatitis A and the pathogen that causes lung infection were likely infected at an earlier age, and no longer carry the pathogens in their system, according to the researchers. CMV and H. pylori antibodies, in contrast, indicate the person continues to carry those pathogens, but may not have any symptoms of the illnesses they can cause.

People with antibodies in their blood to all four of the tested pathogens were 41% more likely to have a heart attack or stroke or die from cardiovascular disease than those with antibodies to one or none of the pathogens.

The findings by Dr. Marek Smieja of McMaster University in Hamilton, Ontario and his colleagues were published Monday in the rapid access online issue of Circulation: Journal of the American Heart Association.

In an interview with Reuters Health, Smieja suggested that CMV itself could raise the risk of blood vessel problems by directly infecting the vessels. Alternatively, infection with CMV could indirectly lead to cardiovascular problems by raising the activity of the immune system in general, encouraging the immune system to attack blockages in blood vessels, which can lead to problems, he said.

No previous evidence has surfaced linking H. pylori and hepatitis A to heart disease, and this study confirms the absence of any connection, he noted. "I say this as there has never been any convincing evidence that these infections can be found within blood vessels, and both of these infections are very common in parts of the world where heart disease is less common than in industrialized nations," Smieja said.

But all four pathogens, together, increased the risk more than CMV alone--a finding that might stem from the fact that the bacteria behind a respiratory infection does, in fact, contribute to blood vessel problems, Smieja said. Findings on infection with this bacterium alone indicated that it carried a slightly higher risk of blood vessel problems, but that this increase was small enough to be caused by chance.

The researchers obtained their findings by analyzing blood samples from 3,168 patients with heart disease. During 4-1/2 years of follow-up, 494 patients had a heart attack or stroke, or died from cardiovascular disease.

Antibodies to each pathogen were discovered in the blood samples of the majority of patients. Smieja said in an interview that the average age of participants was 65, and that these infections were almost universal earlier in the 20th century. The participants lived in Canada, he added, and many Canadian residents come from other countries where these infections occur more commonly.

However, the high rate of pathogens may reflect another explanation for why CMV and many simultaneous infections are linked to blood vessel problems--one that is unrelated to the immune system, Smieja added.

"Is exposure to these infections a measure of an actual cause of heart disease, are we measuring the socioeconomic environment in which these people grew up, or are we measuring non-specific immune activity?" he asked.

"I think it will take several years to work this out," Smieja said.

SOURCE: Circulation: Journal of the American Heart Association 2002;107.