By Randy Dotinga
TUESDAY, June 16, 2015 (HealthDay News) -- There seems to be a higher risk of angina -- chest pain related to clogged blood vessels -- in the small number of people who have a type of herpes virus lurking in their genes, a new study suggests.
Canadian researchers found that people with this inherited condition face three times the risk of angina as others. About 1 percent of people in the world appear to have this increased risk.
There's no way to get rid of the genetic condition, because it is in a person's DNA, said study co-author Louis Flamand, vice chair of the department of microbiology-immunology at Laval University in Quebec, Canada. However, "as a preventive measure, subjects could be monitored more closely for the development of cardiovascular diseases," he said.
"Considering that testing is simple, we propose that testing could be added to the list of genetic tests being performed on every newborn," Flamand added.
The condition can develop before conception, when an egg or sperm cell becomes infected with a strain of herpes virus that causes the common childhood disease known as roseola, Flamand said. When that happens, he said, "subjects are born with a copy of the virus in every cell of their body."
To figure out whether the condition had any impact on health, "we opted to conduct a large population study on 20,000 healthy and diseased individuals aged between 40 to 69 years old, the ages where chronic diseases are most often observed," he said.
The researchers hit pay dirt when they checked their statistics for higher rates of angina. The risk of angina for those with the genetic condition rose from 3 percent to 10 percent, although the findings don't prove that the chromosome quirk is the cause of the chest pain.
Angina is estimated to strike more than 3 million people in the United States each year. According to the U.S. National Library of Medicine, the chest pain and discomfort of angina from blocked blood vessels is a symptom of heart disease. In some cases, angina appears before a heart attack.
What might be going on? Flamand said one theory is that the virus destroys cells lining the arteries and contributes to clogs in the pipes of the circulatory systems.
Dr. Hugh Watkins, head of the Radcliffe Department of Medicine at the University of Oxford in England, said, "This might be one more example to add to the long list of known genetic effects. But it will need replication, as lots of diseases were tested for association with this genetic variant, and it needs to be shown that this finding didn't just happen by chance."
Watkins, who was not involved with the study, disagrees with the need for newborn testing for the variant.
"It won't be helpful to test individuals for this gene or the other common heart disease susceptibility variants, as each has too small an effect to be predictive," he said, although he added, "maybe one day testing for all known variants together might be worthwhile."
Instead, he said, "the true value is in understanding why the effect is seen as that can pinpoint new mechanisms of disease and new targets for future drug treatments."
What's next? Flamand said researchers want to better understand how the virus affects the body, and figure out if it affects less common conditions.
The study was published in the June 15 issue of the Proceedings of the National Academy of Sciences.