Even though the evidence implicating infectious agents in heart disease remains circumstantial it continues to accumulate in favor of the hypothesis that certain bacteria and viruses may play a causative role in the formation of artery clogging plaques. Since this link was first reported further experiments worth mentioning have been conducted. These experiments strengthen the association of Chlamydia pneumoniae (which is primarily known as a sexually transmitted disease) and cytomegalovirus (a common virus that causes respiratory infections) with atherosclerosis.
The initial experiments, as previously mentioned, involved the detection of antibodies in heart attack patients or bacterial proteins in arterial plaques. More recently animal studies have yielded more direct evidence that Chlamydia infection measurably thickens arterial walls particularly in animals with a genetic predisposition to high blood cholesterol or animals that were fed a high fat diet. In the same study it was shown that when the rabbits were given an antibiotic that is used to treat Chlamydia infections the arteries more closely resembled those of uninfected animals.
An additional microbial contributor to heart disease may be the same bacterium that causes gum disease. This was determined from the dental data of 1200 men and it was found that those with dental infections had a higher risk of heart disease and strokes. Another small scale study may lead to the implication of the bacteria that causes ulcers (Helicobacter pylori) in heart disease. However one cautionary note is raised in interpreting this data is that the people with these infections tend to have higher risk factors for both infection and heart disease such as smoking, living in poverty, being older and therefore it is difficult to sort out correlation from causation. Further research must be done to determine the mechanism by which these infections may cause arterial plaques. It may be found that these are merely opportunistic infections that take advantage of the weakened health of someone with heart disease.
The clinical evidence in humans is inconclusive so far. However some ambitious studies are currently be undertaken and the results should be available within a few years. If antibiotic therapies prove to be successful in treating heart disease then this powerful new paradigm of chronic diseases being caused by infectious agents may be applied to other diseases of old age with some exciting results. We have learned in the twentieth century how to fight infectious diseases and it seems less daunting to be fighting a microscopic enemy than what was assumed to be the "natural" progression into old age.
Towards long life!