"Can infection produce heart attacks?"

Although we know that CAD is much more prevalent in high-risk groups, it will not account for about 50% of the patient population who have no conventional cardiac risk factors. Our great emphasis on cholesterol reduction with the use of statins did not start until the early 1990s. Aggressive efforts in blood pressure reduction did not start until the late 1970s. Smoking cessation, at the very best, is partially successful only since the late 1980s. Of course, the prevalence of obesity is certainly on the rise since we have been keeping track of it.

However, it is quite interesting to see that in the United States the coronary epidemic that was rampant in the 1950s peaked out in 1963, and ever since has shown a steady decline. This raises some logical questions: What exactly is the major force in this spectacular decline in CAD incidence? Is it due to the liberal and widespread use of antibiotics for so many common conditions? Is there a link between infection and CAD? Is the rise and fall of CAD in the 1950s and early 1960s related to prolonged infectious conditions not properly accounted for?

Amongst a few infectious agents investigated, the bacteria Chlamydia pneumoniae, which is responsible for as much as 10% of the community-acquired pneumonia is linked to atherosclerosis and myocardial infarction. Several studies have proved that men with AMI have increased seropositivity for Chlamydia pneumoniae than the control group. This bug has been isolated from 50-79% of the atherectomy specimens in some studies. There have even been some studies that show reduced incidence of myocardial infarction and angina in subjects treated with antibiotics (Azithromycin) when compared to the control group. However, the antibiotics used also have some anti-inflammatory effect, and therefore the full credit cannot be attributed to the bactericidal properties.

It is quite interesting to see that in the United States the coronary epidemic that was rampant in the 1950s peaked out in 1963, and ever since has shown a steady decline.

Inflammation and C-reactive protein

High sensitivity C-reactive proteins and elevated fibrinogen levels have a predictive value for future coronary events and death. In many high-risk patients such as diabetics and smokers, there exists a chronic low-grade inflammation resulting in sustained elevation of C-reactive protein and fibrinogen. However, it is safe to assume that with a positive high sensitivity C-reactive protein, the atherosclerotic plaque may be unstable due to inflammation.

At this point we do not know what to do with this data. Until further convincing data is at hand, there is no specific recommendation to treat all patients with angina or MI with an antibiotic.

From exertion comes wisdom and purity, from sloth ignorance and sensuality. Henry David Thoreau 1817-1862