Q- WHAT IS A CORONARY ARTERY DISEASE(CAD)?
Coronary artery disease develops when the major blood vessels
that supply your heart with blood, oxygen, and nutrients (coronary arteries) become damaged or diseased. Cholesterol-containing deposits (plaque) in your
arteries and inflammation are usually to blame for coronary artery disease. When plaque builds up, it narrows your coronary arteries, decreasing blood flow to your heart. Eventually, the decreased blood flow may cause chest pain (angina), shortness of breath, or other coronary artery disease signs and symptoms. A complete blockage can cause a heart attack.
IS COMMON COLD A POTENTIAL CULPRIT IN CORONARY ARTERY DISEASE?
This sounds like a rather unusual and scary question. However, the intention is not to create a panic situation like the recent ruckus about swine flu.
Rather, the focus is on a very interesting aspect of the cause of Coronary Artery Disease (CAD). CAD continuous to be the commonest cause of death in the industrialized world and is ever-increasing in developing countries. The huge burden of disease in terms of mortality, morbidity, and socioeconomic hardship remains a challenge. The conventional risk factors for CAD are smoking, diabetes mellitus, hypertension, and dyslipidemia. However, these factors fail to account for the difference in prevalence and severity of the disease in different populations.
Therefore, a number of ‘novel’ markers for the disease have been recently proposed, one of them being infection by certain micro-organisms. Yes, indeed, a bacterium might just be the culprit behind those cholesterol plaques that narrow our coronary arteries and cause angina, heart attacks, etc.
Atherosclerosis, the process of formation of cholesterol deposits (‘plaques’) in the blood vessel walls is the initiating event in CAD. Research has established that this is an inflammatory process. That is, a process the body initiates when faced with any kind of
infection (bacterial, viral or fungal). Of course, that is not to oversimplify things by saying that CAD could be caused by infection! But evidence suggests that the presence of infective antigens in the blood may act as a ‘signal’ for this inflammatory process to commence and lead to plaque formation and CAD.
Interestingly, as far back as in 1908, Osler the legendary physician proposed that infection could be an etiological factor in atherosclerosis. But it is only in recent decades that a number of potential culprit pathogens have been implicated, foremost among them being Chlamydia pneumonia. This is a gram-negative obligate intracellular pathogen, causing 5-20% of adult pneumonia. This infection itself runs a rather benign course,
with cough, sneezing, fever and body ache being the prominent symptoms. The trouble is that this bacterium tends to linger in the body cells as a dormant organism for an extended period, unrecognized by the immune system. But do we have cold, hard evidence of this? Perhaps yes, in the following forms:
Sero-epidemiological data Saikku et
al (1988) were the first to demonstrate that elevated serological markers of C pneumonia were positively associated with CAD. Since then there have been various studies linking levels of
antibodies against C pneumonia to severity and distribution of atherosclerosis lesions, with differing conclusions.
C pneumonia has actually been isolated from atherosclerotic plaques from autopsy specimens. It has also been isolated
from other human tissues, demonstrating its ubiquitous presence. This does not mean that its presence in atherosclerotic plaques indicates a causative role. But on the flip side, it has been found that C pneumonia detection rate was 29-50% in cardiovascular tissue, versus 5-13% in noncardiovascular tissue. The recent development of the culture of live organisms from plaque tissue may add more evidence in favor of an infectious etiology.
Rabbits experimentally infected with C pneumonia developed
not only pneumonia but also atherosclerotic changes in the aortic wall. Further, cholesterol supplementation in these rabbits caused thickening of the inner walls of their blood vessels. Azithromycin, an antibiotic active against C pneumonia, reduced these arterial lesions in infected rabbits.
Laboratory studies have shown that C pneumonia infects and proliferates in vascular cells (macrophages, endothelial and smooth muscle cells), the main constituents of the atherosclerotic plaque apart from the well-known cholesterol deposits. This may lead to the expression of inflammatory mediators by these cells that set the ball rolling for the inflammatory process leading to atherosclerosis.
Antibiotic studies in humans
Two pilot clinical studies were published in the UK in 1997. Briefly, they involved screening of survivors of major heart attacks for antibiotics to C pneumonia, increasing antibodies were found to be associated with the increasing incidence of adverse cardiovascular events like recurrent heart attacks and angina. Indeed, patients with increased antibody levels received azithromycin and were found to have a 5-fold reduction of events compared to the others not getting the antibiotic.
Understandably, these studies led to a rash of prescriptions of azithromycin and roxithromycin, both antibiotics active against the organism! Unfortunately, subsequent structured studies addressing the issue failed to demonstrate any significant
clinical or survival benefit with the administration of these antibiotics.
Where do we stand?
So can we look forward to popping a course of antibiotics to actually cure CAD, while we continue to enjoy our burgers, French fries, TV, stress, and diabetes? Unfortunately, the jury is still out on that one. No study has conclusively proved the link between C pneumonia infection and CAD and the beneficial effect (if any) of antibiotic therapy in these patients. All said and done, there is a group of pessimists who maintain that the link could be merely coincidental. On the other hand, there are some
practitioners, who are already treating CAD patients with antibiotics!!
One encouraging aspect is the search for a vaccine against C pneumonia the administration of which could determine if there is really a link between the bacterium and the disease. Until then, we would do well to be content with fighting the tradition demons of obesity, diabetes, smoking, hypertension and dyslipidemia.
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