September 10, 2010
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A New Way of Looking at AtherosclerosisClinical Evidence
Recent studies have found increased levels of other "immune system" substances (MCSF, IL-1b, IL-6 and CRP) in patients with coronary (heart) atherosclerosis as compared with healthy subjects.(23)(24) Indeed, the level of both MCSF and IL-1b in the bloodstream correlates closely with the extent of coronary artery disease.
Furthermore, large studies in patients with heart disease have found that those with high blood levels of other "immune system" substances — C-reactive protein, leukocytes and fibrinogen — are more likely to suffer further symptoms, including heart attack.(25)(26) The presence of these substances suggests that inflammatory processes interacting with or, perhaps, originating from atherosclerotic blood vessels may somehow cause or promote thrombosis, or blockage of the artery by a blood clot.(27) Fibrinogen is the precursor of fibrin, the constituent of blood clots. The Physicians' Health Study, which tracked a large group of initially healthy middle-aged male doctors for approximately 10 years, found that blood levels of two inflammatory markers were significantly higher in individuals who subsequently developed heart attack and stroke.(28)(29) These inflammatory markers may well indicate the presence of atherosclerosis at its earliest stages. Risk Factors or Inflammatory Stimuli?
The well-known association between atherosclerosis and various risk factors may in fact support, rather than contradict the theory that the origins of the disease lie in the workings of the immune system. Rather than being causes in themselves, the evidence suggests that some or all of these factors may act to stimulate or enhance the underlying inflammatory process.
LDL
The so-called "bad cholesterol" seems to contribute to the formation of atherosclerotic lesions by binding to the surface of macrophages and smooth muscle cells attached to the artery wall. Studies have shown that lowering LDL concentrations in the blood can reverse atherosclerotic plaques in animals and humans and, thus, reduce the incidence of heart attack and death.(30)
Homocysteine
This substance, found in the bloodstream, has been shown to promote the formation of plaques.(31) Patients with severely high levels of homocysteine are much more likely to die prematurely of diseases related to atherosclerosis.(32) Trials to investigate the possible benefits of reducing homocysteine levels with folic acid are currently under way.
Infectious agents
Studies have found that the presence of two germs, Chlamydia pneumoniae and Helicobacter pylori, as well as the herpes virus, Cytomegalovirus, is strongly associated with coronary artery disease.(33)(34)
Because these infections are so common in the general population, however, it is likely that if they do indeed contribute to atherogenesis in step with other genetic or environmental factors. Two small-scale trials on patients with coronary artery disease have shown that there may be some benefit from antimicrobial drug therapy.(35) At this time, however, there is insufficient evidence to justify widespread use of these drugs to treat coronary artery disease. Hypertension, smoking and diabetes
High blood pressure, whether caused by hypertension, tobacco-related toxins or some types of diabetes may interfere with endothelial cell function or promote the formation of plaques. Successful treatment or correction of these conditions can significantly reduce the risk of cardiovascular disease.(36)
Conclusion
The more we learn about how the lesions of atherosclerosis are formed, the more connections we see to chronic inflammatory disease. Exactly what triggers the early stages of arterial inflammation remains a mystery and may well vary among individuals. Nevertheless, at the cellular level, we have enough evidence that suggests that the role played by inflammatory cytokines and growth factors may be very important. Treatments aimed at these parts of the inflammatory process may be a promising area to look for new, more effective treatments or methods of prevention.
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