The role of inflammation in coronary artery disease

The role of inflammation in coronary artery disease
The year 2000 marks the year in which the link between inflammation and coronary artery disease gained widespread recognition among cardiologists.
Several lines of evidence converged last year to suggest that atherosclerosis, unstable angina and heart attacks are all associated with inflammation of the coronary arteries. This evidence includes the following:
- Elevated levels of C-reactive protein (CRP), a protein that appears in the bloodstream during many inflammatory processes, are associated with acute coronary events. (See CRP and fibrinogen – newer risk factors for coronary artery disease.)
- Patients with acute heart attacks who also have elevated white blood cell counts (the white cells are produced in response to inflammation and infection) were found to have poorer outcomes (increased risk of heart failure and death) than patients with normal white blood cell counts.
- Older patients (> 65) who had antibodies to the herpes simplex virus had an increased risk of heart attack and cardiac death.
- DNA to the bacteria Chlamydia pneumoniae was found in a certain type of white blood cell (the CD3+ lymphocytes) in a high proportion of patients with coronary artery disease. The CD3+ lymphocytes are known to accumulate in atherosclerotic plaques.
These observations have sealed the now generally-accepted notion that vascular inflammation is an important component of coronary artery disease, and have opened many brand new lines of research into novel approaches to the prevention and treatment of coronary artery disease.
The efficacy of the statin drugs and aspirin in reducing the incidence of acute coronary events, for instance, may be related, at least in part, to their anti-inflammatory effects in addition to the cholesterol-lowering effect of statins, and the anti-clotting effect of aspirin.
And, seeing the pot of gold at the end of the rainbow, the pharmaceutical industry is now investing tens of millions of dollars in exploiting the new line of evidence that inflammation plays a major role in causing heart attacks. The clinical payoff from this important conceptual advance in coronary artery disease should begin to appear quite soon.