A recent Associated Press story by Daniel Q. Haney has lead to numerous stories in the news and press concerning the importance of inflammation in the role of coronary artery disease development and progression.

Inflammation (triggered by environmental factors or genetic influences) causes a sequence of actions in the coronary artery such as, plaque rupture, thrombus formation and embolization into the blood vessels within the heart - placing one at increased risk for heart attack.

The American Heart Association and the Centers for Disease Control and Prevention recently published a joint scientific statement about using inflammatory markers in clinical and public health practice.  This statement was developed after systematically reviewing the evidence of association between inflammatory markers (mainly CRP) and coronary heart disease and stroke.

Dr. Paul Ridker, a cardiologist at Boston's Brigham and Women's Hospital has conducted several studies over the past few years, suggesting the importance of inflammation in triggering heart attacks. This may explain why those with a normal cholesterol level may still have a heart attack.

How is inflammation measured?
Inflammation can be determined by measuring your CRP level, short for "C-reactive protein," a protein found in the blood. Presence of CRP indicates a heightened state of inflammation in the body. Inflammation is a normal response to many physical states including fever, injury and infection - as well as the initiation and progression of cardiovascular disease. Elevated CRP is related to increased risk for heart attack, restenosis of coronary arteries after angioplasty, stroke, and peripheral vascular disease (PVD).

What does this mean in the future?
Cleveland Clinic interventional cardiologist Deepak L. Bhatt, M.D. recently conducted a study on patients undergoing percutaneous coronary intervention. He found that by pre-treating patients with high CRP levels with the antithrombotic agent clopidogrel prior to angioplasty and stenting, decreased the rate of myocardial infarction or death from 24 to 10.2 percent for patients with C-reactive protein levels in the highest quartile. Those who were diabetic benefited most by this strategy. This indicates a clinical role for measuring CRP prior to interventional procedures and targeting medical therapies accordingly.

For now, those at high risk for heart disease should consider including a CRP test in their standard lipid analysis. This includes people with a combination of other risk factors. In the future, we may see more people tested for CRP - discussion is currently underway to change national standards to include CRP testing in risk factor evaluations.

Dr. Eric Topol, Department Chairman, Cleveland Clinic Heart Center states the new information about inflammation will, "change everything we do in heart disease." He adds that in the past, people talked about their cholesterol levels. In the next decade everyone will need to know their C-reactive protein level.

What is the treatment of high CRP?
Inflammation should be treated by lifestyle change, such as losing weight, exercising, controlling diabetes, stopping smoking, controlling high blood pressure, stabilizing Insulin levels and reducing alcohol intake. Antithrombotic medications such as aspirin may provide protection.

"Inflammation" is the process by which the body responds to injury. Laboratory evidence and findings from clinical and population studies suggest that inflammation is important in arteriosclerosis. This is the process in which fatty deposits build up in the lining of arteries.

C-reactive protein (CRP) is one of the acute phase proteins that increase during systemic inflammation. It’s been suggested that testing CRP levels in the blood may be a new way to assess cardiovascular disease risk.  A high sensitivity assay for CRP test is now widely available.

A growing number of studies have examined whether CRP can predict recurrent cardiovascular disease and stroke and death in different settings. High levels of CRP consistently predict new coronary events in patients with unstable angina and acute myocardial infarction (heart attack). Higher CRP levels also are associated with lower survival rate of these people.  Many studies suggested that after adjusting for other prognostic factors, CRP was still useful as a risk predictor.

Recent studies also suggest that higher levels of CRP may increase the risk that an artery will reclose after it’s been opened by balloon angioplasty.  High levels of CRP in the blood seem to predict prognosis and recurrent events in patients with stroke and peripheral arterial disease.

Most studies show that the higher the CRP levels, the higher the risk of developing heart attack. In fact, scientific studies have found that the risk for heart attack in people in the upper third of CRP levels is twice that of those whose CRP is in the lower third. These prospective studies include men, women and the elderly. Recent studies also found an association between sudden cardiac death, peripheral arterial disease and CRP.

If CRP level is lower than 1.0 mg/L, a person has a low risk of developing cardiovascular disease.

If CRP is between 1.0 and 3.0 mg/L, a person has an average risk.

If CRP is higher than 3.0 mg/L, a person is at high risk.

If, after repeated testing, patients have persistently unexplained, markedly elevated CRP (greater than 10.0 mg/L), other evaluation should be considered to exclude noncardiovascular causes.