Recently, two new blood tests have been promoted as predictors of heart disease.  Both of these blood tests – C-reactive protein (CRP) and fibrinogen – have now been correlated with a significantly increased risk of future heart attacks.  Two recent articles,
a)  C-reactive protein and fibrinogen - Newer risk factors for coronary artery disease (by Dr. Richard N. Fogoros - DrRich - dateline: 11/14/2000) and b) C-Reactive Protein Headlines (by H. Robert Superko, MD, FAAC) discuss the correlation between elevated CRP levels and coronary artery disease (CAD).  The problem is, unlike other risk factors (such as obesity, smoking and cholesterol) it is not at all clear what should be done about high CRP levels.

C-REACTIVE PROTEIN (CRP) is a protein released into the bloodstream any time there is active inflammation in the body. (Inflammation occurs in response to infection, injury, or various conditions such as arthritis.)  Evidence is accumulating that atherosclerosis (coronary artery disease) is an inflammatory process.  Some even think that coronary artery disease may be promoted by infection.  The fact that elevated CRP levels are associated with an increased risk of heart attack tends to support the proposed relationship between inflammation and atherosclerosis.

Large studies were published this year that clinch the relationship between this blood protein and the risk of heart attack.  Secondly, new commercial tests for measuring this protein has been developed.  (Aside to conspiracy theorists: this means there is money to be made by measuring them.) Thus, physicians now have a clinically relevant reason to do the tests, and a means for doing so.  However, presently there are no known therapies for elevated levels of CRP.  What should doctors and patients do when CRP levels are elevated?  If there aren’t any specific treatments that can be used in response to elevated CRP levels, why should it be measured?

It is not the CRP level itself that is considered to be the problem, but the presumed inflammation in the coronary arteries that is reflected by the high CRP level.  So the real question is whether the inflammation (and not the CRP) can be treated.  There is some evidence that infection with an organism called Chlamydia pneumoniae may be a factor in the development of coronary artery disease.  If so, then antibiotics might be effective in eliminating the infection and reducing the risk of heart attacks (and, dentally, in reducing CRP levels).  But the only published trial testing whether antibiotics help to prevent heart attacks (in patients with serum markers for Chlamydia) showed no benefit. Two larger trials are underway, however.  If antibiotics should prove effective in the future, measuring CRP levels may turn out to be a useful screening tool to select patients who might benefit from antibiotic therapy.  Further, there is accumulating evidence that the statin drugs – drugs used to treat high cholesterol – may also have the effect of reducing inflammation in the coronary arteries.  Trials are underway to assess this possible beneficial effect of the statin drugs.  CRP levels may turn out to be a useful screening tool here, also.

At the moment, the only good answer to this question is: knowing the CRP levels may help to more accurately characterize the risk of coronary artery disease, so the doctor and patient can decide how aggressive to be in attacking risk factors that can be changed.  For instance, both the patient and the doctor may be reluctant to begin statin drugs when cholesterol levels are only borderline elevated.  In this case, elevated CRP  levels may tip the scales in favor of beginning therapy, whereas normal CRP levels may tip the scales in favor of withholding therapy.  Measuring this new risk factor may therefore play directly into therapeutic decisions.

Conceivably, knowing that the CRP level is elevated might be the straw that finally breaks the camel’s back – the factor that finally compels the smoker to quit, the sedentary to exercise, or the obese to radically alter their lifestyles. But it is also possible that measuring risk factors that cannot themselves be changed might merely provoke unrequited anxiety.  In a nonsmoker with normal weight, normal cholesterol, and an active lifestyle, for instance, it is hard to see what benefit might be gained by knowing the CRP is elevated. Indeed, it might cause anxiety that could not be easily allayed.  It would not be wrong to make the measurements, but (analogous to measuring genetic markers) the patient should be made aware before doing the test that there is no specific treatment available.  And (like genetic markers) having such a risk factor on the medical record might conceivably affect insurability in the future.

A lot of research is being done to find ways of treating inflammation affecting the coronary arteries. If antibiotics, statins, or some other therapy eventually were shown to be of benefit, it would make a lot of sense to measure CRP levels, even in patients with no other risk factors.  Measuring CRP levels can be useful in many circumstances, and is likely to be far more useful in the future.  But before ordering these tests, the doctor and the patient ought to be able to say ahead of time how the results might be useful. Especially  in patients with no other risk factors, doing these tests may cause more harm than good, and patients need to understand that before the measurements are made.

Related Links:

C-reactive protein and fibrinogen - Newer risk factors for coronary artery disease (by Dr. Richard N. Fogoros - Dr.Rich - dateline: 11/14/2000)

C-Reactive Protein Headlines (by H. Robert Superko, MD, FAAC)

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