Is hs-CRP useful after acute MI?

Publication
Article
Cardiology Review® OnlineOctober 2006
Volume 23
Issue 10

Biomarkers seem to be proliferating everywhere, with at least 1 "major" new marker appearing each year.

Biomarkers seem to be proliferating everywhere, with at least 1 “major” new marker appearing each year. A new biomarker may be made available for a particular clinical scenario and then be applied to a totally different clinical circumstance. In a hospital environment, markers may appear on the chart of a patient while clinicians struggle to understand their significance. I personally still grapple with the cryptic low-level troponin elevation in patients with medical or surgical conditions. The article by Aronson and Suleiman goes a step further in identifying a helpful role for high-sensitivity C-reactive protein (hs-CRP) in the setting of acute myocardial infarction (MI).

Low-normal elevations of hs-CRP are most well described and understood to predict the risk of future events independent of cholesterol and other traditional “risk factors.”1 In the office, the test can be particularly helpful if a patient or physician is on the fence about whether to begin statin therapy, as an elevated hs-CRP level not only identifies increased risk, but is a target for statin therapy, as well.

Aronson and Suleiman direct their focus at patients hospitalized with acute MI, where there are already many well-established predictors of death and heart failure in the ensuing months. The authors found that even after ejection fraction, infarct size and location, degree of heart failure, and a few other factors were accounted for, higher levels of hs-CRP (well above the normal range) identified patients with worse outcomes. Although the degree of hs-CRP elevation may simply be a surrogate marker for infarct size, the authors suggest that it may more precisely identify patients who have poorer results after reperfusion, have a greater degree of endothelial dysfunction or reperfusion injury, or may be more likely to have ventricular remodeling and enlargement after hospital discharge. The study lacks echocardiographic follow-up, so the relationship of hs-CRP elevation to subsequent ventricular changes is conjectural.

The study, although interesting and useful, does not offer therapeutic alternatives. After MI, patients are already candidates for treatment with angiotensin-converting enzyme inhibitors, β blockers, aspirin, statins, and defibrillators, particularly those with heart failure or left ventricular dysfunction. But the findings do raise the possibility that new drugs that address inflammation, complement activation, or cytokine activity might be useful and that hs-CRP elevations might be predictive of patients who respond favorably to such interventions. Thus, although hs-CRP measurements are not established for acute MI patients, this exciting study suggests that many more potential opportunities may exist to prevent left ventricular dysfunction, heart failure, and death after MI.

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