Clinical Decision Making

The independent information offered by CRP testing for risk stratification is now largely accepted. Its clinical use, however, has not yet been widely implemented primarily owing to uncertainty regarding appropriate therapeutic response. For example, although the AHA/ CDC guidelines have recognized the use of CRP as an independent tool for risk stratification in secondary prevention (class IIa), the expert committee cautioned against altering therapy based on CRP results (class III) (3). This recommendation derives from the fact that no prospective, randomized study has tested a strategy based on tailoring therapy using the results oftesting for CRP. However, based on expanding information regarding the effect of different classes of drugs on CRP, the hypothesis that therapy may be tailored using this inflammatory marker has come to the forefront (54). The observation that lower achieved levels of CRP on statin therapy at 30 d in patients recovering from ACS are associated with more favorable outcomes has offered a major piece of evidence in support of this hypothesis and the achievement of lower levels of CRP as a specific goal of treatment (55).

Nevetheless, more data are needed before specific responses to elevated levels of CRP other than control of obesity, treatment of diabetes and dyslipidemia, and exercise can be recommended. Until such time, measurement of CRP may be useful to provide additional independent information with respect to risk in situations in which the patient's risk appears intermediate or is uncertain using traditional tools, or in which the patient is insufficiently motivated to follow established preventive strategies. CRP may be of value for triage of patients with suspected ACS in the emergency department (Fig. 6), particularly when biomarkers of necrosis are normal. In addition, elevated levels of CRP in patients with ACS might also identify those who warrant particularly close follow-up and aggressive postdischarge therapy, such as increased dose of statin, length of clopidogrel therapy, or addition of angiotensin-converting enzyme inhibitors or ARBs in nondiabe-tic, nonhypertensive patients with normal ejection fraction (Fig. 7).

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