Timing ofTesting

Another issue frequently debated is when to test CRP in patients with ACS. Most studies ofCRP in ACS have provided data based on determination ofCRP at admission. Therefore, taking an evidence-based approach supports the use of CRP levels at admission for risk stratification. Admission levels are unaffected by revascularizationn procedures (because PCI may increase CRP levels) and are less likely to be affected by the inflammatory response to necrosis, and more likely to reflect the patient's basal inflammatory status. In addition, measurement at hospital discharge would obviously preclude use for assessment of the risk of in-hospital complications.

Fig. 6. Proposed algorithm for short-term risk stratification of patients with non-ST-elevation ACS using CRP. Troponin (cTn) levels identify patients at high risk for in-hospital death and recurrent MI CRP levels appear to further risk stratify patients without troponin elevation. If CRP is >10 mg/L, the patient is at high risk of AMI and death, wheres the risk is low if CRP is <3 mg/L. Patients with intermediate CRP levels (3-10 mg/L) are at intermediate risk and have increased rates of complicated hospital courses and need for urgent revascularization.

Fig. 6. Proposed algorithm for short-term risk stratification of patients with non-ST-elevation ACS using CRP. Troponin (cTn) levels identify patients at high risk for in-hospital death and recurrent MI CRP levels appear to further risk stratify patients without troponin elevation. If CRP is >10 mg/L, the patient is at high risk of AMI and death, wheres the risk is low if CRP is <3 mg/L. Patients with intermediate CRP levels (3-10 mg/L) are at intermediate risk and have increased rates of complicated hospital courses and need for urgent revascularization.

Fig. 7. Proposed algorithm for mid to long-term risk stratification of patients recovering from ACS, including CRP. Clinical parameters such as depressed left ventricular (LV) function, inducible ischemia, and severe CAD indicate patients at high risk of recurrence and death and identify those who benefit from more aggressive preventive strategies. CRP determination may be useful for risk stratification in those without high-risk features. The risk strata are as described for Fig. 4. LM, left main coronary artery disease; 3 V, triple-vessel coronary artery disease.

Fig. 7. Proposed algorithm for mid to long-term risk stratification of patients recovering from ACS, including CRP. Clinical parameters such as depressed left ventricular (LV) function, inducible ischemia, and severe CAD indicate patients at high risk of recurrence and death and identify those who benefit from more aggressive preventive strategies. CRP determination may be useful for risk stratification in those without high-risk features. The risk strata are as described for Fig. 4. LM, left main coronary artery disease; 3 V, triple-vessel coronary artery disease.

Additional determinations during and after hospitalization may be of value. In patients without evidence of myocardial necrosis, reassessment may refine the prognostic assessment for secondary prevention. For example, Biasucci et al. (18) showed that CRP levels at discharge were a better predictor of long-term recurrence than CRP levels on admission. In patients with MI, CRP is expected to rise in response to the inflammatory reaction to necrosis and, thus, the clinical value is debated. However, in patients with AMI, peak CRP levels were associated with the risk of heart failure and/or mechanical complications of AMI (56,57). Therefore, even if CRP elevation is to be expected when myocardial necrosis is present, a higher CRP level may be predictive either of greater myocyte loss or of greater inflammatory burden and in both cases may be associated with adverse outcome. For patients undergoing PCI, an elevated level of CRP 48-72 h after stent implantation may reflect an inflammatory response to PCI and predict clinical recurrence (57). Finally, testing during outpatient follow-up one or more months after presentation appears to assist in long-term risk stratification and may provide a basis for titration of therapy with anti-inflammatory actions (58). Moreover, a lower achieved level of CRP at 6 mo after PCI is associated with a favorable outcome (23,57).

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