Inflammation Contributes to Cardiovascular Risk in Patients Receiving Statin Therapy
Recent studies have highlighted the importance of inflammation as a contributing cause to the development of coronary artery disease (CAD). Three large randomized trials (PROMINENT, REDUCE-IT, and STRENGTH) involving 31,000 patients already receiving statin therapy demonstrated that the presence of higher concentrations of hs-CRP significantly increased the risk of major adverse cardiovascular events, cardiovascular mortality, and all-cause mortality.1 The data showed that hs-CRP concentration was a far more powerful predictor of cardiovascular mortality (HR, 2.68; P < .0001) and all-cause mortality (HR, 2.42; P < .0001) than LDL-C level (comparable HRs, 1.27 and 1.17, respectively; P < .03). Moreover, among statin-treated patients with hs-CRP levels >2 mg/L, the risk of cardiovascular death was high regardless of LDL-C level. These observations have resulted in the conclusion that residual inflammatory risk is a stronger predictor of future cardiovascular events and death than residual cholesterol risk. This raises two major clinical issues: the presence of inflammation by measuring hs-CRP levels as well as treatment with anti-inflammatory drugs are both underutilized in treating patients with CAD. Recent studies with colchicine (0.5 mg daily) added to statins have demonstrated a further reduction in MACE,2 consistent with these observations (and, interestingly, have led to a price jump in the cost of colchicine). In the new clinical paradigm, clinicians will need to factor in the role of inflammation in their evaluation and treatment of patients with CAD.