CORONA, Statins, and Heart Failure: Who Lost the Crown?

Abstract

Several small, nonrandomized studies suggested that statin use is associated with improved outcomes in CHF irrespective of aetiology (ischemic or not) or baseline cholesterol levels. Recently, 2 large cohort studies provided more convincing evidence that statins can improve the outcome in this population. In 24,598 patients with CHF who were eligible for treatment with statins, incident statin use was associated with a 21% and 24% reduction in hospitalization for CHF and total mortality, respectively. In an even larger study of 54,960 patients older than 65 y who were hospitalized due to CHF, statin therapy at discharge was associated with a 20% and 18% reduction in 1and 3-y mortality, respectively. Similar findings were reported in small, subgroup analyses of RCT. The Treating to New Targets (TNT) trial randomized 10,001 patients with stable coronary heart disease (CHD) to receive either 10 mg or 80 mg atorvastatin. In the CHF TNT subgroup analysis, rates of the predefined secondary endpoint of CHF hospitalization were significantly lower in the high-dose atorvastatin group (26% lower, P = .0116). Among the TNT population, 7.8% had a prior diagnosis of CHF; their mean age was 64 y. In these patients, high-dose atorvastatin reduced CHF hospitalization rates by 41% (P = .008). In patients without a history of CHF, hospitalization rates for CHF were similar in the Observational studies and subgroup analyses of randomized controlled studies (RCT) suggest that statins exert beneficial effects in patients with congestive heart failure (CHF). However, RCT that specifically evaluate the efficacy of statin treatment in patients with CHF had not been conducted. In this context, the COntrolled ROsuvastatin MultiNAtional Trial in Heart Failure (CORONA) was expected to provide new insights in this field. In the CORONA trial, 5011 elderly patients (mean age, 73 y) with moderate to severe systolic CHF of ischemic origin were randomized to receive 10 mg of rosuvastatin or placebo. After a median follow-up of 32.8 mo, rosuvastatin did not reduce the occurrence of the primary endpoint of cardiovascular death, nonfatal myocardial infarction, or stroke. Rosuvastatin also had no effect on cardiovascular mortality, a prespecified secondary endpoint. These negative findings occurred despite rosuvastatin producing the expected reductions in low-density lipoprotein–cholesterol (LDL-C) levels (–45%). There were significantly fewer hospitalizations for cardiovascular causes or for worsening CHF in the rosuvastatin group than in the placebo group (P < .001 and P = .01, respectively). However, rosuvastatin did not improve