In this trial, treatment with rosuvastatin did not confer a significant benefit with respect to the primary end point, a composite of death resulting from cardiovascular causes, nonfatal MI, or nonfatal stroke, or several secondary end points, including all-cause mortality, coronary events, and worsening HF, despite a significant decrease in low-density lipoprotein choles- terol and C-reactive protein. Interestingly, rosuvastatin reduced the total number of hospitalizations for cardio- vascular causes and hospitalizations for HF, raising the possibility that the drug could have prevented the de- velopment of acute coronary disease that would have contributed to such episodes.273 The second trial, GISSI- HF (Gruppo Italiano per lo Studio della Sopravvivenza nell Infarto Miocardico Heart Failure), randomized 4574 patients with NYHA class II to IV chronic HF regardless of pathogenesis to rosuvastatin 10 mg or placebo; 40% of the patients had ischemic cardiomyopathy. The 2 copri- mary end points, time to death and time to death or admission to hospital for cardiovascular reasons, were not significantly different between the rosuvastatin- and placebo-treated patients. Similarly, the rates of second- ary outcomes, which included cardiovascular death, ischemic end points, and admissions for HF, were not different between the 2 groups.274 However, similar to CORONA, treatment with rosuvastatin was shown to be safe in patients with HF. In summary, low cholesterol levels are associated with increased mortality in patients with chronic HF and in those presenting with acute decompensated Bozkurt et al HF of ischemic and nonischemic origin. Despite retro- spective analyses and small trials demonstrating ben- eficial effects of statins in patients with HF, 2 large, well-executed, prospective, randomized trials revealed that statin treatment does not confer significant clini- cal benefit in patients with HF of either ischemic or nonischemic origin. 