Routine statin treatment after acute coronary syndromes?

HMG CoA (3-hydroxy-3-methylglutaryl coenzyme A) reductase inhibitors are profoundly underused in secondary prevention subjects. Pathways to improve usage of these agents are imperative. Two recent studies demonstrated that the initiation of statin therapy in patients at the time of hospital discharge at least doubled statin usage rates, resulting in a reduction in short-term mortality. The recently released Adult Treatment Panel guidelines (ATP III) have reemphasized the importance of lipid lowering at hospital discharge for continued compliance. This has become particularly compelling in the subset of hospitalized patients with acute coronary syndromes (ACS), in which a currently evolving series of reports have suggested universal statin use as particularly protective. The ATP guidelines currently mandate low-density lipoprotein cholesterol (LDL-C) testing with values 130 mg/dL or, optionally, 100 mg/dL before statin initiation. This recommendation represents a trade-off between operational and preventive benefits of universal statin use after ACS and the lack of clear evidence for statin-induced cardiovascular protection in patients with low baseline LDL-C values. This latter concern has been lessened recently by the results from the Heart Protection Study, in which statin-related protection from cardiovascular events was observed in patients at high risk with LDL 100 mg/dL (AHA presentation, 2001). The prevalence of LDL-C testing within the narrow first–24-hour window of the event (a unique interval that continues to reflect steady-state lipid levels) is quite low and out of step with current national recommendations. We believe that this guideline-based decision on statin therapy after ACS merits further review. Perhaps it is time to allow statins to travel the aspirin pathway in patients after ACS. Two series of reports in the literature recommending continued or initial use of statins are persuasive. First, introduction of statin use in the acute setting in which thrombosis, inflammation, and vasoconstriction more critically define outcomes may be particularly valuable. Investigators from the recent Myocardial Ischemia Reduction with Aggressive Cholesterol Lowering Study (MIRACL) trial randomly assigned patients to receive 80 mg of atorvastatin or placebo within the first 24 to 96 hours of a non–Q-wave myocardial infarction (MI) (54%) or unstable angina (46%). A total of 3806 patients at high risk were observed for 4 months, incurring an LDL-C decrease of 40% (124-72 mg/dL). Although more patients receiving atorvastatin developed liver enzyme elevations (2.5% vs 0.6%, treatment vs placebo group), overall serious adverse events were rare and equivalent between groups ( 1% in both). At the 16-week follow-up observation, there was a 16% reduction (relative risk ratio 0.84, 95% CI 0.7-1.0, P .048) in the combined primary end point of death, nonfatal acute MI, cardiac arrest, or worsening angina with hospitalization in the treatment group (14.8% vs 17.4% in the placebo group). Further, LDL-C lowering did not correlate with these outcomes, suggesting nontraditional benefits from the statin agent. These could include a decrease in thrombus formation, improved fibrinolysis, and both inhibition of thromboxane A2 biosynthesis and platelet function, 19