PubMed · 3336289
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J J McNeil. 1988-01-04. Cholesterol: action or caution?. https://doi.org/10.5694/j.1326-5377.1988.tb104467.x
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OBJECTIVE: To determine the best time to administer statins for optimal lowering of low-density lipoprotein cholesterol (LDL-C) by reviewing the clinical evidence evaluating the chronobiologic effects of morning versus evening statin administration. DATA SOURCES: Using the MeSH terms HMG-CoA reductase inhibitors, statins, morning and evening dosing, and clinical trials, a literature review was conducted to identify articles in MEDLINE (1966-December 2006), International Pharmaceutical Abstracts (1970-December 2006), and IOWA Drug Information Systems (1985-December 2006). DATA SYNTHESIS: Seven English-language studies evaluating morning and evening statin administration were identified and evaluated. Based on the available data, simvastatin demonstrated a pronounced LDL-C percentage reduction with evening dosing. Although not statistically significant, a trend in the LDL-C percentage reduction favoring evening statin administration was noted with lovastatin, pravastatin, and rosuvastatin. Atorvastatin demonstrated similar LDL-C reduction regardless of administration time. With the exception of simvastatin, the trials comparing morning versus evening effects of statins on LDL-C have several significant methodologic shortcomings, including small sample size, lack of statistical power, and inappropriate exclusion criteria that did not include or did not mention drug-induced effects on lipids. CONCLUSIONS: There are sufficient data to support evening administration of simvastatin to achieve optimal lowering of LDL-C levels. Rigorous and robust trials are necessary to determine the best administration time to achieve optimal LDL-C lowering for lovastatin, pravastatin, rosuvastatin, atorvastatin, and fluvastatin.
Scientists are seeking ways to increase high-density lipoprotein (HDL) cholesterol to lower coronary heart disease (CHD). Emerging from this search is torcetrapib, a partial inhibitor of cholesteryl ester transfer protein. Via this mechanism, cholesteryl ester is prevented from being transferred to apolipoprotein B-containing lipoproteins and is retained in HDL particles, where ostensibly it may be delivered directly to the liver for elimination. Proof that this may reduce atherosclerotic vascular disease is provided by population studies of cholesteryl ester transfer protein (CETP) deficiencies and single nucleotide polymorphisms of CETP, and experiments in animal models treated with torcetrapib. Torcetrapib effectively raises HDL cholesterol when used alone and when added to background therapy with atorvastatin. The drug appears to be well tolerated. Large surrogate and survival outcome trials are underway to document its impact on CHD.