Study results published in JAMA showed that patients with a genetic condition causing them to produce low levels of HDL cholesterol had no greater risk of ischemic heart disease than patients who did not have the condition. Lead author Anne Tybjaerg-Hansen commented that the findings demonstrate that HDL cholesterol does not play a role in preventing heart attacks, and the results call into question the strategy of developing drugs that increase HDL cholesterol, based on the theory that raising HDL removes plaque from the arteries.
The author suggested that one possible reason why the study results do not support the theory about the role of HDL in preventing heart attacks is that other research evaluated patients with high triglyceride levels. She said that "triglycerides, not patients' low HDL levels, may have caused their increased heart risk." The study researchers also speculated that triglycerides may explain why torcetrapib, which Pfizer stopped developing in 2006, raised HDL levels without showing any benefit for the heart.
The study published in JAMA examined data from around 57 000 patients in Denmark between 1976 and 2007, and included 148 patients with Tangier disease. Merck & Co.'s senior vice president of cardiovascular disease research, Yale Mitchel, remarked that the study was small and in a rare patient population. He explained that the company will continue with its plans to develop an HDL-raising drug. "The hypothesis on whether CETP inhibition is a benefit or not hasn't been tested and it is too attractive a mechanism to disregard right now... There is a large contextual database that suggests low HDL levels are associated with an increased risk," he said.
Roche, which has a HDL-raising drug in the final stages of testing, noted that it hasn't "had an opportunity to evaluate this study yet, but epidemiological data does show there is a strong inverse relationship between HDL and cardiovascular risk." The drugmaker expects to file its product for approval after 2011.
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