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Nature's Randomized Trial in the Post–Genome Era

George Thanassoulis, MD; Christopher J. O’Donnell, MD, MPH

JAMA. 2009;301(22):2386-2388.

	Since this article does not have an abstract, we have provided the first 150 words of the full text and any section headings.

Despite several observational studies showing that lipoprotein(a) is associated with myocardial infarction (MI),^1-2 only circumstantial evidence exists regarding the causal nature of this association. Observational epidemiological studies, even with a sound prospective design, can provide hints to disease pathogenesis when the effect size is modest but cannot provide definitive evidence for causal relationships. Much of the current understanding of the causal factors in cardiovascular disease, such as the role of low-density lipoprotein, has been confirmed by randomized controlled trials (RCTs).^3-4 However, RCTs are not always feasible. In the case of lipoprotein(a), the modest effect size and the lack of specific lipoprotein(a)-lowering therapy are major obstacles to obtaining causal evidence for its role in cardiovascular disease. In this issue of JAMA, Kamstrup and colleagues⁵ provide insights using a mendelian randomization approach and provide evidence for the causal role of lipoprotein(a) in MI. . . . [Full Text of this Article]

Author Affiliations: National Heart, Lung, and Blood Institute's Framingham Heart Study, Framingham, Massachusetts (Drs Thanassoulis and O’Donnell); Division of Intramural Research, National Heart, Lung, and Blood Institute, Bethesda, Maryland (Dr O’Donnell); Boston University School of Medicine, Boston, Massachusetts (Dr Thanassoulis); and Cardiology Division, Department of Medicine, Massachusetts General Hospital, Boston (Dr O’Donnell).

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