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Genetically Elevated Levels of Lipoprotein Associated With Increased Risk of MI CHICAGO -- June 9, 2009 -- A genetic analysis of data from 3 studies suggests that genetically elevated levels of lipoprotein(a) are associated with an increased risk of myocardial infarction (MI), according to a study published in the June 10 issue of JAMA. “The need for identification of additional causal factors, and thus potential new targets for prophylactic treatment, is apparent. Elevated levels of lipoprotein(a) represent such a candidate; however, whether lipoprotein(a) causes MI is unclear,” the authors wrote. “A randomised intervention trial showing that a reduction in lipoprotein(a) levels leads to a reduction in risk of MI would favor causality. Such a study has yet to be conducted.” They add that a mendelian randomisation study could also provide evidence of a causal relationship. “Simply put, association of elevated levels of lipoprotein(a), as well as association of genetic variation raising levels of lipoprotein(a), with risk of MI would suggest causality.” The most influential LPA variation is the kringle IV type 2 (KIV-2) size variation. The number of KIV-2 repeats correlates inversely with levels of lipoprotein(a), according to background information in the article. Pia R. Kamstrup, MD, Herlev Hospital, Copenhagen University Hospital, Herlev, Denmark, and colleagues examined whether genetically elevated lipoprotein(a) levels are associated with increased risk of MI. Three studies of white individuals from Copenhagen, Denmark, were used: the Copenhagen City Heart Study (CCHS), a general population study with 16 years of follow-up (1991-2007; n = 8,637; 599 MI events); the Copenhagen General Population Study (CGPS), a general population study (2003-2006; n = 29€388; 994 MI events); and the Copenhagen Ischemic Heart Disease Study (CIHDS), a case-control study (1991-2004; n = 2,461; 1,231 MI events). For all participants, plasma lipoprotein(a) levels, lipoprotein(a) KIV-2 size variation genotype, and MIs were recorded from 1976 through July 2007. “We observed an increase in risk of MI with increasing levels of lipoprotein(a), as well as with decreasing numbers of lipoprotein(a) KIV-2 repeats associated with elevated levels of lipoprotein(a),” the authors wrote. “The increase in risk of MI associated with genetically elevated levels of lipoprotein(a) was consistently seen in 3 large independent studies…the KIV-2 genotype explained 21% and 27% of the total lipoprotein(a) concentration variation in the CCHS and the CGPS. Instrumental variable analysis directly demonstrated that genetically elevated lipoprotein(a) is associated with increased risk of MI, like elevations in plasma lipoprotein(a). These findings are consistent with a causal association of elevated lipoprotein(a) levels with increased MI risk.” “Nonetheless, final proof of causality still requires randomised clinical trials demonstrating reduced MI risk in response to lipoprotein(a)-lowering therapy.” SOURCE: JAMA E-mail this page to a friend or colleague! To print, use this version