Abstract

YOCARDIAL INFARCTION(MI) remains a leading cause of morbidity and mortality despite targeting of low-density lipoprotein (LDL) cholesterol by statin therapy.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 1-5 ; however, whether lipoprotein(a) causes MI is unclear.A randomized 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.][8] 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.Lipoprotein(a) consists of what is essentially an LDL particle bound to a plasminogen-like glycoprotein, apolipoprotein(a). 9Levels of lipoprotein(a) may vary up to a thousand-fold among individuals, and levels are partly determined by polymorphisms in the LPA gene (OMIM 152200) coding for the apolipoprotein(a) moiety of