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Article
November 10, 1993

Has Lipoprotein 'Little' (a) Shrunk?

Author Affiliations

From the Cardiovascular Division, Department of Medicine, University of Pennsylvania School of Medicine, Philadelphia.

JAMA. 1993;270(18):2224-2225. doi:10.1001/jama.1993.03510180094042
Abstract

Lipoprotein(a), or Lp(a), refers to lipoprotein particles composed of disulfide-linked apolipoprotein(a) and apolipoprotein B-100 around a cholesterol-rich lipid core. Since Berg's1 initial discovery in 1963 of Lp(a) as distinct from low-density lipoprotein, many studies (most of them retrospective and cross-sectional in nature) have demonstrated an association of atherosclerotic cardiovascular disease with high blood Lp(a) levels.2-4 The Lp(a) level, which remains relatively constant throughout life, has been suggested to be a strong, independent risk factor for acute myocardial infarction (MI), particularly in younger individuals5 or those without other predisposing risk factors. Population studies have revealed a skewed distribution of Lp(a) levels, particularly in white and Asian populations, while black populations tend to have a more normal distribution,6 with higher mean levels, yet without a substantial increase in cardiovascular risk. Genetic analyses have revealed that Lp(a) levels are primarily controlled by a series of autosomal alleles at a

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