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  Vol. 270 No. 18, November 10, 1993 TABLE OF CONTENTS
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Has Lipoprotein 'Little' (a) Shrunk?

Elliot S. Barnathan, MD

JAMA. 1993;270(18):2224-2225.

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

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 . . . [Full Text PDF of this Article]


Author Affiliations

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


Footnotes

Reprint requests to 524 Johnson Pavilion, University of Pennsylvania School of Medicine, 36th and Hamilton Walk, Philadelphia, PA 19104-6060 (Dr Barnathan).



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