This Article  • References  • Full text PDF  • Send to a friend  • Save in My Folder  • Save to citation manager  • Permissions  Citing Articles  • Citation map  • Contact me when this article is cited  Related Content  • Similar articles in JAMA  Social Bookmarking   What's this?

Henry C. McGill, Jr, MD

JAMA. 1994;271(4):317-318.

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

Debate over the role of hyperlipidemia in causing coronary heart disease has dominated discussion of this disease since it emerged on an epidemic scale in industrialized countries after World War II. Although many questions remain about how, the question about whether hyperlipidemia causes atherosclerosis and its sequelae (the so-called lipid hypothesis) has been settled: it does. Nearly two decades of clinical trials have confirmed predictions derived from observational epidemiology and animal experimentation that control of hyperlipidemia reduces the frequency of coronary heart disease and causes regression of coronary atherosclerosis. This knowledge is now modifying public health and clinical medical practice.¹

See also p 289.

However, continued investigation discloses new aspects of this disease. A few years ago, lipoprotein (a) was a laboratory curiosity of uncertain significance; now, its similarity to plasminogen suggests that it may predispose to coronary heart disease by augmenting thrombosis.² The discovery of oxidized low-density . . . [Full Text PDF of this Article]

Author Affiliations
From the Department of Physiology and Medicine, Southwest Foundation for Biomedical Research, San Antonio, Tex.

Footnotes
Reprint requests to Department of Physiology and Medicine, Southwest Foundation for Biomedical Research, PO Box 28147, San Antonio, TX 78228-0147 (Dr McGill).

CiteULike    Connotea    Del.icio.us    Digg    Reddit    Technorati    Twitter     What's this?