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Circulation. 1998;98:2785-2787

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(Circulation. 1998;98:2785-2787.)
© 1998 American Heart Association, Inc.


Editorials

To E or Not To E—How Do We Tell?

Joseph L. Witztum, MD

From the Department of Medicine, University of California San Diego.

Correspondence to Joseph L. Witztum, MD, Department of Medicine Division of Endocrinology/Metabolism, University of California San Diego, La Jolla, CA 92093.


Key Words: Editorials • atherosclerosis • arteries • lipid peroxidation

Clinical disease resulting from atherosclerosis continues to cause extensive mortality and morbidity and uses an exorbitant amount of the financial resources available for health care. Atherosclerosis is a complex, multifactorial, and chronic disease influenced by a wide variety of genetic, environmental, and behavioral activities. However, it is at last widely recognized that among the known risk factors, hypercholesterolemia is one of the most important. Recent clinical trials indicate that for most individuals, and certainly for those at high risk, the lower the plasma cholesterol level, the lower the risk for subsequent development of clinical events. The mechanisms by which elevated levels of lipoproteins, chiefly the apoB containing lipoproteins such as LDL, cause an acceleration of atherogenesis are only incompletely understood. Yet there seems to be an emerging body of evidence to support the contention that the atherogenicity of LDL derives in large part from the fact that it becomes modified in one or more ways. In particular, it is widely held that the oxidative modification of LDL is intimately involved in the atherogenic process.1

Indeed, there is now considerable evidence to support the so-called oxidation hypothesis of atherosclerosis. This hypothesis suggests that oxidation of lipids and lipoproteins, such as LDL, is important, if not obligatory for the atherogenic process. This formulation has not only been of great heuristic value in guiding research into the pathophysiology of lesion development, but if correct, the corollary is that inhibition of such lipid peroxidation should ameliorate or even prevent atherosclerosis and its clinical sequelae.2 . . . [Full Text of this Article]




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