This Article Full Text Full Text (PDF) Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Grundy, S. M. Search for Related Content PubMed Articles by Grundy, S. M. Related Collections Risk Factors Related Article

(Circulation. 2008;117:569-573.)
© 2008 American Heart Association, Inc.

Controversies in Cardiovascular Medicine

Is lowering low-density lipoprotein an effective strategy to reduce cardiac risk?

Promise of Low-Density Lipoprotein–Lowering Therapy for Primary and Secondary Prevention

Scott M. Grundy, MD, PhD

From the Center for Human Nutrition, Departments of Clinical Nutrition and Internal Medicine, University of Texas Southwestern Medical Center at Dallas.

Correspondence to Scott M. Grundy, MD, PhD, Center for Human Nutrition, Departments of Clinical Nutrition and Internal Medicine, University of Texas Southwestern Medical Center at Dallas, 5323 Harry Hines Blvd, Ste Y3.206, Dallas, TX 75390–9052. E-mail scott.grundy@utsouthwestern.edu

An extract of the first 250 words of the full text is provided, because this article has no abstract.

	Introduction

 
One of the foremost medical advances of the past 2 decades has been proof that elevated low-density lipoprotein (LDL) is a cause of atherosclerotic cardiovascular disease (ASCVD) and that lowering of LDL levels will reduce risk for ASCVD.^1,2 The application of this knowledge in clinical and public health arenas offers the opportunity to greatly reduce morbidity and mortality from ASCVD. This article outlines the rationale underlying this opportunity.

Response by Superko and King p 573

	LDL: The Driving Force of Atherogenesis

 
Although several major risk factors for ASCVD exist, the realization that elevated plasma LDL is the driving force of atherogenesis highlights the possibilities for prevention. Many studies in laboratory animals have shown that high serum cholesterol levels induce atherosclerotic lesions resembling those found in humans.¹ Similarly, humans with severe forms of hypercholesterolemia commonly exhibit premature atherosclerotic disease. Epidemiological studies reveal a strong association between serum cholesterol levels and ASCVD prevalence³; moreover, in populations in which cholesterol levels are low, ASCVD is correspondingly low even when other risk factors are common.⁴ The latter observation has recently been confirmed through genetic epidemiology; in those persons who carry a mutation causing low cholesterol levels over a lifetime, ASCVD is virtually absent even in the presence of other risk factors.⁵ Finally, many recent clinical trials have documented that LDL-lowering therapy reduces risk for ASCVD.⁶ All told, these several lines of evidence indicate that a lifetime of low LDL levels lowers risk for ASCVD by up to 80% to 90% compared with the general population of the United States,⁵ . . . [Full Text of this Article]

Related Article:

Lipid Management to Reduce Cardiovascular Risk: A New Strategy Is Required

H. Robert Superko and Spencer King, III
Circulation 2008 117: 560-568. [Extract] [Full Text]

This article has been cited by other articles:

				A. J. King, J. A. Segreti, K. J. Larson, A. J. Souers, P. R. Kym, R. M. Reilly, G. Zhao, S. W. Mittelstadt, and B. F. Cox Diacylglycerol Acyltransferase 1 Inhibition Lowers Serum Triglycerides in the Zucker Fatty Rat and the Hyperlipidemic Hamster J. Pharmacol. Exp. Ther., August 1, 2009; 330(2): 526 - 531. [Abstract] [Full Text] [PDF]

				G. D Brinkworth, M. Noakes, J. D Buckley, J. B Keogh, and P. M Clifton Long-term effects of a very-low-carbohydrate weight loss diet compared with an isocaloric low-fat diet after 12 mo Am. J. Clinical Nutrition, July 1, 2009; 90(1): 23 - 32. [Abstract] [Full Text] [PDF]

				M. J. Budoff Not all diabetics are created equal (in cardiovascular risk) Eur. Heart J., September 2, 2008; 29(18): 2193 - 2194. [Full Text] [PDF]