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J Clin Lipidol. 2015 Mar-Apr;9(2):129-69. doi: 10.1016/j.jacl.2015.02.003. Epub 2015 Apr 7.

National lipid association recommendations for patient-centered management of dyslipidemia: part 1--full report.

Author information

Department of Medicine, Emory University School of Medicine, Atlanta, GA, USA. Electronic address:
Oregon State University/Oregon Health & Science University, College of Pharmacy, Portland, OR, USA.
Midwest Center for Metabolic & Cardiovascular Research and DePaul University, Chicago, IL, USA.
University of Miami Health System, Miami, FL, USA.
Louisville Metabolic and Atherosclerosis Research Center, Louisville, KY, USA.
Baylor College of Medicine, Houston, TX, USA.
Virginia Commonwealth University and National Clinical Research, Richmond, VA, USA.
The University of Texas Southwestern Medical Center, Dallas, TX, USA.
University of Washington/Harborview Medical Center, Seattle, WA, USA.
Oklahoma University Health Sciences Center, Oklahoma City, OK, USA.
Cook Children's Medical Center, Fort Worth, TX, USA.
Emory University School of Medicine, Atlanta, GA, USA.


The leadership of the National Lipid Association convened an Expert Panel to develop a consensus set of recommendations for patient-centered management of dyslipidemia in clinical medicine. An Executive Summary of those recommendations was previously published. This document provides support for the recommendations outlined in the Executive Summary. The major conclusions include (1) an elevated level of cholesterol carried by circulating apolipoprotein B-containing lipoproteins (non-high-density lipoprotein cholesterol and low-density lipoprotein cholesterol [LDL-C], termed atherogenic cholesterol) is a root cause of atherosclerosis, the key underlying process contributing to most clinical atherosclerotic cardiovascular disease (ASCVD) events; (2) reducing elevated levels of atherogenic cholesterol will lower ASCVD risk in proportion to the extent that atherogenic cholesterol is reduced. This benefit is presumed to result from atherogenic cholesterol lowering through multiple modalities, including lifestyle and drug therapies; (3) the intensity of risk-reduction therapy should generally be adjusted to the patient's absolute risk for an ASCVD event; (4) atherosclerosis is a process that often begins early in life and progresses for decades before resulting a clinical ASCVD event. Therefore, both intermediate-term and long-term or lifetime risk should be considered when assessing the potential benefits and hazards of risk-reduction therapies; (5) for patients in whom lipid-lowering drug therapy is indicated, statin treatment is the primary modality for reducing ASCVD risk; (6) nonlipid ASCVD risk factors should also be managed appropriately, particularly high blood pressure, cigarette smoking, and diabetes mellitus; and (7) the measurement and monitoring of atherogenic cholesterol levels remain an important part of a comprehensive ASCVD prevention strategy.


Atherogenic cholesterol; Atherosclerotic cardiovascular disease; Clinical recommendations; Coronary heart disease; Dyslipidemia; Lipoproteins; Low-density lipoprotein cholesterol

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