Journal
JOURNAL OF CLINICAL LIPIDOLOGY
Volume 9, Issue 2, Pages 129-169Publisher
ELSEVIER SCIENCE INC
DOI: 10.1016/j.jacl.2015.02.003
Keywords
Clinical recommendations; Dyslipidemia; Atherogenic cholesterol; Low-density lipoprotein cholesterol; Lipoproteins; Atherosclerotic cardiovascular disease; Coronary heart disease
Categories
Funding
- Merck and Co
- Amarin
- AstraZeneca
- Regeneron/Sanofi-Aventis
- Kowa Pharmaceuticals
- Abbvie
- Matinas BioPharma
- Pharmavite
- Sancilio
- Trygg Pharmaceuticals
- Ardea
- Amgen
- Arisaph
- California Raisin Marketing Board
- Catabasis
- Cymabay
- Eisai
- Elcelyx
- Eli Lilly
- Esperion
- Gilead
- Hanmi
- Hisun
- Hoffman-La Roche
- Home Access
- Janssen
- Johnson and Johnson
- Merck
- Necktar
- Novartis
- Novo Nordisk
- Omthera
- Orexigen
- Pfizer
- Pronova
- Regeneron
- Sanofi
- Takeda
- TIMI
- VIVUS Inc
- Wpu Pharmaceuticals
- Lily
- Philips Medical Systems
- Merck Sharpe Dohme
- Novo Nordisk Inc.
- Bristol-Myers Squibb
- Genzyme
- Pfizer, Inc,
- LipoScience, Inc
- GlaxoSmithKline
- Medtelligence
- Vindico
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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. (C) 2015 National Lipid Association. All rights reserved.
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