Defining specific goals of therapy in treating dyslipidemia in the patient with low high-density lipoprotein cholesterol

Ligia Belalcazar, C. M. Ballantyne

Research output: Contribution to journalArticle

31 Citations (Scopus)

Abstract

Because patients with low high-density lipoprotein (HDL) cholesterol (HDL-C) are at high risk for clinical coronary artery disease (CAD) events, these patients require aggressive treatment with lifestyle modifications increased exercise, smoking cessation, and weight loss in overweight patients- and available pharmacological agents. Drugs that raise HDL-C include nicotinic acid, fibric acid derivatives, estrogens, 3-hydroxy-3- methylglutaryl coenzyme A reductase inhibitors (statins), α-blockers, and alcohol. However, all agents that increase HDL-C may not have the same clinical benefit, just as, as shown in genetic studies in humans and mice, genetic causes of high HDL-C do not always protect against CAD, nor do genetic causes of low HDL-C always increase risk for CAD. Better understanding of the complexities of HDL metabolism and the mechanisms by which HDL protects against CAD is needed to enable the development of new therapeutic strategies-novel drugs or gene delivery systems to increase HDL- C and reduce CAD events. The statins are the agents with the greatest evidence for slowing progression of CAD and reducing clinical events in patients with low HDL-C, but additional research is needed to determine the potential benefits of additional interventions that increase HDL-C, including combination therapy, which may provide greater improvements in the entire lipid profile.

Original languageEnglish (US)
Pages (from-to)151-174
Number of pages24
JournalProgress in Cardiovascular Diseases
Volume41
Issue number2
DOIs
StatePublished - 1998
Externally publishedYes

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HDL Lipoproteins
Dyslipidemias
LDL Cholesterol
HDL Cholesterol
Coronary Artery Disease
Hydroxymethylglutaryl-CoA Reductase Inhibitors
Therapeutics
LDL Lipoproteins
Fibric Acids
Gene Transfer Techniques
Niacin
Medical Genetics
Smoking Cessation
Drug Delivery Systems
Life Style
Weight Loss
Oxidoreductases
Estrogens
Alcohols
Pharmacology

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

Cite this

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abstract = "Because patients with low high-density lipoprotein (HDL) cholesterol (HDL-C) are at high risk for clinical coronary artery disease (CAD) events, these patients require aggressive treatment with lifestyle modifications increased exercise, smoking cessation, and weight loss in overweight patients- and available pharmacological agents. Drugs that raise HDL-C include nicotinic acid, fibric acid derivatives, estrogens, 3-hydroxy-3- methylglutaryl coenzyme A reductase inhibitors (statins), α-blockers, and alcohol. However, all agents that increase HDL-C may not have the same clinical benefit, just as, as shown in genetic studies in humans and mice, genetic causes of high HDL-C do not always protect against CAD, nor do genetic causes of low HDL-C always increase risk for CAD. Better understanding of the complexities of HDL metabolism and the mechanisms by which HDL protects against CAD is needed to enable the development of new therapeutic strategies-novel drugs or gene delivery systems to increase HDL- C and reduce CAD events. The statins are the agents with the greatest evidence for slowing progression of CAD and reducing clinical events in patients with low HDL-C, but additional research is needed to determine the potential benefits of additional interventions that increase HDL-C, including combination therapy, which may provide greater improvements in the entire lipid profile.",
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AB - Because patients with low high-density lipoprotein (HDL) cholesterol (HDL-C) are at high risk for clinical coronary artery disease (CAD) events, these patients require aggressive treatment with lifestyle modifications increased exercise, smoking cessation, and weight loss in overweight patients- and available pharmacological agents. Drugs that raise HDL-C include nicotinic acid, fibric acid derivatives, estrogens, 3-hydroxy-3- methylglutaryl coenzyme A reductase inhibitors (statins), α-blockers, and alcohol. However, all agents that increase HDL-C may not have the same clinical benefit, just as, as shown in genetic studies in humans and mice, genetic causes of high HDL-C do not always protect against CAD, nor do genetic causes of low HDL-C always increase risk for CAD. Better understanding of the complexities of HDL metabolism and the mechanisms by which HDL protects against CAD is needed to enable the development of new therapeutic strategies-novel drugs or gene delivery systems to increase HDL- C and reduce CAD events. The statins are the agents with the greatest evidence for slowing progression of CAD and reducing clinical events in patients with low HDL-C, but additional research is needed to determine the potential benefits of additional interventions that increase HDL-C, including combination therapy, which may provide greater improvements in the entire lipid profile.

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