Literature DB >> 21730827

Optimal pharmacotherapy to combat the atherogenic lipid triad.

M John Chapman1, Jan S Redfern, Mark E McGovern, Philippe Giral.   

Abstract

PURPOSE OF REVIEW: A lipid triad involving an atherogenic dyslipidemia characterized by moderate/high LDL-C, low HDL-C, and elevated triglyceride (TG) occurs in numerous clinical settings associated with high cardiovascular risk. This article focuses on optimizing treatment of atherogenic dyslipidemias involving this lipid triad, emphasizing niacin-based or fibrate-based therapies. RECENT
FINDINGS: Niacin-based therapies comprehensively improve the atherogenic lipid profile, lead to atherosclerosis regression, and exert benefits across a spectrum of cardiovascular endpoints in studies based on limited patient numbers. Fibrates impact TG, HDL-C, and LDL-C according to lipid phenotype and underlying metabolic abnormality. In a recent meta-analysis, fibrates significantly reduced major cardiovascular events (-10%) and coronary events (-13%) across a wide range of lipid phenotypes, but had no impact on stroke, sudden death, or mortality. The Action to Control Cardiovascular Risk in Diabetes (ACCORD) trial in type 2 diabetic patients similarly showed no significant effect of fenofibrate + simvastatin (vs. simvastatin) on nonfatal myocardial infarction, nonfatal stroke, or cardiovascular death; a subgroup (17%) with marked atherogenic dyslipidemia trended toward benefit. Both niacin and fibrates attenuate vascular inflammation but the potential clinical relevance is indeterminate.
SUMMARY: Optimal cardiovascular risk reduction in patients exhibiting the lipid triad requires integrated pharmacotherapy to normalize LDL-C, HDL-C, TGs, and potentially lipoprotein(a). Ongoing studies may provide definitive evidence of the impact of niacin plus statins on cardiovascular outcomes.

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Year:  2011        PMID: 21730827     DOI: 10.1097/HCO.0b013e32834965e9

Source DB:  PubMed          Journal:  Curr Opin Cardiol        ISSN: 0268-4705            Impact factor:   2.161


  4 in total

1.  Nicotinic acid inhibits hepatic APOA gene expression: studies in humans and in transgenic mice.

Authors:  Indumathi Chennamsetty; Karam M Kostner; Thierry Claudel; Manjula Vinod; Sasa Frank; Thomas S Weiss; Michael Trauner; Gerhard M Kostner
Journal:  J Lipid Res       Date:  2012-08-28       Impact factor: 5.922

2.  Genetic loss or pharmacological blockade of testes-expressed taste genes causes male sterility.

Authors:  Bedrich Mosinger; Kevin M Redding; M Rockwell Parker; Valeriya Yevshayeva; Karen K Yee; Katerina Dyomina; Yan Li; Robert F Margolskee
Journal:  Proc Natl Acad Sci U S A       Date:  2013-07-01       Impact factor: 11.205

Review 3.  Fibrates are an essential part of modern anti-dyslipidemic arsenal: spotlight on atherogenic dyslipidemia and residual risk reduction.

Authors:  Alexander Tenenbaum; Enrique Z Fisman
Journal:  Cardiovasc Diabetol       Date:  2012-10-11       Impact factor: 9.951

Review 4.  Balanced pan-PPAR activator bezafibrate in combination with statin: comprehensive lipids control and diabetes prevention?

Authors:  Alexander Tenenbaum; Enrique Z Fisman
Journal:  Cardiovasc Diabetol       Date:  2012-11-14       Impact factor: 9.951

  4 in total

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