Literature DB >> 21722900

Cardiovascular implications of HIV-induced dyslipidemia.

Chiara Giannarelli1, Robert S Klein, Juan J Badimon.   

Abstract

Cardiovascular disease (CVD) is currently the second most frequent cause of death (after cancer) among HIV-positive subjects. The clinical use of highly active antiretroviral therapy (HAART) has dramatically reduced mortality and morbidity in HIV-positive population, leading to prolonged and improved quality of life. However, as mortality and morbidity from AIDS-related conditions improve, CVD assumes increasing magnitude. It is estimated that by 2015 more than 50% of HIV-positive patients will be older than 50 years. Since age is a major unmodifiable cardiovascular risk factor, the risk for CVD in this population will significantly and progressively increase in the near future. A large part of the risk for cardiovascular events appears to be a result of lipid abnormalities characterizing HIV-positive persons. This review focuses on HIV-associated lipid abnormalities and CVD. Lipid abnormalities may be related to either viral infection, HAART or both. Dyslipidemia characterizing HIV-infected patients has become a therapeutic target to reduce cardiovascular risk of HIV-treated patients. HAART-treated patients show an atherogenic lipid profile comprised of low HDL-cholesterol levels, hypertrigliceridemia and increased levels of small-LDL particles. Current guidelines for the treatment of dyslipidemia and reducing cardiovascular risk in HIV-positive patients suggest that when lifestyle modifications (i.e., diet and exercise) and switching antiretroviral therapy are not enough, statins should be the first-line therapy for dyslipidemia. HDL raising interventions (niacin and fibrates) should be considered to raise HDL levels and lower triglyceride in HIV-infected patients. Implications of lipid-related interventions in HIV-treated patients to avoid drug interactions and their adverse effects are also discussed.
Copyright © 2011 Elsevier Ireland Ltd. All rights reserved.

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Year:  2011        PMID: 21722900     DOI: 10.1016/j.atherosclerosis.2011.06.003

Source DB:  PubMed          Journal:  Atherosclerosis        ISSN: 0021-9150            Impact factor:   5.162


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