Abstract
In the era of highly active antiretroviral therapy (HAART), human immunodeficiency virus (HIV) infection has become a chronic disease in which patients may develop significant metabolic complications and risk factors for cardiovascular disease (CVD), including insulin resistance, visceral fat deposition, and increases in atherogenic cholesterol and triglyceride levels. Epidemiologic studies have found that persons infected with HIV are likely to be at higher risk for premature CVD compared with the general population, and clinical studies examining endothelial function in HIV-infected cohorts have supported such conclusions. The mechanisms underlying the regulation of endothelial function in HIV-infected persons appear to be multifactorial, including direct effects of HIV on the endothelium, indirect effects of HIV on lipids and inflammatory cytokines, HAART-related effects, and traditional/host factors. Better understanding of these processes can lead to improved strategies for the long-term management of HIV infection.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 88-92 |
| Number of pages | 5 |
| Journal | Journal of the CardioMetabolic Syndrome |
| Volume | 3 |
| Issue number | 2 |
| State | Published - Mar 2008 |
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ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine
- Internal Medicine
- Endocrinology, Diabetes and Metabolism
Cite this
Determinants of endothelial function in human immunodeficiency virus infection : a complex interplay among therapy, disease, and host factors. / Mondy, Kristin E.
In: Journal of the CardioMetabolic Syndrome, Vol. 3, No. 2, 03.2008, p. 88-92.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Determinants of endothelial function in human immunodeficiency virus infection
T2 - a complex interplay among therapy, disease, and host factors.
AU - Mondy, Kristin E.
PY - 2008/3
Y1 - 2008/3
N2 - In the era of highly active antiretroviral therapy (HAART), human immunodeficiency virus (HIV) infection has become a chronic disease in which patients may develop significant metabolic complications and risk factors for cardiovascular disease (CVD), including insulin resistance, visceral fat deposition, and increases in atherogenic cholesterol and triglyceride levels. Epidemiologic studies have found that persons infected with HIV are likely to be at higher risk for premature CVD compared with the general population, and clinical studies examining endothelial function in HIV-infected cohorts have supported such conclusions. The mechanisms underlying the regulation of endothelial function in HIV-infected persons appear to be multifactorial, including direct effects of HIV on the endothelium, indirect effects of HIV on lipids and inflammatory cytokines, HAART-related effects, and traditional/host factors. Better understanding of these processes can lead to improved strategies for the long-term management of HIV infection.
AB - In the era of highly active antiretroviral therapy (HAART), human immunodeficiency virus (HIV) infection has become a chronic disease in which patients may develop significant metabolic complications and risk factors for cardiovascular disease (CVD), including insulin resistance, visceral fat deposition, and increases in atherogenic cholesterol and triglyceride levels. Epidemiologic studies have found that persons infected with HIV are likely to be at higher risk for premature CVD compared with the general population, and clinical studies examining endothelial function in HIV-infected cohorts have supported such conclusions. The mechanisms underlying the regulation of endothelial function in HIV-infected persons appear to be multifactorial, including direct effects of HIV on the endothelium, indirect effects of HIV on lipids and inflammatory cytokines, HAART-related effects, and traditional/host factors. Better understanding of these processes can lead to improved strategies for the long-term management of HIV infection.
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UR - http://www.scopus.com/inward/citedby.url?scp=65849138983&partnerID=8YFLogxK
M3 - Article
C2 - 18453808
AN - SCOPUS:65849138983
VL - 3
SP - 88
EP - 92
JO - Journal of the CardioMetabolic Syndrome
JF - Journal of the CardioMetabolic Syndrome
SN - 1559-4564
IS - 2
ER -