TY - JOUR
T1 - Impact of HIV and highly active antiretroviral therapy on leukocyte adhesion molecules, arterial inflammation, dyslipidemia, and atherosclerosis
AU - Fisher, Stacy D.
AU - Miller, Tracie L.
AU - Lipshultz, Steven E.
N1 - Funding Information:
This work was supported in part by grants CA68484, CA79060, HL69800, HL59837, and HL53392 from the National Institutes of Health, Bethesda, MD and Boehringer Ingelheim.
PY - 2006/3
Y1 - 2006/3
N2 - Highly active antiretroviral therapy (HAART) has greatly extended the lives of people infected with the human immunodeficiency virus (HIV). This reduced risk of early death from opportunistic infections or other sequelae of HIV infection, however, means that other possible causes of death emerge. Myocardial infarction has become a matter of particular concern. Two of the main sources of cardiovascular disease in this population are believed to be vascular inflammation and dyslipidemia. We review the evidence for this hypothesis and discuss the relationship of HIV to vascular inflammation. Current treatment guidelines do not recommend the immediate initiation of HAART unless warranted, potentially allowing long-term, unchecked viral impact on the development of atherosclerosis. Finally, we consider the protease inhibitors traditionally included in HAART regimens and their relationship to the development of dyslipidemia, as well as other classes of antiretrovirals, such as the non-nucleoside reverse transcriptase inhibitors, which might be a better choice for patients with cardiovascular risks. Other strategies, such as pharmacologic, nutritional, and physical activity interventions are discussed. The patients who might benefit most are those in whom the precursors of vascular plaques, such as fatty streak, smooth muscle cell, macrophage, and T-lymphocyte aggregation not yet identified by echocardiographic and biopsy findings have already developed as a result of unchecked viral inflammation and replication.
AB - Highly active antiretroviral therapy (HAART) has greatly extended the lives of people infected with the human immunodeficiency virus (HIV). This reduced risk of early death from opportunistic infections or other sequelae of HIV infection, however, means that other possible causes of death emerge. Myocardial infarction has become a matter of particular concern. Two of the main sources of cardiovascular disease in this population are believed to be vascular inflammation and dyslipidemia. We review the evidence for this hypothesis and discuss the relationship of HIV to vascular inflammation. Current treatment guidelines do not recommend the immediate initiation of HAART unless warranted, potentially allowing long-term, unchecked viral impact on the development of atherosclerosis. Finally, we consider the protease inhibitors traditionally included in HAART regimens and their relationship to the development of dyslipidemia, as well as other classes of antiretrovirals, such as the non-nucleoside reverse transcriptase inhibitors, which might be a better choice for patients with cardiovascular risks. Other strategies, such as pharmacologic, nutritional, and physical activity interventions are discussed. The patients who might benefit most are those in whom the precursors of vascular plaques, such as fatty streak, smooth muscle cell, macrophage, and T-lymphocyte aggregation not yet identified by echocardiographic and biopsy findings have already developed as a result of unchecked viral inflammation and replication.
KW - Atherogenesis
KW - Cardiovascular disease
KW - Highly active antiretroviral therapy
KW - Human immunodeficiency virus
KW - Myocardial infarction
KW - Non-nucleoside reverse transcriptase inhibitors
KW - Protease inhibitors
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U2 - 10.1016/j.atherosclerosis.2005.09.025
DO - 10.1016/j.atherosclerosis.2005.09.025
M3 - Review article
C2 - 16297390
AN - SCOPUS:30944431733
VL - 185
SP - 1
EP - 11
JO - Atherosclerosis
JF - Atherosclerosis
SN - 0021-9150
IS - 1
ER -