The consequences of HIV infection and antiretroviral therapy use for cardiovascular disease risk: shifting paradigms

被引:36
作者
Baker, Jason V. [1 ,2 ]
Henry, W. Keith [1 ,2 ]
Neaton, James D. [1 ]
机构
[1] Univ Minnesota, Minneapolis, MN USA
[2] Hennepin Cty Med Ctr, Minneapolis, MN 55415 USA
关键词
antiretroviral therapy; cardiovascular disease; dyslipidemia; early treatment; endothelial dysfunction; HIV infection; inflammation; C-REACTIVE PROTEIN; INTIMA-MEDIA THICKNESS; IMMUNODEFICIENCY-VIRUS-INFECTION; CORONARY-HEART-DISEASE; MYOCARDIAL-INFARCTION; ENDOTHELIAL FUNCTION; LOPINAVIR-RITONAVIR; IMMUNE ACTIVATION; BODY-FAT; ATHEROSCLEROSIS;
D O I
10.1097/COH.0b013e328329c62f
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 ;
摘要
Purpose of review To explore the mechanisms by which HIV infection and antiretroviral therapy (ART) may increase risk for atherosclerotic cardiovascular disease (CVD), with attention to the implications of earlier initiation of ART (i.e. at higher CD4 cell counts than currently recommended by guidelines). Recent findings Compared with the general population, HIV-infected patients who receive ART have a greater burden of subclinical and clinical atherosclerotic disease. Findings from a recent international treatment interruption trial (SMART) have redirected attention from ART-related drug toxicity toward a better appreciation for the consequences of untreated HIV infection, which may increase CVD risk through inflammation, upregulation of thrombotic pathways, and ultimately early vascular damage and dysfunction. In addition, CVD risk may increase with some ART, and this risk may be class-specific and/or drug-specific. Summary Compared with untreated HIV, ART may increase or decrease risk of CVD. Reliable data on the relative risk do not exist. A randomized trial of early ART will provide the best data for assessment of the net risks and benefits of ART use on CVD.
引用
收藏
页码:176 / 182
页数:7
相关论文
共 85 条
[1]   Inflammation: A pivotal link between autoimmune diseases and atherosclerosis [J].
Abou-Raya, Anna ;
Abou-Raya, Suzan .
AUTOIMMUNITY REVIEWS, 2006, 5 (05) :331-337
[2]  
[Anonymous], 2007, 4 INT AIDS SOC C HIV
[3]  
[Anonymous], 2008, CIRCULATION
[4]   Immune activation and inflammation in HIV-I infection: causes and consequences [J].
Appay, V. ;
Sauce, D. .
JOURNAL OF PATHOLOGY, 2008, 214 (02) :231-241
[5]  
Aukrust P, 2000, THROMB HAEMOSTASIS, V84, P183
[6]   AIDS-related vasculopathy: evidence for oxidative and inflammatory pathways in murine and human AIDS [J].
Baliga, RS ;
Chaves, AA ;
Jing, L ;
Ayers, LW ;
Bauer, JA .
AMERICAN JOURNAL OF PHYSIOLOGY-HEART AND CIRCULATORY PHYSIOLOGY, 2005, 289 (04) :H1373-H1380
[7]   Endothelial cell activation, injury, damage and dysfunction: separate entities or mutual terms? [J].
Blann, AD .
BLOOD COAGULATION & FIBRINOLYSIS, 2000, 11 (07) :623-630
[8]   Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection [J].
Bozzette, SA ;
Ake, CF ;
Tam, HK ;
Chang, SW ;
Louis, TA .
NEW ENGLAND JOURNAL OF MEDICINE, 2003, 348 (08) :702-710
[9]   Efficacy of contact lens systems against recent clinical and tap water Acanthamoeba isolates [J].
Shoff, Megan E. ;
Doslin, Charlotte E. ;
Tu, Elmer Y. ;
Kubatko, Laura ;
Fuerst, Paul A. .
CORNEA, 2008, 27 (06) :713-719
[10]   Microbial translocation is a cause of systemic immune activation in chronic HIV infection [J].
Brenchley, Jason M. ;
Price, David A. ;
Schacker, Timothy W. ;
Asher, Tedi E. ;
Silvestri, Guido ;
Rao, Srinivas ;
Kazzaz, Zachary ;
Bornstein, Ethan ;
Lambotte, Olivier ;
Altmann, Daniel ;
Blazar, Bruce R. ;
Rodriguez, Benigno ;
Teixeira-Johnson, Leia ;
Landay, Alan ;
Martin, Jeffrey N. ;
Hecht, Frederick M. ;
Picker, Louis J. ;
Lederman, Michael M. ;
Deeks, Steven G. ;
Douek, Daniel C. .
NATURE MEDICINE, 2006, 12 (12) :1365-1371