Article information
Resumen
Los pacientes infectados por el virus de la inmunodeficiencia humana (VIH) comparten los factores de riesgo cardiovascular tradicionales con la población general. Además, el propio VIH incrementa significativamente el riesgo de enfermedad cardiovascular. Por este motivo, el control de la infección por el VIH con tratamiento antirretroviral de gran actividad (TARGA) ayuda a reducir el riesgo vascular de los pacientes infectados por el VIH. Hay evidencias de que el TARGA incrementa el riesgo cardiovascular, y se ha asociado el uso de abacavir, ddI, lopinavir/r e indinavir con el desarrollo de infarto agudo de miocardio (IAM). Sin embargo, el riesgo absoluto de desarrollar IAM en pacientes que reciben TARGA es muy bajo con relación al alto beneficio obtenido por la terapia antirretroviral.
Palabras clave:
VIH
Riesgo cardiovascular
Tratamiento antirretroviral de gran actividad (TARGA)
Abacavir
Abstract
HIV-infected patients share traditional cardiovascular risk factors with the general population. Moreover, HIV per se significantly increases the risk of cardiovascular disease. Consequently, control of HIV infection with highly-active antiretroviral therapy (HAART) helps to reduce vascular risk in HIV-infected patients. However, there is evidence that HAART increases cardiovascular risk and the use of abacavir, didanosine, lopinavir/ritonavir and indinavir has been associated with the development of acute myocardial infarction (AMI). However, the absolute risk of AMI in patients receiving HAART is very low in relation to the benefit obtained with antiretroviral therapy.
Keywords:
HIV
Cardiovascular risk
Highly-active antiretroviral therapy (HAART)
Abacavir
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Bibliografía
[1.]
V.D. Lima, R.S. Hogg, P.R. Harrigan, D. Moore, B. Yip, E. Wood, et al.
Continued improvement in survival among HIV-infected individuals with newer forms of highly active antiretroviral therapy.
AIDS, 21 (2007), pp. 685-692
[2.]
F.J. Palella Jr, K.M. Delaney, A.C. Moorman, M.O. Loveless, J. Fuhrer, G.A. Satten, et al.
Declining morbidity and mortality among patients with advanced human immunodeficiency virus infection. HIV Outpatient Study Investigators.
N Engl J Med, 338 (1998), pp. 853-860
[3.]
A. Mocroft, B. Ledergerber, C. Katlama, O. Kirk, P. Reiss, A. D’Arminio Monforte, et al.
Decline in the AIDS and death rates in the EuroSIDA study: an observational study.
Lancet, 362 (2003), pp. 22-29
[4.]
R. Manfredi, S. Sabbatani, D. Agostini.
Trend of mortality observed in a cohort of drug addicts of the metropolitan area of Bologna, North-Eastern Italy, during a 25-year-period.
Coll Antropol, 30 (2006), pp. 479-488
[5.]
M.D. Wong, M.F. Shapiro, W.J. Boscardin, S.L. Ettner.
Contribution of major diseases to disparities in mortality.
N Engl J Med, 347 (2002), pp. 1585-1592
[6.]
W. Rosamond, K. Flegal, K. Furie, A. Go, K. Greenlund, N. Haase, et al.
Heart disease and stroke statistics-2008 update: a report from the American Heart Association Statistics Committee and Stroke Statistics Subcommittee.
Circulation, 117 (2008), pp. e25-146
[7.]
J.A. Aberg.
Cardiovascular complications in HIV management: past, present, and future.
J Acquir Immune Defic Syndr, 50 (2009), pp. 54-64
[8.]
N. Friis-Moller, C.A. Sabin, R. Weber, A. D’Arminio Monforte, W.M. El-Sadr, P. Reiss, et al.
Combination antiretroviral therapy and the risk of myocardial infarction.
N Engl J Med, 349 (2003), pp. 1993-2003
[9.]
D. Finzi, J. Blankson, J.D. Siliciano, J.B. Margolick, K. Chadwick, T. Pierson, et al.
Latent infection of CD4+ T cells provides a mechanism for lifelong persistence of HIV-1, even in patients on effective combination therapy.
Nat Med, 5 (1999), pp. 512-517
[10.]
W.M. El-Sadr, J.D. Lundgren, J.D. Neaton, F. Gordin, D. Abrams, R.C. Arduino, et al.
Strategies for Management of Antiretroviral Therapy (SMART) Study Group. CD4+ count-guided interruption of antiretroviral treatment.
N Engl J Med, 355 (2006), pp. 2283-2296
[11.]
S. Bozzette, C. Ake, H. Tam, S.W. Chang, T.A. Louis.
Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection.
N Engl J Med, 348 (2003), pp. 702-710
[12.]
A. Carr, K. Samaras, S. Burton, M. Law, J. Freund, D.J. Chisholm, et al.
A syndrome of peripheral lipodystrophy, hyperlipidaemia and insulin resistance in patients receiving HIV protease inhibitors.
AIDS, 12 (1998), pp. F51-58
[13.]
M. Dube, F. Sattler.
Metabolic complications of antiretroviral therapies.
AIDS Clin Care, 10 (1998), pp. 41-44
[14.]
R. SoRelle.
Vascular and lipid syndromes in selected HIV-infected patients.
Circulation, 98 (1998), pp. 829-830
[15.]
B. Gallet, M. Pulik, P. Genet, P. Chedin, M. Hiltgen.
Vascular complications associated with use of HIV protease inhibitors.
Lancet, 351 (1998), pp. 1958-1959
[16.]
K. Henry, H. Melroe, J. Huebsch, J. Hermundson, C. Levine, L. Swensen, et al.
Severe premature coronary artery disease with protease inhibitors.
Lancet, 351 (1998), pp. 1328
[17.]
D. Klein, L.B. Hurley, C.P. Quesenberry Jr, S. Sidney.
Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection?.
J Acquir Immune Defic Syndr, 30 (2002), pp. 471-477
[18.]
M. Mary-Krause, L. Cotte, A. Simon, M. Partisani, D Costagliola, Clinical Epidemiology Group from the French Hospital Database.
Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men.
AIDS, 17 (2003), pp. 2479-2486
[19.]
J. Currier, A. Taylor, F. Boyd, C.M. Dezii, H. Kawabata, B. Burtcel, et al.
Coronary heart disease in HIV-infected individuals.
J Acquir Immune Defic Syndr, 33 (2003), pp. 506-512
[20.]
R.C. Kaplan, L.A. Kingsley, A.R. Sharrett, X. Li, J. Lazar, P.C. Tien, et al.
Ten-year predicted coronary heart disease risk in HIV-infected men and women.
Clin Infect Dis, 44 (2007), pp. 1074-1081
[21.]
N. Obel, H.F. Thompsen, G. Kronborg, C.S. Larsen, P.R. Hildebrandt, H.T. Sorensen, et al.
Ischemic heart disease in HIV-infected and HIV-uninfected individuals: a population- based cohort study.
Clin Infect Dis, 44 (2007), pp. 1625-1631
[22.]
S.D. Holmberg, A.C. Moorman, J.M. Williamson, T.C. Tong, D.J. Ward, K.C. Wood, HIV Outpatient Study (HOPS) investigators, et al.
Protease inhibitors and cardiovascular outcomes in patients with HIV-1.
Lancet, 360 (2002), pp. 1747-1748
[23.]
G. Vaughn, R. Detels.
Protease inhibitors and cardiovascular disease: analysis of the Los Angeles County adult spectrum of disease cohorte.
AIDS Care, 19 (2007), pp. 492-499
[24.]
N. Friis-Moller, C. Sabin, R. Weber, A. D’Arminio Monforte, W.M. El-Sadr, P. Reiss, et al.
Combination antiretroviral therapy and the risk of myocardial infarction.
N Engl J Med, 349 (2003), pp. 1993-2003
[25.]
G. Vaughn, R. Detels.
Protease inhibitors and cardiovascular disease: análisis of the Los Angeles County adult spectrum of disease cohorte.
AIDS Care, 19 (2007), pp. 492-499
[26.]
J.H. Stein.
Cardiovascular risks of antiretroviral therapy.
N Engl J Med, 356 (2007), pp. 1773-1775
[27.]
J.Q. Purnell, A. Zambon, R.H. Knopp, D.J. Pizzuti, R. Achari, J.M. Leonard, et al.
Effect of ritonavir on lipids and post-heparin lipase activities in normal subjects.
AIDS, 14 (2000), pp. 51-57
[28.]
D. Periard, A. Telenti, P. Sudre, J.J. Cheseaux, P. Halfon, M.J. Reymond, et al.
Atherogenic dyslipidemia in HIV-infected individuals treated with protease inhibitors.
Circulation, 100 (1999), pp. 700-705
[29.]
A.D. Roberts, R.A. Muesing, D.M. Parenti, J. Hsia, A.G. Wasserman, G.L. Simon.
Alterations in serum levels of lipids and lipoproteins with indinavir therapy for human immunodeficiency virus-infected patients.
Clin Infect Dis, 29 (1999), pp. 441-443
[30.]
K. Mulligan, C. Grunfeld, V.W. Tai, H. Algren, M. Pang, D.N. Chernoff, et al.
Hyperlipidemia and insulin resistance are induced by protease inhibitors independent of changes in body composition in patients with HIV infection.
J Acquir Immune Defic Syndr, 23 (2000), pp. 35-43
[31.]
M.A. Noor, J.C. Lo, K. Mulligan, J.M. Schwarz, R.A. Halvorsen, M. Schambelan, et al.
Metabolic effects of indinavir in healthy HIV-seronegative men.
AIDS, 15 (2001), pp. F11-F18
[32.]
K. Squires, A. Lazzarin, J.M. Gatell, W.G. Powderly, V. Pokrovskiy, J.F. Delfraissy, et al.
Comparison of once-daily atazanavir to efavirenz each in combination with fixeddose zidovudina and lamivudine, as initial therapy for patients infected with HIV.
J Acquir Immune Defic Syndr, 36 (2004), pp. 1011-1019
[33.]
D.RN. Malan, E. Krantz, N. David, V. Wirtz, J. Hammond, D. McGrath, 089 Study Group.
Efficacy and safety of atazanavir, with or without ritonavir, as part of once-daily highly active antiretroviral therapy regimens in antiretroviral-naive patients.
J Acquir Immune Defic Syndr, 47 (2008), pp. 161-167
[34.]
K.Y. Smith, W.G. Weinberg, E. Dejesus, M.A. Fischl, Q. Liao, L. Ross, et al.
Fosamprenavir or atazanavir once daily boosted with ritonavir 100 mg, plus tenofovir/emtricitabine, for the initial treatment of HIV infection: 48-week results of ALERT.
AIDS Res Ther, 5 (2008), pp. 5
[35.]
J. Eron Jr, P. Yeni, J. Gathe Jr, V. Estrada, E. DeJesus, S. Staszewski, et al.
The KLEAN study of fosamprenavirritonavir versus lopinavir-ritonavir, each in combination with abacavirlamivudine, for initial treatment of HIV infection over 48 weeks: a randomised non-inferiority trial.
Lancet, 368 (2006), pp. 476-482
[36.]
J.M. Molina, J. Andrade-Villanueva, J. Echevarria, P. Chetchotisakd, J. Corral, N. David, et al.
Once-daily atazanavir/ritonavir versus twice-daily lopinavir/ritonavir, each in combination with tenofovir and emtricitabine, for management of antiretroviral- naive HIV-1-infected patients: 48 week efficacy and safety results of the CASTLE study.
Lancet, 372 (2008), pp. 646-655
[37.]
R. Ortiz, E. Dejesus, H. Khanlou, E. Voronin, J. Van Lunzen, J. Andrade-Villanueva, et al.
Efficacy and safety of once-daily darunavir/ritonavir versus lopinavir/ritonavir in treatment-naive HIV-1-infected patients at week 48.
AIDS, 22 (2008), pp. 1389-1397
[38.]
S. Walmsley, A. Avihingsanon, J. Slim, D.J. Ward, K. Ruxrungtham, J. Brunetta, et al.
Gemini: a noninferiority study of saquinavir/ritonavir versus lopinavir/ritonavir as initial HIV-1 therapy in adults.
J Acquir Immune Defic Syndr, 50 (2009), pp. 367-374
[39.]
Lundgren J, Reiss P, Worm S, Weber R, El-Sadr W, De Wit S, et al. Risk of myocardial infarction with exposure to specific ARV from the PI, NNRTI, and NRTI drug classes: the D:A:D study. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11,Montreal. Abstract 44LB.
[40.]
C.M. Shikuma, Y. Yang, M.J. Glesby, W.A. Meyer 3rd, K.T. Tashima, H.J. Ribaudo, et al.
Metabolic effects of protease inhibitor-sparing antiretroviral regimens given as initial treatment of HIV-1 infection (AIDS Clinical Trials Group Study A5095).
J Acquir Immune Defic Syndr, 44 (2007), pp. 540-550
[41.]
Haubrich R, Riddler S, DiRienzo G, L Komarow l, W Powderly W, Garren K, et al. Metabolic outcomes of ACTG 5142: a prospective, randomized phase III trial of NRTI-, PI-, and NNRTIsparing regimens for initial treatment of HIV-1. Presented at: 14th Conference on Retroviruses and Opportunistic Infections (CROI); 2007; Los Angeles, CA. Abstract.
[42.]
Van Leth F, Phanuphak P, Stroes E, Gazzard B, Cahn P, Raffi, F, et al. Nevirapine and efavirenz elicit different changes in lipid profiles in antiretroviral-therapy-naive patients infected with HIV-1 PLoS Med. 2004;1:e19.
[43.]
P.N. Kumar, A. Rodriguez-French, M.A. Thompson, K.T. Tashima, D. Averitt, P.G. Wannamaker, et al.
A prospective, 96-week study of the impact of Trizivir, Combivir/ nelfinavir, and lamivudine/stavudine/nelfinavir on lipids, metabolic parameters and efficacy in antiretroviral-naive patients: effect of sex and ethnicity.
HIV Med, 7 (2006), pp. 85-98
[44.]
C.A. Sabin, S.W. Worm, R. Weber, P. Reiss, W. El-Sadr, F. Dabis, et al.
Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients enrolled in the D:A:D study: a multi-cohort collaboration.
Lancet, 371 (2008), pp. 1417-1426
[45.]
Benson C, Ribaudo H, Zheng E, Koletar S, Smurzynski M, Bosch R, et al. No association of abacavir use with risk of myocardial infarction or severe cardiovascular disease events: results from ACTG A5001. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11 2009, Montreal, Canada. Abstract 721.
[46.]
Reiss P. Abacavir and Cardiovascular Risk. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11 2009, Montreal, Canada. Abstract 152.
[47.]
Cooper D, Bloch M, Humphries A, Amin J, Baker D, Emery S, for the STEAL Study Investigators. Simplification with Fixed-dose Tenofovir/Emtricitabine or Abacavir/ Lamivudine in Adults with Suppressed HIV Replication: The STEAL Study, a Randomized, Open-label, 96-Week, Non-inferiority Trial. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11 2009, Montreal, Canada. Abstract 576.
[48.]
Lang S, Mary-Krause M, Cotte L, Gilquin J, Partisani M, Simon A, et al. Impact of specific NRTI and PI exposure on the risk of myocardial infarction: a case-control study nested within FHDH ANRS CO4. 16th Conference on Retroviruses and Opportunistic Infections February 8-11 2009, Montreal, Canada. Abstract 43LB.
[49.]
Hsue P, Wu Y, Schnell A, Ganz P, Hunt P, Hatano H, et al. Association of abacavir and HIV disease factors with endothelial function in patients on long-term suppressive ART. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11 2009, Montreal, Canada. Abstract 723.
[50.]
Satchell C, O’Connor E, Peace A, Cotter A, Sheehan G, Tedesco T, et al. Platelet hyper- reactivity in HIV-1-infected patients on abacavir-containing ART. 16th Conference on Retroviruses and Opportunistic Infections, February 8-11 2009, Montreal, Canada. Abstract 151LB.
[51.]
C. Hadigan, J.B. Meigs, C. Corcoran, P. Rietschel, S. Piecuch, N. Basgoz, et al.
Metabolic abnormalities and cardiovascular disease risk factors in adults with human immunodeficiency virus infection and lipodystrophy.
Clin Infect Dis, 32 (2001), pp. 130-139
[52.]
M.P. Dubé, J.H. Stein, J.A. Aberg, C.J. Fichtenbaum, J.G. Gerber, K.T. Tashima, et al.
Guidelines for the evaluation and management of dyslipidemia in human immunodeficiency virus (HIV)-infected adults receiving antiretroviral therapy: recommendations of the HIV Medical Association of the Infectious Disease Society of America and the Adult AIDS Clinical Trials Group.
Clin Infect Dis, 37 (2003), pp. 613-627
[53.]
J.S. Liang, O. Distler, D.A. Cooper, H. Jamil, R.J. Deckelbaum, H.N. Ginsberg, et al.
HIV protease inhibitors Project apolipoprotein B from degradation by the proteasome: a potential mechanism for protease inhibitor-induced hyperlipidemia.
Nat Med, 7 (2001), pp. 1327-1331
[54.]
R.R. Sankatsing, F.W. Wit, N. Pakker, J. Vyankandondera, F. Mmiro, P. Okong, et al.
Effects of nevirapine, compared with lamivudine, on lipids and lipoproteins in HIV-1-uninfected newborns: the stopping infection from mother-to-child via breast-feeding in Africa lipid substudy.
J Infect Dis, 196 (2007), pp. 15-22
[55.]
Lazzaretti R, Pinto-Ribeiro J, Kummer R, Polanczyk C, Sprinz E. Dietary intervention when starting HAART prevents the increase in lipids independently of drug regimen: a randomized trial. Presented at: 4th International AIDS Society Conference on HIV Pathogenesis, Treatment and Prevention; July 22-25, 2007; Sydney, Australia. Abstract WEAB303.
[56.]
J.B. Meigs, M.K. Rutter, L.M. Sullivan, C.S. Fox, R.B. D’Agostino Sr, P.W. Wilson.
Impact of insulin resistance on risk of type 2 diabetes and cardiovascular disease in people with metabolic syndrome.
Diabetes Care, 30 (2007), pp. 1219-1225
[57.]
F. Wollesen, L. Berglund, C. Berne.
Insulin resistance and atherosclerosis in diabetes mellitus.
Metabolism, 51 (2002), pp. 941-948
[58.]
M.P. Dube, D. Sprecher, W.K. Henry, J.A. Aberg, F.J. Torriani, H.N. Hodis, et al.
Preliminare guidelines for the evaluation and management of dyslipemia in HIV-infected adults receiving antiretroviral therapy: recommendations of the adult ACTG Cardiovascular Disease Focus Group.
Clin Infect Dis, 31 (2000), pp. 1216-1224
[59.]
C. Hadigan, C. Corcoran, T. Stanley, S. Piecuch, A. Klibanski, S. Grinspoon.
Fasting hyperinsulinemia in human immunodeficiency virus-infected men: relationship to body composition gonadal function, and proteasa inhbitor use.
J Clin Endocrinol Metab, 85 (2000), pp. 35-41
[60.]
M. Caron, M. Auclair, C. Vigouroux, M. Glorian, C. Forest, J. Capeau.
The HIV proteasa inhibitor indinavir impairs sterol regulatory element-binding protein-1 intranuclear localization, inhibits preadipocyte differentiation, and induces insulin resistance.
Diabetes, 50 (2001), pp. 1378-1388
[61.]
L. Nolte, K.E. Yarasheski, K. Kawanaka, J. Fisher, N. Le, J.O. Holloszy.
The HIV protease inhibitor indinavir decreases insulin-and coraction-stimulated glucose transport in skeletal muscle.
Diabetes, 50 (2001), pp. 1397-1401
[62.]
H. Murata, P.W. Hruz, M. Mueckler.
The mechanism of insulin resistance caused by HIV proteasa inhibitor therapy.
J Biol Chem, 27 (2000), pp. 20251-20354
[63.]
O. Andersen, S.B. Haugaard, U.B. Andersen, N. Friis-Møller, H. Storgaard, A. Vølund, et al.
Lipodystrophy in human immunodeficiency virus patients impairs insulin action and induces defects in beta-cell function.
Metabolism, 52 (2003), pp. 1343-1353
[64.]
G.M. Behrens, A.R. Boerner, K. Weber, J. Van den Hoff, J. Ockenga, G. Brabant, et al.
Impaired glucose phosphorylation and transport in skeletal muscle cause insulin resistance in HIV-1-infected patients with lipodystrophy.
J Clin Invest, 110 (2002), pp. 1319-1327
[65.]
J.M. Lenhard, E.S. Furfine, R.J. Jain, O. Ittoop, L.A. Orband-Miller, S.G. Blanchard, et al.
HIV protease inhibitors block adipogenesis and increase lipolysis in vitro.
Antiviral Res, 47 (2000), pp. 121-129
[66.]
Z.V. Man, T. Hirashima, S. Mori, K. Kawano.
Decrease in triglyceride accumulation in tissues by restricted diet and improvement of diabetes in Otsuka Long-Evans Tokushima fatty rats, a non-insulin-dependent diabetes model.
Metabolism, 49 (2000), pp. 108-114
[67.]
E. Ledru, N. Christeff, O. Patey, P. De Truchis, J.C. Melchior, M.L. Gougeon.
Alteration of tumor necrosis factor-alpha T-cell homeostasis following potent antiretroviral therapy: contribution to the development of human immunodeficiency virus-associated lipodystrophy syndrome.
Blood, 95 (2000), pp. 3191-3198
[68.]
D.P. Kotler.
HIV and antiretroviral therapy: lipid abnormalities and associated cardiovascular risk in HIV-infected patients.
J Acquir Immune Defic Syndr, 49 (2008), pp. S79-85
[69.]
A. Carr, K. Samaras, A. Thorisdottir, G.R. Kaufmann, D.J. Chisholm, D.A. Cooper.
Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: a cohort study.
Lancet, 353 (1999), pp. 2093-2099
[70.]
D.A. Wohl, G. McComsey, P. Tebas, T.T. Brown, M.J. Glesby, D. Reeds.
Current concepts in the diagnosis and management of metabolic complications of HIV infection and its therapy.
Clin Infect Dis, 43 (2006), pp. 645-653
[71.]
K. Mulligan, V.W. Tai, H. Algren, D.I. Abrams, R.J. Leiser, J.C. Lo, et al.
Altered fat distribution in HIV-positive men on nucleoside analog reverse transcriptase inhibitor therapy.
J Acquir Immune Defic Syndr, 26 (2001), pp. 443-448
[72.]
S.A. Mallal, M. John, C.B. Moore, I.R. James, E.J. McKinnon.
Contribution of nucleoside analogue reverse transcriptase inhibitors to subcutaneous fat wasting in patients with HIV infection.
AIDS, 14 (2000), pp. 1309-1316
[73.]
J.E. Gallant, S. Staszewski, A.L. Pozniak, E. DeJesus, J.M. Suleiman, M.D. Miller, et al.
Efficacy and safety of tenofovir DF vs stavudine in combination therapy in antiretroviralnaive patients: a 3-year randomized trial.
JAMA, 292 (2004), pp. 191-201
[74.]
M. Casula, M. Van der Valk, F.W. Wit, M.A. Nievaard, P. Reiss.
Mitochondrial DNA assessment in adipocytes and peripheral blood mononuclear cells of HIV-infected patients with lipodystrophy according to a validated case definition.
HIV Med, 8 (2007), pp. 32-37
[75.]
C. Lagathu, J.P. Bastard, M. Auclair, M. Maachi, M. Kornprobst, J. Capeau, et al.
Antiretroviral drugs with adverse effects on adipocyte lipid metabolism and survival alter the expression and secretion of proinflammatory cytokines and adiponectin in vitro.
Antivir Ther, 9 (2004), pp. 911-920
[76.]
P.WG. Mallon, P. Unemori, R. Sedwell, A. Morey, M. Rafferty, K. Williams, et al.
In vivo, nucleoside reverse transcriptase inhibitors alter expression of both mitochondrial and lipid metabolism genes in the absence of mitochondrial DNA depletion.
J Infect Dis, 191 (2005), pp. 1686-1696
[77.]
S.M. Grundy, H.B. Brewer, J.I. Cleeman, S.C. Smith Jr, C Lenfant.
American Heart Association; National Heart, Lung, and Blood Institute. Definition of metabolic syndrome: Report of the National Heart, Lung, and Blood Institute/American Heart Association conference on scientific issues related to definition.
Circulation, 109 (2004), pp. 433-438
[78.]
P. Bonfanti, C. Giannattasio, E. Ricci, R. Facchetti, E. Rosella, M. Franzetti, et al.
HIV and metabolic syndrome: a comparison with the general population.
J Acquir Immune Defic Syndr, 45 (2007), pp. 426-431
[79.]
K. Samaras, H. Wand, M. Law, S. Emery, D. Cooper, A. Carr.
Prevalence of metabolic syndrome in HIV-infected patients receiving highly active antiretroviral therapy using International Diabetes Foundation and Adult Treatment Panel III criteria: associations with insulin resistance, disturbed body fat compartmentalization, elevated C-reactive protein, and [corrected] hypoadiponectinemia.
Diabetes Care, 30 (2007), pp. 113-119
[80.]
D.L. Jacobson, A.M. Tang, D. Spiegelman, A.M. Thomas, S. Skinner, S.L. Gorbach, et al.
Incidence of metabolic syndrome in a cohort of HIV-infected adults and prevalence relative to the US population (National Health and Nutrition Examination Survey).
J Acquir Immune Defic Syndr, 43 (2006), pp. 458-466
[81.]
R. Palacios, J. Santos, M. González, J. Ruiz, M. Márquez.
Incidence and prevalence of the metabolic syndrome in a cohort of naive HIV-infected patients: prospective analysis at 48 weeks of highly active antiretroviral therapy.
Int J STD AIDS, 18 (2007), pp. 184-187
[82.]
H. Wand, A. Calmy, D.L. Carey, K. Samaras, A. Carr, M.G. Law, et al.
Metabolic syndrome, cardiovascular disease and type 2 diabetes mellitus after initiation of antiretroviral therapy in HIV-infection.
AIDS, 21 (2007), pp. 2445-2453
[83.]
A. Mangili, D.L. Jacobson, J. Gerrior, J.F. Polak, S.L. Gorbach, C.A. Wanke.
Metabolic syndrome and subclinical atherosclerosis in patients infected with HIV.
Clin Infect Dis, 44 (2007), pp. 1368-1374
[84.]
P.Y. Hsue, P.W. Hunt, E. Sinclair, B. Bredt, A. Franklin, M. Killian, et al.
Increased carotid intima-media thickness in HIV patients is associated with increased cytomegalovirusspecific T-cell responses.
AIDS, 20 (2006), pp. 2275-2283
[85.]
B. Lau, A.R. Sharrett, L.A. Kingsley, W. Post, F.J. Palella, B. Visscher, et al.
C-reactive protein is a marker for human immunodeficiency virus disease progression.
Arch Intern Med, 166 (2006), pp. 64-70
[86.]
G. Sitia, A. De Bona, S. Bagaglio, L. Galli, C.T. Paties, C. Uberti-Foppa, et al.
Naive HIV/ HCV-coinfected patients have higher intrahepatic pro-inflammatory cytokines than coinfected patients treated with antiretroviral therapy.
Antivir Ther, 11 (2006), pp. 385-389
[87.]
D.C. Mynarcik, M.A. McNurlan, R.T. Steigbigel, J. Fuhrer, M.C. Gelato, et al.
Association of severe insulin resistance with both loss of limb fat and elevated serum tumor necrosis factor receptor levels in HIV lipodystrophy.
J Acquir Immune Defic Syndr, 25 (2000), pp. 312-321
[88.]
Kuller L and the SMART Study Group. Elevated levels of interleukin-6 and D-dimer are associated with an increased risk of death in patients with HIV. Presented at: 15th Conference on Retroviruses and Opportunistic Infections; 2008; Boston, M.A.
[89.]
Strategies for Management of Anti-Retroviral Therapy/INSIGHT and DAD Study Groups.
Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients.
AIDS, 22 (2008), pp. F17-24
[90.]
J.H. Stein, M.A. Klein, J.L. Bellehumeur, P.E. McBride, D.A. Wiebe, J.D. Otvos, et al.
Use of human immunodeficiency virus-1 protease inhibitors is associated with atherogenic lipoprotein changes and endothelial dysfunction.
Circulation, 104 (2001), pp. 257-262
[91.]
D. Nolan, G.F. Watts, S.E. Herrmann, M.A. French, M. John, S. Mallal.
Endothelial function in HIV-infected patients receiving protease inhibitor therapy: does immune competence affect CV risk?.
QJM, 96 (2003), pp. 825-832
[92.]
Murphy L, Zala C, Berzins B, Fichtenbaum C, Dube M, Guaraldi G, et al. Endothelial function, lipoproteins, and cardiovascular inflammatory markers in treated HIV-infected patients with hyperlipidemia who were switched to an atazanavirwith atazanavir-containing regimen or continued on other protease inhibitor inhibitor-based therapy: switch to atazanavir brachial artery reactivity study. 16th Conference on Retroviruses and Opportunistic Infections February 8-11 2009, Montreal, Canada. Abstract 722LB.
[93.]
B. Conklin, W. Fu, P. Lin, A. Lundsen, Q. Yao, C. Chen.
HIV protease inhibitor ritonavir induces endothelial dysfunction in porcine arteries.
J Surg Res, 114 (2003), pp. 249
[94.]
S.S. Shankar, M.P. Dubé, J.C. Gorski, J.E. Klaunig, H.O. Steinberg.
Indinavir impairs endothelial function in healthy HIV-negative men.
Am Heart J, 150 (2005), pp. 933
[95.]
E. Seminari, A. Pan, G. Voltini, G. Carnevale, R. Maserati, L. Minoli, et al.
Assessment of atherosclerosis using carotid ultrasonography in a cohort of HIV-positive patients treated with protease inhibitors.
Atherosclerosis, 162 (2002), pp. 433-438
[96.]
P.Y. Hsue, J.C. Lo, A. Franklin, A.F. Bolger, J.N. Martin, S.G. Deeks, et al.
Progression of atherosclerosis as assessed by carotid intima-media thickness in patients with HIV infection.
Circulation, 109 (2004), pp. 1603-1608
[97.]
M. Duong, Y. Cottin, L. Piroth, A. Fargeot, I. Lhuiller, M. Bobillier, et al.
Exercise stress testing for detection of silent myocardial ischemia in human immunodeficiency virus-infected patients receiving antiretroviral therapy.
Clin Infect Dis, 34 (2002), pp. 523-528
[98.]
L.J. Shaw, P. Raggi, D.S. Berman, T.Q. Callister.
Cost effectiveness of screening for CV disease with measures of coronary calcium.
Prog Cardiovasc Dis, 46 (2003), pp. 171-184
[99.]
L.A. Kingsley, J. Cuervo-Rojas, A. Muñoz, F.J. Palella, W. Post, M.D. Witt, et al.
Subclinical coronary atherosclerosis, HIV infection and antiretroviral therapy: Multicenter AIDS Cohort Study.
AIDS, 22 (2008), pp. 1589-1599
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