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Resumen
Las enfermedades cardiovasculares son un problema creciente en pacientes infectados por el virus de inmunodeficiencia humana (VIH). El aumento del riesgo cardiovascular en población infectada tiene un ori gen multifactorial. En el momento actual, no se puede concluir qué elemento tiene más peso en esta ecuación, si los factores de riesgo clásicos, el propio virus o el tratamiento antirretroviral. El riesgo absoluto de enfermedad cardiovascular de cada paciente dependerá de su perfil de riesgo global. En la actualidad no hay datos que obliguen a evaluar de forma diferente al paciente con VIH a la hora de manejar los factores de riesgo cardiovascular. Se debería incorporar a la rutina clínica diaria la evaluación cuidadosa de los factores de riesgo y el cálculo del riesgo cardiovascular mediante la aplicación de ecuaciones de riesgo.
Palabras clave:
Infección VIH
TARGA
Factores de riesgo
Enfermedad cardiovascular
Abstract
Cardiovascular diseases are an increasing problem in patients with HIV infection. The causes of the increased cardiovascular risk in HIV-infected patients are multifactorial. Currently, the question of which factor has the most weight in this equation - whether traditional risk factors, the virus per se or antiretroviral therapy - remains to be determined. The absolute risk of cardiovascular disease in a particular patient depends on the composite risk profile. At present, there are no data to support a distinct approach to cardiovascular risk evaluation in HIV-infected patients. Cardiovascular risk equations should be incorporated into routine daily clinical assessment in order to identify patients in need of specific interventions.
Key words:
HIV infection
HAART
Risk factors
Cardiovascular disease
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Bibliografía
[1]
S.A. Bozzette, C.F. Ake, H.K. 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
[2]
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
[3]
W.M. El-Sadr, J.D. Lundgren, J.D. Neaton, F. Gordin, D. Abrams, R.C. Arduino, et al.
CD4+ count-guided interruption of antiretroviral treatment.
N Engl J Med, 355 (2006), pp. 2283-2296
[4]
N. Friis-Moller, P. Reiss, C.A. Sabin, R. Weber, A. Monforte, W. El-Sadr, et al.
Class of antiretroviral drugs and the risk of myocardial infarction.
N Engl J Med, 356 (2007), pp. 1723-1735
[5]
V.A. Triant, H. Lee, C. Hadigan, S.K. Grinspoon.
Increased acute myocardial infarction rates and cardiovascular risk factors among patients with human immunodeficiency virus disease.
J Clin Endocrinol Metab, 92 (2007), pp. 2506-2512
[6]
M. Saves, G. Chene, P. Ducimetiere, C. Leport, G. Le Moal, P. Amouyel, et al.
Risk factors for coronary heart disease in patients treated for human immunodeficiency virus infection compared with the general population.
Clin Infect Dis, 37 (2003), pp. 292-298
[7]
M.J. Silverberg, W. Leyden, L. Hurley, A.S. Go, C.P. Quesenberry Jr., D. Klein, et al.
Response to newly prescribed lipid-lowering therapy in patients with and without HIV infection.
Ann Intern Med, 150 (2009), pp. 301-313
[8]
S. Yusuf, S. Hawken, S. Ounpuu, T. Dans, A. Avezum, F. Lanas, et al.
Effect of potentially modifiable risk factors associated with myocardial infarction in 52 countries (the INTERHEART study): case-control study.
Lancet, 364 (2004), pp. 937-952
[9]
S.W. Worm, S. De Wit, R. Weber, C.A. Sabin, P. Reiss, W. El-Sadr, et al.
Diabetes mellitus, preexisting coronary heart disease, and the risk of subsequent coronary heart disease events in patients infected with human immunodeficiency virus: the Data Collection on Adverse Events of Anti-HIV Drugs (D:A:D Study).
Circulation, 119 (2009), pp. 805-811
[10]
D.S. Celermajer.
Endothelial dysfunction: does it matter? Is it reversible?.
J Am Coll Cardiol, 30 (1997), pp. 325-333
[11]
F.J. Torriani, L. Komarow, R.A. Parker, B.R. Cotter, J.S. Currier, M.P. Dube, et al.
Endothelial function in human immunodeficiency virus-infected antiretroviral-naive subjects before and after starting potent antiretroviral therapy: The ACTG (AIDS Clinical Trials Group) Study 5152s.
J Am Coll Cardiol, 52 (2008), pp. 569-576
[12]
L.H. Kuller, R. Tracy, W. Belloso, S. De Wit, F. Drummond, H.C. Lane, et al.
Inflammatory and coagulation biomarkers and mortality in patients with HIV infection.
PLoS Med, 5 (2008), pp. e203
[13]
P. Tebas, W.K. Henry, R. Matining, D. Weng-Cherng, J. Schmitz, H. Valdez, et al.
Metabolic and immune activation effects of treatment interruption in chronic HIV-1 infection: implications for cardiovascular risk.
PLoS ONE, 3 (2008), pp. e2021
[14]
Grunfeld C, Delaney JAC, Wanke C, Currier J, Scherzer R, Biggs ML, et al. HIV infection is an independent risk factor for atherosclerosis similar in magnitude to tradicional cardiovascular disease risk factors. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Oral presentation 146.
[15]
Hsue P, Deeks S, Schnell A, Krone M, Xie Y, Lee T, et al. HIV infection is independently associated with detectable coronary artery calcium. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 724.
[16]
Baker J, Duprez D, Rapkin J, Grima R, Neaton JKH. Untreated HIV infection is associated with impaired arterial elasticity. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 725.
[17]
Mestek M, Stauffer B, Westby C, Weil B, Van Guilder G, Greiner J, et al. Endotelial fibrinolytic capacity is impaired in HIV infected men. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 728.
[18]
M.W. Smith, M. Dean, M. Carrington, C. Winkler, G.A. Huttley, D.A. Lomb, et al.
Contrasting genetic influence of CCR2 and CCR5 variants on HIV-1 infection and disease progression. Hemophilia Growth and Development Study (HGDS), Multicenter AIDS Cohort Study (MACS), Multicenter Hemophilia Cohort Study (MHCS), San Francisco City Cohort (SFCC), ALIVE Study.
Science, 277 (1997), pp. 959-965
[19]
Z. Mujawar, H. Rose, M.P. Morrow, T. Pushkarsky, L. Dubrovsky, N. Mukhamedova, et al.
Human immunodeficiency virus impairs reverse cholesterol transport from macrophages.
PLoS Biol, 4 (2006), pp. e365
[20]
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
[21]
Lundgren J, Reiss P, Worm SW, El-Sadr W, De Wit S, Weber R, et al. Risk of myocardial infarction and exposure to specific antiretrovirals from the PI, NNRTI and NRTI drug classes: The D:A:D. study. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 44LB.
[22]
Use of nucleoside reverse transcriptase inhibitors and risk of myocardial infarction in HIV-infected patients. Aids. 2008;22:F17-24.
[23]
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 the French Hospital Database on HIV ANRS CO4. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 43LB.
[24]
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 Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 721.
[25]
C.H. Brothers, J.E. Hernández, A.G. Cutrell, L. Curtis, M. Ait-Khaled, S.J. Bowlin, et al.
Risk of myocardial infarction and abacavir therapy: no increased risk across 52 GlaxoSmithKline- Sponsored Clinical Trials in Adult Subjects.
J Acquir Immune Defic Syndr, 51 (2009), pp. 20-28
[26]
P.M. Coplan, A. Nikas, A. Japour, K. Cormier, H. Maradit-Kremers, R. Lewis, et al.
Incidence of myocardial infarction in randomized clinical trials of protease inhibitorbased antiretroviral therapy: an analysis of four different protease inhibitors.
AIDS Res Hum Retroviruses, 19 (2003), pp. 449-455
[27]
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
[28]
A. Solages, J.A. Vita, D.J. Thornton, J. Murray, T. Heeren, D.E. Craven, et al.
Endothelial function in HIV-infected persons.
Clin Infect Dis, 42 (2006), pp. 1325-1332
[29]
M.P. Dube, C. Shen, M. Greenwald, K.J. Mather.
No impairment of endothelial function or insulin sensitivity with 4 weeks of the HIV protease inhibitors atazanavir or lopinavir-ritonavir in healthy subjects without HIV infection: a placebo-controlled trial.
Clin Infect Dis, 47 (2008), pp. 567-574
[30]
P. Mercie, R. Thiebaut, V. Aurillac-Lavignolle, J.L. Pellegrin, M.C. Yvorra-Vives, C. Cipriano, et al.
Carotid intima-media thickness is slightly increased over time in HIV-1- infected patients.
HIV Med, 6 (2005), pp. 380-387
[31]
J.S. Currier, M.A. Kendall, W.K. Henry, B. Alston-Smith, F.J. Torriani, P. Tebas, et al.
Progression of carotid artery intima-media thickening in HIV-infected and uninfected adults.
Aids, 21 (2007), pp. 1137-1145
[32]
C.A. Sabin, A. D’Arminio Monforte, N. Friis-Moller, R. Weber, W.M. El-Sadr, P. Reiss, et al.
Changes over time in risk factors for cardiovascular disease and use of lipidlowering drugs in HIV-infected individuals and impact on myocardial infarction.
Clin Infect Dis, 46 (2008), pp. 1101-1110
[33]
P.W. Wilson, R.B. D’Agostino, D. Levy, A.M. Belanger, H. Silbershatz, W.B. Kannel.
Prediction of coronary heart disease using risk factor categories.
Circulation, 97 (1998), pp. 1837-1847
[34]
J. Marrugat, P. Solanas, R. D’Agostino, L. Sullivan, J. Ordovás, F. Cordón, et al.
Estimación del riesgo coronario en España mediante la ecuación de Framingham calibrada.
Rev Esp Cardiol, 56 (2003), pp. 253-261
[35]
R.M. Conroy, K. Pyorala, A.P. Fitzgerald, S. Sans, A. Menotti, G. De Backer, et al.
Estimation of ten-year risk of fatal cardiovascular disease in Europe: the SCORE project.
Eur Heart J, 24 (2003), pp. 987-1003
[36]
G. Mancia, G. De Backer, A. Dominiczak, R. Cifkova, R. Fagard, G. Germano, et al.
2007 Guidelines for the management of arterial hypertension: The Task Force for the Management of Arterial Hypertension of the European Society of Hypertension (ESH) and of the European Society of Cardiology (ESC).
Eur Heart J, 28 (2007), pp. 1462-1536
[37]
G. Assmann, P. Cullen, H. Schulte.
Simple scoring scheme for calculating the risk of acute coronary events based on the 10-year follow-up of the prospective cardiovascular Munster (PROCAM) study.
Circulation, 105 (2002), pp. 310-315
[38]
M.G. Law, N. Friis-Moller, W.M. El-Sadr, R. Weber, P. Reiss, A. D’Arminio Monforte, et al.
The use of the Framingham equation to predict myocardial infarctions in HIVinfected patients: comparison with observed events in the D:A:D Study.
HIV Med, 7 (2006), pp. 218-230
[39]
H. Knobel, C. Jerico, M. Montero, M.L. Sorli, M. Velat, A. Guelar, et al.
Global cardiovascular risk in patients with HIV infection: concordance and differences in estimates according to three risk equations (Framingham, SCORE, and PROCAM).
AIDS Patient Care STDS, 21 (2007), pp. 452-457
[40]
M. May, J.A. Sterne, M. Shipley, E. Brunner, R. D’Agostino, P. Whincup, et al.
A coronary heart disease risk model for predicting the effect of potent antiretroviral therapy in HIV-1 infected men.
Int J Epidemiol, 36 (2007), pp. 1309-1318
[41]
C. Jericó, H. Knobel, N. Calvo, M.L. Sorli, A. Guelar, J.L. Gimeno-Bayón, et al.
Subclinical carotid atherosclerosis in HIV-infected patients: role of combination antiretroviral therapy.
Stroke, 37 (2006), pp. 812-817
[42]
Falcone L, Mangili A, Skinner S, Polak JCW. Framingham risk scores and markers of early atherosclerosis in a cohort of HIV-infected subjects. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 726.
[43]
Lichtenstein K, Armon C, Buchacz K, Moorman AC, Wood KC, Brooks J. Analysis of cardiovascular risk factors in the HIV Outpatient Study Cohort. 13th Conference on Retrovirus and Oportunistic Infections. Denver; 5-8 February 2006. Abstract 735.
[44]
Hurley L, Leyden W, Xu L, Silverberg M, Chao C, Tang B, et al. Updated surveillance of cardiovascular event rates among HIV infected and HIV uninfected Californians, 1996-2008. 16th Conference on Retrovirus and Oportunistic Infections. Montreal; February 2009. Abstract 710.
[45]
L. Calza, R. Manfredi, V. Colangeli, L. Tampellini, T. Sebastiani, D. Pocaterra, et al.
Substitution of nevirapine or efavirenz for protease inhibitor versus lipid-lowering therapy for the management of dyslipidaemia.
Aids, 19 (2005), pp. 1051-1058
[46]
B. Zethelius, L. Berglund, J. Sundstrom, E. Ingelsson, S. Basu, A. Larsson, et al.
Use of multiple biomarkers to improve the prediction of death from cardiovascular causes.
N Engl J Med, 358 (2008), pp. 2107-2116
[47]
Triant VA, Meigs JB, Grinspoon S. Association of C-reactive protein and HIV infection with acute myocardial infarction. 10th International Workshop on Adverse Drug Reactions and Lipodystrophy in HIV. London; November 2008.
[48]
S.K. Gupta, R.M. Johnson, C. Saha, K.J. Mather, M.L. Greenwald, J.S. Waltz, et al.
Improvement in HIV-related endothelial dysfunction using the anti-inflammatory agent salsalate: a pilot study.
Aids, 22 (2008), pp. 653-655
[49]
E.R. Kline, D.J. Kleinhenz, B. Liang, S. Dikalov, D.M. Guidot, C.M. Hart, et al.
Vascular oxidative stress and nitric oxide depletion in HIV-1 transgenic rats are reversed by glutathione restoration.
Am J Physiol Heart Circ Physiol, 294 (2008), pp. H2792-H2804
[50]
O. López, D. Bonnefont-Rousselot, M. Edeas, J. Emerit, F. Bricaire.
Could antioxidant supplementation reduce antiretroviral therapy-induced chronic stable hyperlactatemia?.
Biomed Pharmacother, 57 (2003), pp. 113-116
[51]
J.S. 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
[52]
M. Mary-Krause, L. Cotte, A. Simon, M. Partisani, D. Costagliola.
Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men.
Aids, 17 (2003), pp. 2479-2486
[53]
V. Rickerts, H. Brodt, S. Staszewski, W. Stille.
Incidence of myocardial infarctions in HIV-infected patients between 1983 and 1998: the Frankfurt HIV-cohort study.
Eur J Med Res, 5 (2000), pp. 329-333
[54]
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
[55]
Martínez E, Arribas JR, López-Aldeguer J, Gutiérrez F, Miralles C, Lozano F, et al. Factors associated with a high cardiovascular risk in HIV-infected patients in Spain: a multicenter, nationwide cross-sectional study. 12th Conference on Retrovirus and Oportunistic Infections. Boston; 22-25 February. 2005. Abstract 870.
[56]
C. Jericó, H. Knobel, M.L. Sorli, M. Montero, A. Guelar, J. Pedro-Botet.
Prevalencia de factores de riesgo cardiovascular en pacientes con infección por el VIH.
Rev Clin Esp, 206 (2006), pp. 556-559
[57]
D. Pere, S.L. Ignacio, T. Ramón, L. Fernando, T. Alberto, V. Pompeyo, et al.
Dyslipidemia and cardiovascular disease risk factor management in HIV-1-infected subjects treated with HAART in the Spanish VACH cohort.
Open AIDS J, 2 (2008), pp. 26-38
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