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Riesgo Cardiovascular en el paciente VIH

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X Congreso de la Sociedad de Medicina Interna de Aragón, Navarra, La Rioja y País Vasco.

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Riesgo Cardiovascular en el paciente VIH

  1. 1. Riesgo Cardiovascular en el paciente VIH DR. JAVIER PINILLA MORAZA MEDICINA INTERNA HOSPITAL SAN PEDRO
  2. 2. <ul><li>Epidemiología </li></ul>
  3. 3. Copyright ©2008 American Heart Association Rosamond, W. et al. Circulation 2008;117:e25-e146 CVD and other major causes of death: total, <85 years of age, and 85 years of age. Deaths among both sexes, United States, 2004. Source: NCHS and NHLBI.
  4. 4. 2. Triant VA, et al. J Clin Endocrin Metab. 2007;92(7):2506-2512 (*) Ajustado por edad, género, raza, HTA, Diabetes e HTA…pero NO POR TABAQUISMO!! <ul><li>Tasas de IAM (x 1000 pers-año) en 3.851 VIH+ y en 1.044.589 VIH-(1996-2004): </li></ul><ul><li>VIH+: 11,13 episodios por 1.000 pers-año. VIH- : 6,98 episodios por 1.000 pers-año. </li></ul><ul><li>Riesgo Relativo* : 1,75 (IC 95% entre 1,51-2,02). </li></ul><ul><ul><li>Mujeres: 2,98 (IC 95% entre 2,33 y 3,75). </li></ul></ul><ul><ul><li>Hombres: 1,40 (IC 95% entre 1,16 y 1,67). </li></ul></ul>¿ES MÁS FRECUENTE?
  5. 5. Higher Incidence of CHD in HIV- Infected vs HIV-Uninfected Patients Klein D, et al. CROI 2007. Abstract 807 . <ul><li>5000 HIV-infected men followed for 10.5 years compared with 43,000 age-matched HIV-uninfected men </li></ul><ul><li>HIV-infected men had significantly higher rates of CHD ( P < .0001) and MI ( P < .002) vs HIV-uninfected men </li></ul><ul><ul><li>Trend for HIV-infected men on PI-based regimens to be at higher risk of CHD ( P = .11) and MI ( P = .14) vs those not taking PIs </li></ul></ul>Age-Adjusted Rates* From 1996-2004, Events per 1000 Person-Yrs (95% CI) All HIV- Infected Patients HIV-Infected Patients on Any PI HIV-Infected Patients Not on PI HIV-Uninfected Comparator Group CHD 6.1 (4.9-7.3) 6.9 (5.3-8.6) 4.9 (3.1-6.8) 2.9 (2.7-3.1) MI 3.8 (2.8-4.7) 4.4 (3.1-5.8) 2.9 (1.5-4.4) 2.2 (2.0-2.4)
  6. 6. ¿QUE TENDENCIA MUESTRA EN EL TIEMPO? <ul><li>Datos de 68.669 muertes de VIH+ en New York. </li></ul><ul><li>Incremento de causas No VIH (ECV, Cáncer y Uso de Drogas) : </li></ul><ul><ul><li>1999: 19,8% </li></ul></ul><ul><ul><li>2006: 23,2% </li></ul></ul><ul><li>ECV: Principal causa de muerte en pacientes > 55 años. </li></ul>4. Sackoff JE, et al. Ann Intern Med. 2006;145(6):397-406
  7. 7. CV disease Patient Antiretroviral drugs HIV (and other infections) Drug consumption Tobacco Alcohol Cocaine Other? There are reasons to consider that the risk of CV disease may be increased in HIV-infected patients Metabolic abnormalities Dyslipidemia Insulin resistance / DM Body fat changes Lipoatrophy Lipoaccumulation Degree of immunedeficiency PIs Dyslipidemia Insulin resistance ? Body fat changes? Other? NRTIs Dyslipidemia? Insulin resistance? Body fat changes? Other? HIV, HCV, HBV?, other? Dyslipidemia Systemic inflammation Inmune activation Vascular infection
  8. 8. Increased risk of CV disease in HIV+ persons relative to HIV- ones: impact of traditional factors <ul><li>Approximately 2-fold higher incidence of CAD / MI </li></ul><ul><li>Higher prevalence of other types of CV disease in HIV+ vs HIV-: </li></ul><ul><ul><li>Peripheral arterial disease 1, 2 </li></ul></ul><ul><ul><li>Increased cIMT 3-5 </li></ul></ul>1. Palacios R et al. AIDS Res Human Retrovir 2008; 2. Periard D et al. Clin Infect Dis 2008; 3. Hsue PY et al. Circulation 2004; 4. Mercie P et al. HIV Medicine 2005; 5. Lekakis J et al. Clin Sci 2008; 6. Lorenz MW et al. Atherosclerosis 2008 In these studies, higher prevalence of traditional CV risk factors (smoking, HT, DM, and dyslipidemia) in HIV+ relative to HIV- References Size Outcome HIV+ vs HIV- Klein, JAIDS, ’02 4,159 / 39,877 CAD  (6.5 vs 3.8/1000 PYFU) Klein, CROI, ’07 5,000 / 43000 CAD  (4.5 vs 2.9/1000 PYFU) Currier, JAIDS, ’03 28,513 / 3 mill CAD  (only in young) Triant, JCEM, ’07 3,851 / 1 mill MI  (75%) Obel, CID, ’07 3,953 / 0.4mill CAD  (39-112%)
  9. 9. Risk factors for CHDin patients treated for HIVcompared with the general population. Clin Infect Dis. 2003 Jul 15;37(2):292-8.
  10. 10. <ul><li>Influencia del propio VIH </li></ul>
  11. 11. SMART: Study Design <ul><li>Independent data and safety monitoring board reviewed interim study data annually </li></ul><ul><ul><li>Board recommended that study enrollment halted on January 11, 2006 </li></ul></ul><ul><ul><li>Significant safety risk in treatment interruption group </li></ul></ul>El-Sadr WM, et al. N Engl J Med. 2006; 355:2283-2296 HIV-infected patients with CD4+ cell count > 350 cells/mm 3 (N = 5472) Treatment Interruption Arm Treatment stopped when CD4+ cell count > 350 cells/mm 3 ; restarted when CD4+ cell count < 250 cells/mm 3 (n = 2720) Continuous Treatment Arm HAART continuously administered (n = 2752) 16 months mean follow-up
  12. 12. SMART: Higher Risk of Opportunistic Disease or Death With Tx Interruption Favors CT ► ► Favors TI Hazard Ratio (TI/CT) (95% CI) 2.6 1.8 3.6 0.1 1 10 4.0 1.2 P < .001 *Among those on ART at BL El-Sadr WM, et al. N Engl J Med 2006; 355:2283-2296 6.6 Endpoint Opportunistic infection or death (OI/death) OI (nonserious) OI (serious) Death from any cause OI/death by BL VL * ≤ 400 copies/mL > 400 copies/mL
  13. 13. SMART: Non-AIDS Event Rates With Continuous vs Intermittent Therapy <ul><li>Significantly more individuals in treatment interruption arm developed major CV, renal, or hepatic disease than individuals in viral suppression arm </li></ul><ul><li>Significantly more individuals in treatment interruption arm experienced grade 4 event or death from any cause than individuals in viral suppression arm </li></ul>*Treatment interruption group vs viral suppression group El-Sadr WM, et al. N Engl J Med 2006; 355:2283-2296 Endpoint, n Viral Suppression Arm (n = 2752) Treatment Interruption Arm (n = 2720) HR (95% CI)* P Value Major cardiovascular, renal, or hepatic disease 39 65 1.7 (1.1-2.5) .009 <ul><li>Fatal/nonfatal cardiovascular disease </li></ul>31 48 1.6 (1.0-2.5) .05 <ul><li>Fatal/nonfatal renal disease </li></ul>2 9 4.5 (1.0-20.9) .05 <ul><li>Fatal/nonfatal liver disease </li></ul>7 10 1.4 (0.6-3.8) .46 Grade 4 event or death from any cause 164 205 1.3 (1.0-1.6) .03
  14. 14. 0 % with a Major CVD Event Years from Randomization 2752 0.5 1306 1.5 713 2.5 379 3.5 10 5 10 15 20 DC VS 2720 1292 696 377 10 DC VS No. at Risk 31 48 All major CVD events 14 22 Coronary artery disease requiring surgery for invasive procedure 3 8 Non-fatal stroke 5 11 Non-fatal silent MI 12 12 Non-fatal clinical MI 4 7 Death from CVD VS DC 0 1 2 3 4 SMART Study Phillips A, et al. 14th CROI, Los Angeles, CA, February 25-28, 2007 ART discontinuation increases the risk of CV disease relative to standard, continuous ART SMART Study
  15. 15. Grunfeld C, et al. CROI 2009. Oral presentation 114
  16. 16. The FRAM Study Grunfeld C, et al. CROI 2009. Oral presentation 114
  17. 17. The FRAM Study Grunfeld C, et al. CROI 2009. Oral presentation 114
  18. 18. The FRAM Study Grunfeld C, et al. CROI 2009. Oral presentation 114
  19. 19. <ul><li>Marcadores evaluados: </li></ul><ul><ul><li>Inflamatorios: TNF, IL-6, PCR ultrasensible (us), IL-10, amiloide A y P, MCP-1. </li></ul></ul><ul><ul><li>De Trombosis: PAI, Dímero D. </li></ul></ul><ul><ul><li>De activación endotelial: sICAM-1, sVCAM-1, FvW. </li></ul></ul>43. Masiá et al. Artheriosclerosis 2007; 195(1):167-71; 44. Kuller L, et al. CROI 2008. Abstract 139; 45. Ross A, et al. CROI 2008. Abstract 949; 46. Gupta S, et al. CROI 2008. Abstract 955 BIOMARCADORES CARDIOVASCULARES EN PACIENTES CON INFECCIÓN POR EL VIH
  20. 20. <ul><li>Estudio transversal en 62 pacientes con infección VIH y en 32 controles seronegativos. </li></ul><ul><li>Mediciones de GMI y de marcadores inflamatorios (PCRus, IL-6, TNF, mieloperoxidasa) y endoteliales (sICAM, sVCAM, factor von Willebrand). </li></ul><ul><ul><li>GMI mayor en VIH+. </li></ul></ul><ul><ul><li>PCRus, IL-6, TNF-alfa y sICAM más elevadas en VIH+. </li></ul></ul><ul><ul><li>Correlación entre las concentraciones de IL-6 y TNF alfa, y el GMI en VIH+. </li></ul></ul><ul><ul><li>Marcadores inflamatorios correlacionados con marcadores endoteliales . </li></ul></ul><ul><li>Activación endotelial, aumento de citoquinas inflamatorias y GMI más altos en VIH. </li></ul><ul><li>Papel de la inflamación en la activación endotelial y en la arteriosclerosis asociada a la infección VIH. </li></ul>45. Ross A, et al. CROI 2008. Abstract 949 BIOMARCADORES CARDIOVASCULARES EN PACIENTES CON INFECCIÓN POR EL VIH: ESTUDIOS TRANSVERSALES OTROS MARCADORES INFLAMATORIOS Y ENDOTELIALES
  21. 21. BIOMARCADORES CARDIOVASCULARES EN PACIENTES CON INFECCIÓN POR EL VIH: ESTUDIOS LONGITUDINALES: SMART <ul><li>Subestudio de biomarcadores: </li></ul><ul><ul><li>Aumentos en las concentraciones de IL-6 (TAR intermitente: +60%; TAR contínuo: +12%) y dímero D (TAR intermitente: +5%; TAR contínuo: 0%) en el primer mes del ensayo. </li></ul></ul><ul><ul><li>En el grupo de TAR intermitente los aumentos de IL-6 y dímero D se correlacionaron con incrementos en la carga viral del VIH. </li></ul></ul>44. Kuller L, et al. CROI 2008. Abstract 139 <ul><li>Con la interrupción del TAR se produce un aumento de IL-6 y DD que podría explicar la mayor mortalidad y la mayor incidencia de enfermedad cardiovascular. </li></ul>
  22. 23. <ul><li>Influencia del tratamiento AR </li></ul>
  23. 24. Tasa relativa ajustada/año de IP : 1.15 (1.06, 1.25) Tasa relativa ajustada/año de NNRTI : 0.94 (0.74, 1.19) Número de IAMs por 1.000 pacientes por año (IC 95%) Años de exposición a IP o NNRTI 0 2 4 6 8 10 >6 5–6 2–3 3–4 4–5 0 1–2 <1 La exposición a IP se ha asociado con un riesgo aumentado de infarto de miocardio Friis-Møller N et al, N Engl J Med 2007. Estudio D:A:D
  24. 25. *Adjusted for conventional risk factors (sex, cohort, HIV transmission group, ethnicity, age, BMI, family history of CVD, smoking, previous CVD events, lipids, diabetes, and hypertension). † Unadjusted model. Relative Rate of MI* (95% CI) 0.72 (0.52–0.99); P =0.05* 1.58 (1.43–1.75); P <0.001 † 1.26 (1.19–1.35); P <0.001* 1.10 (1.01–1.18); P =0.002 * 1.00 (0.93–1.09); P =0.92* Total cholesterol (per mmol/L) Triglycerides (per log 2 mmol/L higher) HDL cholesterol (per mmol/L) PI exposure (per additional year) NNRTI exposure (per additional year) 1 10 0.1 Friis-Moller N et al. N Engl J Med. 2007 Contribution of dyslipidemia to MI risk
  25. 26. Ajustado para sexo, edad, cohorte, año, ECV previa, H a familiar de ECV, tabaco, índice de masa corporal, y la otra clase de 3 er fármaco Exposición a NNRTI (por cada año) 0.9 1.0 1.1 1.2 1.3 0.9 1.0 1.1 1.2 1.3 Tasa relativa de IAM (IC 95%) TR 1,00 TR 1,10 TR 1,05 TR 1,16 Exposición a IP (por cada año) Parte (pero no todo) del RCV atribuido a IP puede explicarse por los lípidos Friis-Møller N et al, N Engl J Med 2007. Sin embargo, no se ajustó para exposición a NRTI. NRTI’s timidínicos tienen un impacto en sensibilidad a insulina y en lípidos. Uso de NRTI’s timidínicos pudo ser diferente en pacientes expuestos a IP vs NNRTI.
  26. 27. IDV NFV LPV/r SAQ NVP EFV #PYFU: 68,469 56,529 37,136 44,657 61,855 58,946 #MI: 298 197 150 221 228 221 LPV/r e IDV fueron los IPs asociados con mayor riesgo de IAM en el análisis del D:A:D J Lundgren & D:A:D Study Group et al CROI 2009 LB abstr 44. Pis/NNRTIs y riesgo de IAM: exposición acumulada a cada fámaco RR por año IC95% *Prueba aproximada de heterogeneidad: P=0,02 PI* NNRTI 1,2 1,13 1,1 1 0,9
  27. 28. <ul><li>reciente= usado en la actualidad o al menos últimos 6 meses </li></ul><ul><li>**: not shown (low number of patient currently on ddC) </li></ul>RR sí/no IC95% 1 1.9 1.5 1.2 0.8 0.6 1 1.9 1.5 1.2 0.8 0.6 RR por año 95%CI * NRTIs y riesgo de IAM : reciente * y acumulada exposici ón J Lundgren & D:A:D Study Group et al CROI 2009 LB abstr 44. El análisis actual del D:A:D confirma  riesgo de IAM con uso reciente de ABC o ddI ZDV ddI ddC d4T 3TC ABC TDF #PYFU: 138,109 74,407 29,676 95,320 152,009 53,300 39,157 #MI: 523 331 148 405 554 221 139
  28. 29. 0 2 4 6 8 1 0 A b a c a v i r S p a r i n g R e g i m e n A b a c a v i r C o n t a i n i n g R e g i m e n P = 0 . 0 1 Endothelium- dependent FMD (%) After adjustment for age, gender, traditional risk factors, HIV-specific factors, and baseline brachial artery diameter, current abacavir use was independently associated with lower FMD (p=0.02) Cross-sectional study No data on antiretrovirals other than ABC and other epidemiological characteristics Hsue P et al, CROI 2009 abstract 723 ABC use associated with  endothelial function among patients on ART with HIV suppression
  29. 30. 13 [23]% .v. 1 [4]% P = 0.009 30 [25]% .v. 18 [18]% P = 0.032 12 [19]% .v. 5 [2]% P = 0.06 31 [20]% .v. 21 [17]% P = 0.043 Satchell C et al, CROI 2009 abstract 151LB Cross-sectional study No data on antiretrovirals other than ABC and other epidemiological characteristics 25% patients had detectable viral load Significance lost when adjusted for HIV RNA for ADP and epinephrine ABC use associated with  platelet reactivity
  30. 31. No Association of Myocardial Infarction with ABC Use: An FDA Meta-analysis. 18th CROI2011; Abstrac 808
  31. 32. <ul><li>Patients switching to ABC/3TC (n = 46) or TDF/FTC (n = 34) </li></ul><ul><li>Markers of inflammation, endothelial dysfunction, insulin resistance, and hypercoagulability compared at BL and Wk 48 </li></ul><ul><li>None of these markers were significantly different between arms at Wk 48 </li></ul>15 0.1 Median Change From BL at Wk 48 (%) -5 0 5 10 20 ABC/3TC TDF/FTC -3.9 hsCRP 5.9 4.0 MCP-1 5.1 -2.8 OPG 6.6 5.2 ICAM-1 8.4 -2.0 VCAM-1 7.8 -0.4 Selectin-E -2.5 8.8 Insulin 0.05 0.1 D-dimer 12.6 Selectin-P 4.6 15.4 Adiponectin -2.2 P = .26 P = .52 P = .59 P = .12 P = .84 P = .96 P = .13 P = .33 P = .69 P = .73 Martinez et al. IAS 2009. MOAB203 Relative to TDF/FTC, ABC/3TC does not promote mechanisms known to be involved in MI BICOMBO Sub-study: patients with sustained viral suppression, clinical stability, and no prior CVD
  32. 33. <ul><li>HR: Unadjusted HR of AMI for each PY of exposure to each one of the categories </li></ul><ul><li>Most recent estimated GFR (by MDRD method; carried forward) . </li></ul><ul><li>Age, hypercholesterolemia, HTN, type 2 DM, and tobacco use. </li></ul>Bedimo R et al. IAS 2009. MOAB202 The association between ABC and MI may be biased by chronic kidney disease Veterans Cohort Study
  33. 34. Cardiovascular Disease and HIV infection: Pathogenesis
  34. 35. Conclusiones <ul><li>El propio VIH y los factores de riesgo tradicionales son los responsables en gran medida del incremento del riesgo CV </li></ul><ul><li>Algunos fármacos (ABC, LPV/r), podrían ejercer una influencia significativa en este incremento del riesgo en determinadas circunstancias. </li></ul>
  35. 36. <ul><li>Manejo </li></ul>
  36. 37. Estimación del riesgo CV <ul><li>Escala de Framingham </li></ul><ul><ul><li>Riesgo de enfermedad CV a los 5 o 10 años </li></ul></ul><ul><ul><li>Variables incluidas: </li></ul></ul><ul><ul><ul><li>Edad, presión arterial, tabaco, colesterol HDL, diabetes </li></ul></ul></ul><ul><li>Escala SCORE </li></ul><ul><ul><li>Validada para población europea alto/bajo riego </li></ul></ul><ul><ul><li>Riesgo de muerte CV a los 10 años </li></ul></ul><ul><ul><li>Edad, sexo, colesterol total, presión arterial sistólica, tabaco </li></ul></ul><ul><li>Escala PROCAM </li></ul><ul><ul><li>LDL, HDL, triglicéridos, presión arterial, edad, diabetes, historia familiar, tabaquismo. </li></ul></ul>
  37. 38. Law MG, et al. 11th CROI. 2004. Abstract 737. Duration of HAART (years) MI per 1000 PYFU 0 1 2 3 4 5 6 7 8 < 1 1-2 2-3 3-4 4+ 0 Observed Predicted Risk of myocardial infarction in HIV-infected patients can be estimated with the Framingham score DAD Study Law MG et al. HIV Med 2006; 7: 218-230
  38. 39. Framingham Risk Score Used to Estimate 10-Year Cardiovascular Risk <ul><li>Developed for use in general population </li></ul><ul><ul><li>Thought to be reasonable predictor in HIV-infected population </li></ul></ul><ul><li>However, does not include HIV-specific factors </li></ul><ul><ul><li>Immune status </li></ul></ul><ul><ul><li>Increased inflammatory markers </li></ul></ul><ul><ul><li>Insulin resistance </li></ul></ul>Age: Sex: Total cholesterol: HDL cholesterol: Smoker: Systolic blood pressure: Are you currently on any medication to treat high blood pressure? Female Male No Yes No Yes National Cholesterol Education Program
  39. 41. Ecuación D:A:D frente a escala de riesgo de Framingham <ul><li>Estudio de cohortes prospectivo y multinacional de sujetos VIH-positivos </li></ul><ul><li>Más de 33.594 personas-año, se produjeron 157 casos de PCV </li></ul><ul><li>El modelo paramétrico de mejor encaje fue el logarítmico-logístico contando con los factores de riesgo convencionales y la duración de la exposición a IP </li></ul><ul><li>La ecuación del Framingham sobreestimó el riesgo absoluto de PCV y subestimó el riesgo de IM </li></ul>Otras CC Observado Ecuación D:A:D Ecuación de Framingham Cifra absoluta observada y estimada de episodios de PCV y proporción de IM IM Número de episodios de PCV y proporción de IM Friis-Møller N, et al. CROI 2008; Abstract 808 0 20 40 60 80 100 120 140 160 180 200
  40. 42. P = .81 Lichtenstein K et al. CROI 2006. Abstract 735. 0 5 10 15 20 25 30 35 % pts on anti-hypertensive or anti-lipemic agents MI incidence per 1000 pt-yrs, by year Incidence of MI per 1000 PYFU 0 1.5 2.0 2.5 3.0 3.5 4.0 4.5 1993 1994 1995 1996 1997 1998 1999 2000 2001 2002 2004 2005 2003 0.5 1.0 Effect HR adj 95% CI P-value LLAs 0.34 0.14–0.85 0.021 Age >40 y 2.38 0.88–6.43 0.087 Diabetes 2.45 0.99–6.05 0.052 Smoking 2.22 0.98–5.05 0.057 HOPS Cohort The incidence of myocardial infarction can be satisfactorily modified with intervention
  41. 43. Assess CVD risk in next 10 years (Framingham score) Advise on diet and lifestyle in all patients Consider ART modification if CVD risk ≥20% Identify key modifiable risk factors Smoking Blood pressure Coagulation Glucose Li pids Drug treatment if: SBP ≥140 or DBP ≥90 mmHg (especially if 10 year CVD risk ≥20%) Drug treatment if: Established CVD or age ≥50 and 10 year CVD risk ≥20% Confirm DM and drug treatment if: HBA1c ≥6.5% Drug treatment if: Established CVD or T2DM or TC:HDL ratio >6 or 10 year CVD risk ≥20% Target DM or Non-DM; CVD or no CVD: CKD+prot: <130/<80 <140/<90 Target HBA1c <6.5% Target Optimal Standard TC 4 5 (155) (190) LDL 2 3 (80) (115) Target – N/A Treat with acetylsalicylic acid 75-150 mg/d 2009 EACS guidelines on non-infectious co-morbidities in HIV: Prevention of CVD To be released at EACS, Köln 2009.
  42. 45. Clin Infect Dis. 2011 Feb 1;52(3):387-95. Epub 2010 Dec 28. Comparative Effectiveness and Toxicity of Statins Among HIV-Infected Patients. Singh S , Willig JH , Mugavero MJ , Crane PK , Harrington RD , Knopp RH , Kosel BW , Saag MS , Kitahata MM , Crane HM . A retrospective cohort study of patients starting their initial statin medications at 2 large HIV clinics (N = 700). The primary observation : change in lipid levels during statin therapy. Secondary observations : individualized National Cholesterol Education Program (NCEP) goals for low density lipoprotein cholesterol (LDL-C) and non-high density lipoprotein cholesterol (non-HDL-C) levels were reached, and toxicity rates. RESULTS: Atorvastatin (N = 303), pravastatin (N = 280), and rosuvastatin (N = 95). One year after starting a statin therapy, patients who received atorvastatin or rosuvastatin had significantly greater decreases in total cholesterol, LDL-C, and non-HDL-C than patients on pravastatin. The likelihood of reaching NCEP goals for LDL-C levels was higher with the use of rosuvastatin (OR 2.1; P = .03) and atorvastatin (odds ratio [OR], 2.1; P = .001) compared with that of pravastatin. The likelihood of reaching NCEP goals for non-HDL-C levels was higher for rosuvastatin (OR 2.3; P = .045) but not atorvastatin (OR, 1.5; P = .1) compared with pravastatin. Toxicity rates were similar for all 3 statins CONCLUSIONS: Atorvastatin and rosuvastatin are preferable to pravastatin for treatment of HIV-infected patients with dyslipidemia, due to greater declines in total cholesterol, LDL-C, and non-HDL-C, with similar lower toxicity rates.
  43. 47. MUCHAS GRACIAS

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