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REVIEW ARTICLE |
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Year : 2020 | Volume
: 10
| Issue : 1 | Page : 1-5 |
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Myocardial infarction in people living with HIV/AIDS
Shailesh Singh1, Katyayni Singh2
1 Department of Cardiology, Fortis Escorts Heart Institute, New Delhi, India 2 Department of Paediatrics, Lal Bahadur Shastri Hospital, New Delhi, India
Date of Submission | 20-Jan-2020 |
Date of Acceptance | 03-Feb-2020 |
Date of Web Publication | 20-Apr-2020 |
Correspondence Address: Dr. Shailesh Singh M.429, Ashiana Colony, Lucknow - 226 012, Uttar Pradesh India
 Source of Support: None, Conflict of Interest: None
DOI: 10.4103/JICC.JICC_4_20
The advancements in the field of antiretroviral therapy and prevention, diagnosis and treatment of deadly opportunistic infections in HIV has led to prolongation of life of these patients. As these patients now have a higher life expectancy and since they are dying less of infectious diseases, a rise in cardiovascular and metabolic diseases has been seen in these patients. More and more patients have been found to be suffering from acute coronary syndrome, peripheral vascular disease, and stroke.
Keywords: Acute coronary syndrome, HIV/AIDS, myocardial infarction
How to cite this article: Singh S, Singh K. Myocardial infarction in people living with HIV/AIDS. J Indian coll cardiol 2020;10:1-5 |
Introduction | |  |
The advancements in the field of antiretroviral therapy (ART) and prevention, diagnosis, and treatment of deadly opportunistic infections in HIV have led to prolongation of life of these patients. As these patients now have a higher life expectancy and since they are dying less of infectious diseases, a rise in cardiovascular and metabolic diseases has been seen in these patients. More and more patients have been found to be suffering from acute coronary syndrome (ACS), peripheral vascular disease, and stroke.
Incidence of Acute Cardiovascular Complications in Hiv | |  |
Studies have found that HIV-infected patients are more likely to suffer from acute myocardial infarction (MI) than the general population.[1],[2] This becomes even more pronounced in patients who are receiving highly active ART (HAART).[2],[3],[4]
There is some in concrete evidence pointing toward increased incidence of coronary artery disease (CAD) in patients who are being prescribed protease inhibitors.[5] However, the definitive association between the two is not proven.[6]
Spectrum of Disease | |  |
Multiple cases of CAD in HIV-infected patients have been reported worldwide.[7],[8],[9],[10],[11],[12],[13],[14]
Like their noninfected counterparts, HIV-infected patients can either present as chronic stable angina or unstable ACS or ST-elevation MI.
Boccara et al.[14] found among 20 HIV+ patients admitted with an ACS, of which majority suffered from MI and 19 patients were male. Majority of the patients had a history of tobacco consumption (80%). Dyslipidemia was present in 65%. Fourteen patients had received protease inhibitors.
Duong et al.[13] prospectively evaluated the presence of silent MI in HIV+ patients. The authors found that silent myocardial ischemia, as detected by the treadmill test, increased in HIV-infected patients more than the general population (11% vs. 5%). The authors also found that the patients who developed silent myocardial ischemia were older, had fat redistribution with more central fat, and have hypercholesterolemia.
Bergersen et al.[15] demonstrated that the risk of CAD was higher in HIV-infected patients compared to the general population. The study reported that compared to controls, twice as many HIV-infected patients on HAART had an estimated 10-year coronary heart disease (CHD) Framingham risk above 20% (11.9% vs. 5.3%). The main contributors to increased risk of CHD were increased prevalence of daily smoking, elevated total cholesterol and low high-density lipoprotein (HDL) in the patient on HAART.
Neumann et al.[16] demonstrated that the risk of cardiovascular event is related to the age of HIV-infected patients. The authors also found that total cholesterol, low-density lipoprotein cholesterol (LDL-C), and triglycerides increased with increasing age.
Hadigan et al.[17] compared the 10-year CHD risk among HIV-infected patients with noninfected counterparts and concluded that the CHD risk is increased in male HIV patients with fat redistribution.
A study[18] compared three cardiovascular risk-predicting equations, i.e. Framingham, PROCAM, and SCORE, for risk assessment in HIV+ patients. Majority of HIV+ patients were found to be at low cardiovascular risk by all of the methods. However, when the three systems were compared, the Framingham equation classified a higher number of HIV positive male patients with moderate cardiovascular risk.
A French study[19] studied the risk factors for CHD in HIV+ patients treated and compared with the general population. HIV-infected patients were more likely to be a smoker, hypertensive, have lower HDL cholesterol with high triglycerides, and have a higher waist-to-hip ratio.
The Swiss HIV cohort study[20] studied the prevalence of risk factors for cardiovascular disease in HIV-infected patients. Smoking, low HDL cholesterol, high triglycerides, and hypertension were found to be the most common cardiovascular risk factors.
Many studies have shown that HIV+ patients have a higher incidence of risk factors for cardiovascular disease; thus, they are at a higher risk of CHD.[21],[22],[23]
Protease inhibitors have been implicated in the pathogenesis of MI.[24],[25]
Pathophysiology | |  |
Accelerated atherosclerosis in HIV infection can be attributed to factors such as insulin resistance, lipodystrophy syndrome,[23],[26],[27] dyslipidemia,[27],[28],[29],[30],[31],[32] chronic inflammation and inflammatory pathway,[33],[34],[35],[36],[37],[38],[39],[40],[41],[42] prothrombotic state,[34],[43],[44] metabolic abnormalities in HIV,[45],[46] and direct vascular toxicity of the virus.[47]
Prognosis | |  |
The prognosis of HIV-infected patients during the acute phase of ACS has been evaluated in a few studies.[48],[49],[50],[51],[52] The inhospital mortality rate varied from 0% to 8%, and no differences in terms of heart failure and reinfarction were found when a control group was included.[50],[52] However, when long-term follow-up of HIV-infected patients was compared with controls, HIV-positive patients were more likely to have recurrent ischemia, but there was no significant difference in long-term cardiovascular and total mortality.[50],[52]
Primary Prevention | |  |
Aspirin
In primary prevention, aspirin should be given if the level of CHD risk is high and in the absence of contraindications.[53] Recently, questions have been raised about platelet function and activity in HIV-infected patients.[54],[55]
Empiric Statin Therapy – Is There a Role? | |  |
Considering the high risk of atherosclerotic cardiovascular disease in HIV+ patients, empiric statin therapy can be considered in the absence of contraindications.[56]
Lo et al. randomized 40 HIV patients without vascular disease or an existing indication for statin therapy to receive either atorvastatin or placebo. The study showed that statin therapy slowed coronary plaque progression.[57]
Funderburg et al.[58] found that 48 weeks of rosuvastatin treatment reduced significantly several markers of inflammation. Another study found that the patients with HIV infection who received statin therapy had smaller reductions in low-density lipoprotein cholesterol.[59]
Management of Dyslipidemia and Cardiovascular Risk Reduction in Hiv+ Patients | |  |
If dyslipidemia is present, the patient should be screened for secondary causes such as the general population. Underlying causes such as diabetes mellitus, hypothyroidism, excessive alcohol use, obstructive liver disease, chronic renal failure, hypogonadism, and drug-induced elevated LDL-C (progestins, anabolic steroids, and corticosteroids) should be ruled out. Statins and other lipid-lowering agents should be strongly considered.
A study has shown that statin therapy can cause a 26% reduction in LDL-C in HIV+ patients, which is less than that seen in non-HIV-infected individuals.[59]
A study has shown that statin therapy improves high-risk plaque morphology.[57]
Studies have shown that pitavastatin causes more reduction of arterial inflammation and LDL lowering among HIV patients compared to pravastatin, a more commonly used drug.[60],[61]
The standard dose rosuvastatin or pravastatin or fluvastatin is a safe choice because they do not have an interaction with cytochrome P-450 (CYP).
Smoking Cessation | |  |
Compared to the general population, HIV+ patients were more likely to be the prevalence of smoking cigarettes.[62] Smoking cessation should be a priority for HIV-infected patients and physicians, integrated into a global risk reduction approach (dyslipidemia, diabetes mellitus, overweight, and inactivity) to prevent future coronary events.[63]
Systemic Hypertension | |  |
Few studies have studied the prevalence of hypertension in HIV+ patients.[64],[65]
Sattler et al.[65] showed that hypertension was more common in HIV-infected patients with lipodystrophy compared with HIV-infected patients without it (74 vs. 48%, P = 0.01).
The prevalence of systemic hypertension was studied in a cohort of 214 HIV-1-infected patients, and it was found to be 29%. These hypertensive patients were much older and had a higher waist to hip ratio than normotensive individuals. Hypertensive patients were more likely to suffer from CHD and MI.[66]
Crane et al.[67] found that treatment with lopinavir/ritonavir was significantly associated with hypertension. The likely explanation for the phenomenon was an increase in body mass index. Atazanavir was the least likely cause of hypertension among the protease inhibitors.
Renin angiotensin aldosterone system inhibitors (RAAS inhibitors) are considered the first-line therapy for hypertension in HIV+ patients because of their protective effects on glucose metabolism and kidney function.
Secondary Prevention | |  |
HIV+ patients presenting with ACS should be managed as per standard guidelines for the general population in terms of thrombolytic, antithrombotic therapy, and coronary revascularization modalities.
Patients should receive β-blockers, aspirin, angiotensin-converting enzyme inhibitors, and lipid-lowering therapy as a part of medical management.
Antiplatelets | |  |
Dual antiplatelet therapy, which includes aspirin plus clopidogrel, prasugrel, or ticagrelor, should be given to the patients as per the guidelines for the general population.
A study has reported a potential drug interaction between ritonavir and prasugrel.[68] Concerns have been raised about the potential drug interaction between ticagrelor and protease inhibitors as the former is metabolized by CYP 3A4/5 pathway, and the latter is its inhibitor.[69]
Percutaneous Interventions for Hiv+ Patients With Myocardial Infarction | |  |
A study has found that HIV-infected individuals are less likely to undergo percutaneous coronary intervention and, more likely to receive a Bare metal stent (BMS) instead of a Drug- eluting stent (DES), have higher mortality rates, and hospitalization costs are higher than their noninfected counterparts.[70] HIV+ patients have been found to have higher incidences of stent thrombosis, especially when CD4 cell count is low (>200 cells/mm3).[71],[72] Studies have reported a higher frequency of in stent restenosis and target vessel revascularization in HIV+ patients who received BMS, suggesting potential benefits with the use of DES.[73],[74] Studies have reported a higher frequency of in-stent restenosis and target vessel revascularization in HIV+ patients who received BMS, suggesting potential benefits with the use of DES.[75],[76]
Coronary Artery Bypass Graft for Hiv+ Patients With Myocardial Infarction/coronary Artery Disease | |  |
Evidence suggests that the immediate and postoperative periods after coronary artery bypass graft in HIV-infected patients are uneventful and are not different from those in non-HIV-infected patients. There was no difference in the rate of cardiovascular death in long term follow up.[75],[76],[77],[78]
Financial support and sponsorship
Nil.
Conflicts of interest
There are no conflicts of interest.
References | |  |
1. | Klein D, Hurley LB, Quesenberry CP Jr., Sidney S. Do protease inhibitors increase the risk for coronary heart disease in patients with HIV-1 infection? J Acquir Immune Defic Syndr 2002;30:471-7. |
2. | Mary-Krause M, Cotte L, Simon A, Partisani M, Costagliola D; Clinical Epidemiology Group from the French Hospital Database. Increased risk of myocardial infarction with duration of protease inhibitor therapy in HIV-infected men. AIDS 2003;17:2479-86. |
3. | Friis-Møller N, Sabin CA, Weber R, d'Arminio Monforte A, El-Sadr WM, Reiss P, et al. Combination antiretroviral therapy and the risk of myocardial infarction. N Engl J Med 2003;349:1993-2003. |
4. | Holmberg SD, Moorman AC, Williamson JM, Tong TC, Ward DJ, Wood KC, et al. Protease inhibitors and cardiovascular outcomes in patients with HIV-1. Lancet 2002;360:1747-8. |
5. | Bozzette SA, Ake CF, Tam HK, Chang SW, Louis TA. Cardiovascular and cerebrovascular events in patients treated for human immunodeficiency virus infection. N Engl J Med 2003;348:702-10. |
6. | DAD Study Group, Friis-Møller N, Reiss P, Sabin CA, Weber R, Monforte Ad, et al. Class of antiretroviral drugs and the risk of myocardial infarction. N Engl J Med 2007;356:1723-35. |
7. | Henry K, Melroe H, Huebsch J, Hermundson J, Levine C, Swensen L, et al. Severe premature coronary artery disease with protease inhibitors. Lancet 1998;351:1328. |
8. | Behrens G, Schmidt H, Meyer D, Stoll M, Schmidt RE. Vascular complications associated with use of HIV protease inhibitors. Lancet 1998;351:1958. |
9. | Gallet B, Pulik M, Genet P, Chedin P, Hiltgen M. Vascular complications associated with use of HIV protease inhibitors. Lancet 1998;351:1958-9. |
10. | Vittecoq D, Escaut L, Monsuez JJ. Vascular complications associated with use of HIV protease inhibitors. Lancet 1998;351:1959. |
11. | Jütte A, Schwenk A, Franzen C, Römer K, Diet F, Diehl V, et al. Increasing morbidity from myocardial infarction during HIV protease inhibitor treatment? AIDS 1999;13:1796-7. |
12. | Rickerts V, Brodt H, Staszewski S, Stille W. Incidence of myocardial infarctions in HIV-infected patients between 1983 and 1998: The Frankfurt HIV-cohort study. Eur J Med Res 2000;5:329-33. |
13. | Duong M, Cottin Y, Piroth L, Fargeot A, Lhuiller I, Bobillier M, et al. Exercise stress testing for detection of silent myocardial ischemia in human immunodeficiency virus-infected patients receiving antiretroviral therapy. Clin Infect Dis 2002;34:523-8. |
14. | Boccara F, Ederhy S, Janower S, Benyounes N, Odi G, Cohen A. Clinical characteristics and mid-term prognosis of acute coronary syndrome in HIV-infected patients on antiretroviral therapy. HIV Med 2005;6:240-4. |
15. | Bergersen BM, Sandvik L, Bruun JN, Tonstad S. Elevated Framingham risk score in HIV-positive patients on highly active antiretroviral therapy: Results from a Norwegian study of 721 subjects. Eur J Clin Microbiol Infect Dis 2004;23:625-30. |
16. | Neumann T, Woiwod T, Neumann A, Miller M, Von Birgelen C, Volbracht L, et al. Cardiovascular risk factors and probability for cardiovascular events in HIV-infected patients-part III: Age differences. Eur J Med Res 2004;9:267-72. |
17. | Hadigan C, Meigs JB, Wilson PW, D'Agostino RB, Davis B, Basgoz N, et al. Prediction of coronary heart disease risk in HIV-infected patients with fat redistribution. Clin Infect Dis 2003;36:909-16. |
18. | Knobel H, Jericó C, Montero M, Sorli ML, Velat M, Guelar A, 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 2007;21:452-7. |
19. | Savès M, Chêne G, Ducimetière P, Leport C, Le Moal G, Amouyel P, et al. Risk factors for coronary heart disease in patients treated for human immunodeficiency virus infection compared with the general population. Clin Infect Dis 2003;37:292-8. |
20. | Glass TR, Ungsedhapand C, Wolbers M, Weber R, Vernazza PL, Rickenbach M, et al. Prevalence of risk factors for cardiovascular disease in HIV-infected patients over time: The Swiss HIV Cohort Study. HIV Med 2006;7:404-10. |
21. | Sterne JA, May M, Bucher HC, Ledergerber B, Furrer H, Cavassini M, et al. HAART and the heart: Changes in coronary risk factors and implications for coronary risk in men starting antiretroviral therapy. J Intern Med 2007;261:255-67. |
22. | Bergersen BM. Cardiovascular risk in patients with HIV Infection: Impact of antiretroviral therapy. Drugs 2006;66:1971-87. |
23. | Grinspoon S, Carr A. Cardiovascular risk and body-fat abnormalities in HIV-infected adults. N Engl J Med 2005;352:48-62. |
24. | Sudano I, Spieker LE, Noll G, Corti R, Weber R, Lüscher TF. Cardiovascular disease in HIV infection. Am Heart J 2006;151:1147-55. |
25. | Triant VA, Lee H, Hadigan C, Grinspoon SK. Increased acute myocardial infarction rates and cardiovascular risk factors among patients with human immunodeficiency virus disease. J Clin Endocrinol Metab 2007;92:2506-12. |
26. | Carr A, Samaras K, Thorisdottir A, Kaufmann GR, Chisholm DJ, Cooper DA. Diagnosis, prediction, and natural course of HIV-1 protease-inhibitor-associated lipodystrophy, hyperlipidaemia, and diabetes mellitus: A cohort study. Lancet 1999;353:2093-9. |
27. | Périard D, Telenti A, Sudre P, Cheseaux JJ, Halfon P, Reymond MJ, et al. Atherogenic dyslipidemia in HIV-infected individuals treated with protease inhibitors. The Swiss HIV Cohort Study. Circulation 1999;100:700-5. |
28. | Fichtenbaum CJ, Gerber JG, Rosenkranz SL, Segal Y, Aberg JA, Blaschke T, et al. Pharmacokinetic interactions between protease inhibitors and statins in HIV seronegative volunteers: ACTG Study A5047. AIDS 2002;16:569-77. |
29. | Dubé MP, Stein JH, Aberg JA, Fichtenbaum CJ, Gerber JG, Tashima KT, 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 2003;37:613-27. |
30. | Stein JH, Merwood MA, Bellehumeur JL, Aeschlimann SE, Korcarz CE, Underbakke GL, et al. Effects of pravastatin on lipoproteins and endothelial function in patients receiving human immunodeficiency virus protease inhibitors. Am Heart J 2004;147:E18. |
31. | Asztalos BF, Schaefer EJ, Horvath KV, Cox CE, Skinner S, Gerrior J, et al. Protease inhibitor-based HAART, HDL, and CHD-risk in HIV-infected patients. Atherosclerosis 2006;184:72-7. |
32. | Grinspoon SK. Metabolic syndrome and cardiovascular disease in patients with human immunodeficiency virus. Am J Med 2005;118 Suppl 2:23S-28S. |
33. | Khan NA, Di Cello F, Nath A, Kim KS. Human immunodeficiency virus type 1 tat-mediated cytotoxicity of human brain microvascular endothelial cells. J Neurovirol 2003;9:584-93. |
34. | Schecter AD, Berman AB, Yi L, Mosoian A, McManus CM, Berman JW, et al. HIV envelope gp120 activates human arterial smooth muscle cells. Proc Natl Acad Sci U S A 2001;98:10142-7. |
35. | Coll B, Parra S, Alonso-Villaverde C, de Groot E, Aragonés G, Montero M, et al. HIV-infected patients with lipodystrophy have higher rates of carotid atherosclerosis: The role of monocyte chemoattractant protein-1. Cytokine 2006;34:51-5. |
36. | de Larrañaga GF, Petroni A, Deluchi G, Alonso BS, Benetucci JA. Viral load and disease progression as responsible for endothelial activation and/or injury in human immunodeficiency virus-1-infected patients. Blood Coagul Fibrinolysis 2003;14:15-8. |
37. | Fisher SD, Miller TL, Lipshultz SE. Impact of HIV and highly active antiretroviral therapy on leukocyte adhesion molecules, arterial inflammation, dyslipidemia, and atherosclerosis. Atherosclerosis 2006;185:1-11. |
38. | Stein JH, Klein MA, Bellehumeur JL, McBride PE, Wiebe DA, Otvos JD, et al. Use of human immunodeficiency virus-1 protease inhibitors is associated with atherogenic lipoprotein changes and endothelial dysfunction. Circulation 2001;104:257-62. |
39. | Hulgan T, Morrow J, D'Aquila RT, Raffanti S, Morgan M, Rebeiro P, et al. Oxidant stress is increased during treatment of human immunodeficiency virus infection. Clin Infect Dis 2003;37:1711-7. |
40. | de Gaetano Donati K, Rabagliati R, Iacoviello L, Cauda R. HIV infection, HAART, and endothelial adhesion molecules: Current perspectives. Lancet Infect Dis 2004;4:213-22. |
41. | Wu RF, Gu Y, Xu YC, Mitola S, Bussolino F, Terada LS. Human immunodeficiency virus type 1 Tat regulates endothelial cell actin cytoskeletal dynamics through PAK1 activation and oxidant production. J Virol 2004;78:779-89. |
42. | Hsue PY, Hunt PW, Sinclair E, Bredt B, Franklin A, Killian M, et al. Increased carotid intima-media thickness in HIV patients is associated with increased cytomegalovirus-specific T-cell responses. AIDS 2006;20:2275-83. |
43. | Zandman-Goddard G, Shoenfeld Y. HIV and autoimmunity. Autoimmun Rev 2002;1:329-37. |
44. | Karmochkine M, Ankri A, Calvez V, Bonmarchant M, Coutellier A, Herson S. Plasma hypercoagulability is correlated to plasma HIV load. Thromb Haemost 1998;80:208-9. |
45. | Escaut L, Monsuez JJ, Chironi G, Merad M, Teicher E, Smadja D, et al. Coronary artery disease in HIV infected patients. Intensive Care Med 2003;29:969-73. |
46. | David MH, Hornung R, Fichtenbaum CJ. Ischemic cardiovascular disease in persons with human immunodeficiency virus infection. Clin Infect Dis 2002;34:98-102. |
47. | Barbaro G, Barbarini G, Pellicelli AM. HIV-associated coronary arteritis in a patient with fatal myocardial infarction. N Engl J Med 2001;344:1799-800. |
48. | Varriale P, Saravi G, Hernandez E, Carbon F. Acute myocardial infarction in patients infected with human immunodeficiency virus. Am Heart J 2004;147:55-9. |
49. | Ambrose JA, Gould RB, Kurian DC, DeVoe MC, Pearlstein NB, Coppola JT, et al. Frequency of and outcome of acute coronary syndromes in patients with human immunodeficiency virus infection. Am J Cardiol 2003;92:301-3. |
50. | Matetzky S, Domingo M, Kar S, Noc M, Shah PK, Kaul S, et al. Acute myocardial infarction in human immunodeficiency virus-infected patients. Arch Intern Med 2003;163:457-60. |
51. | Hsue PY, Giri K, Erickson S, MacGregor JS, Younes N, Shergill A, et al. Clinical features of acute coronary syndromes in patients with human immunodeficiency virus infection. Circulation 2004;109:316-9. |
52. | Boccara F, Mary-Krause M, Teiger E, Lang S, Lim P, Wahbi K, et al. Acute coronary syndrome in human immunodeficiency virus-infected patients: Characteristics and 1 year prognosis. Eur Heart J 2011;32:41-50. |
53. | Wolff T, Miller T, Ko S. Aspirin for the primary prevention of cardiovascular events: An update of the evidence for the U.S. Preventive Services Task Force. Ann Intern Med 2009;150:405-10. |
54. | Corrales-Medina VF, Simkins J, Chirinos JA, Serpa JA, Horstman LL, Jy W, et al. Increased levels of platelet microparticles in HIV-infected patients with good response to highly active antiretroviral therapy. J Acquir Immune Defic Syndr 2010;54:217-8. |
55. | Satchell CS, Cotter AG, O'Connor EF, Peace AJ, Tedesco AF, Clare A, et al. Platelet function and HIV: A case-control study. AIDS 2010;24:649-57. |
56. | Justice A, Freiberg MS, Lo Re V. Should everyone ageing with HIV take a statin? Lancet HIV 2015;2:e36-7. |
57. | Lo J, Lu MT, Ihenachor EJ, Wei J, Looby SE, Fitch KV, et al. Effects of statin therapy on coronary artery plaque volume and high-risk plaque morphology in HIV-infected patients with subclinical atherosclerosis: A randomised, double-blind, placebo-controlled trial. Lancet HIV 2015;2:e52-63. |
58. | Funderburg NT, Jiang Y, Debanne SM, Labbato D, Juchnowski S, Ferrari B, et al. Rosuvastatin reduces vascular inflammation and T-cell and monocyte activation in HIV-infected subjects on antiretroviral therapy. J Acquir Immune Defic Syndr 2015;68:396-404. |
59. | Silverberg MJ, Leyden W, Hurley L, Go AS, Quesenberry CP Jr, Klein D, et al. Response to newly prescribed lipid-lowering therapy in patients with and without HIV infection. Ann Intern Med 2009;150:301-13. |
60. | Toribio M, Fitch KV, Sanchez L, Burdo TH, Williams KC, Sponseller CA, et al. Effects of pitavastatin and pravastatin on markers of immune activation and arterial inflammation in HIV. AIDS 2017;31:797-806. |
61. | Sponseller CA, Aberg J; INTREPID Team. After 52 weeks pitavastatin is superior to pravastatin for LDL-C lowering in patients with HIV. Conference on Retroviruses and Opportunistic Infections. Abstract 751LB. Boston; 3-6 March, 2014. |
62. | Niaura R, Shadel WG, Morrow K, Tashima K, Flanigan T, Abrams DB. Human immunodeficiency virus infection, AIDS, and smoking cessation: The time is now. Clin Infect Dis 2000;31:808-12. |
63. | Elzi L, Spoerl D, Voggensperger J, Nicca D, Simcock M, Bucher HC, et al. A smoking cessation programme in HIV-infected individuals: A pilot study. Antivir Ther 2006;11:787-95. |
64. | Morse CG, Kovacs JA. Metabolic and skeletal complications of HIV infection: The price of success. JAMA 2006;296:844-54. |
65. | Sattler FR, Qian D, Louie S, Johnson D, Briggs W, DeQuattro V, et al. Elevated blood pressure in subjects with lipodystrophy. AIDS 2001;15:2001-10. |
66. | Jung O, Bickel M, Ditting T, Rickerts V, Welk T, Helm EB, et al. Hypertension in HIV-1-infected patients and its impact on renal and cardiovascular integrity. Nephrol Dial Transplant 2004;19:2250-8. |
67. | Crane HM, Van Rompaey SE, Kitahata MM. Antiretroviral medications associated with elevated blood pressure among patients receiving highly active antiretroviral therapy. AIDS 2006;20:1019-26. |
68. | Daali Y, Ancrenaz V, Bosilkovska M, Dayer P, Desmeules J. Ritonavir inhibits the two main prasugrel bioactivation pathways in vitro: A potential drug-drug interaction in HIV patients. Metabolism 2011;60:1584-9. |
69. | Zhou D, Andersson TB, Grimm SW. In vitro evaluation of potential drug-drug interactions with ticagrelor: Cytochrome P450 reaction phenotyping, inhibition, induction, and differential kinetics. Drug Metab Dispos 2011;39:703-10. |
70. | Singh V, Mendirichaga R, Savani GT, Rodriguez AP, Dabas N, Munagala A, et al. Coronary revascularization for acute myocardial infarction in the HIV population. J Interv Cardiol 2017;30:405-14. |
71. | D'Ascenzo F, Cerrato E, Appleton D, Moretti C, Calcagno A, Abouzaki N, et al. Prognostic indicators for recurrent thrombotic events in HIV-infected patients with acute coronary syndromes: Use of registry data from 12 sites in Europe, South Africa and the United States. Thromb Res 2014;134:558-64. |
72. | Carvalho AS, Osório Valente R, Almeida Morais L, Modas Daniel P, Sá Carvalho R, Ferreira L, et al. HIV and coronary disease – When secondary prevention is insufficient. Rev Port Cardiol 2017;36:569. |
73. | Segev A, Cantor WJ, Strauss BH. Outcome of percutaneous coronary intervention in HIV-infected patients. Catheter Cardiovasc Interv 2006;68:879-81. |
74. | Badr S, Minha S, Kitabata H, Fatemi O, Torguson R, Suddath WO, et al. Safety and long-term outcomes after percutaneous coronary intervention in patients with human immunodeficiency virus. Catheter Cardiovasc Interv 2015;85:192-8. |
75. | Trachiotis GD, Alexander EP, Benator D, Gharagozloo F. Cardiac surgery in patients infected with the human immunodeficiency virus. Ann Thorac Surg 2003;76:1114-8. |
76. | Filsoufi F, Salzberg SP, Harbou KT, Neibart E, Adams DH. Excellent outcomes of cardiac surgery in patients infected with HIV in the current era. Clin Infect Dis 2006;43:532-6. |
77. | Jiménez-Expósito MJ, Mestres CA, Claramonte X, Cartañá R, Josa M, Pomar JL, et al. Mortality and morbidity in HIV-infected patients undergoing coronary artery bypass surgery: A case control study. Rev Esp Cardiol 2006;59:276-9. |
78. | Boccara F, Cohen A, Di Angelantonio E, Meuleman C, Ederhy S, Dufaitre G, et al. Coronary artery bypass graft in HIV-infected patients: A multicenter case control study. Curr HIV Res 2008;6:59-64. |
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