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REVIEW ARTICLE
Year : 2011  |  Volume : 134  |  Issue : 6  |  Page : 898-903

Human immunodeficiency virus & cardiovascular risk


1 Department of Medical Pathophysiology, University "La Sapienza", Rome, Italy
2 Department of Infectious & Parasitic Diseases, Fondazione Policlinico S. Matteo, Pavia, Italy

Date of Submission04-Jun-2011
Date of Web Publication6-Feb-2012

Correspondence Address:
Giuseppe Barbaro
Viale Anicio Gallo 63, 00174 Rome
Italy
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DOI: 10.4103/0971-5916.92634

PMID: 22310821

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   Abstract 

Highly active antiretroviral therapy (HAART) significantly changed the prevalence of the cardiovascular manifestations of human immunodeficiency virus (HIV)/AIDS. In developed countries, a 30 per cent reduction in the prevalence of cardiomyopathy and pericardial effusion was observed, possibly related to a reduction of opportunistic infections and myocarditis. In developing countries, however, where the availablity of HAART is limited, and the pathogenic impact of nutritional factors is significant, a 32 per cent increase was seen in the prevalence of cardiomyopathy and related high mortality rate from congestive heart failure. Also, some HAART regimens in developed countries, especially those including protease inhibitors, may cause, in a high proportion of HIV-infected patients, a lipodystrophy syndrome that is associated with an increased risk of cardiovascular events related to a process of accelerated atherosclerosis. Careful cardiac screening is warranted for patients who are being evaluated for, or who are receiving HAART regimens, particularly for those with known underlying cardiovascular risk factors, according to the most recent clinical guidelines.

Keywords: Acquired immunodeficiency syndrome - cardiovascular disease - highly active antiretroviral therapy - human immunodeficiency virus - lipodystrophy syndrome


How to cite this article:
Barbaro G, Barbarini G. Human immunodeficiency virus & cardiovascular risk. Indian J Med Res 2011;134:898-903

How to cite this URL:
Barbaro G, Barbarini G. Human immunodeficiency virus & cardiovascular risk. Indian J Med Res [serial online] 2011 [cited 2014 Sep 1];134:898-903. Available from: http://www.ijmr.org.in/text.asp?2011/134/6/898/92634


   Introduction Top


The introduction of highly active antiretroviral therapy (HAART) has significantly improved the clinical evolution of human immunodeficiency virus (HIV)/AIDS disease, with an increased survival of infected patients. However, the introduction of HAART has generated contrasting aspects in the clinical manifestation of cardiovascular complications. In developed countries, a reduction has been observed in the prevalence of HIV-associated cardiomyopathy, possibly related to the reduction in the incidence of opportunistic infections and myocarditis. On the other hand, in developing countries, where HAART is not widely available, an increase has been noted in the prevalence of cardiomyopathy and pericardial effusion, with a related high mortality rate for congestive heart failure [1] . In the context of these new clinical findings, it has been observed in developed countries that some HAART regimens, especially those including protease inhibitors, may cause a iatrogenic metabolic syndrome (HIV-associated lipodystrophy syndrome) that is associated with an increased risk for cardiovascular events (myocardial infarction and stroke) because of a process of accelerated atherosclerosis.


   HIV-Associated Cardiology Issues: Pre-HAART vs Post-HAART Period Top


Cardiomyopathy and pericardial effusion: HIV/AIDS is recognized as an important cause of dilated cardiomyopathy, with an estimated annual incidence of 15.9/1,000 before the introduction of HAART [1] . This incidence is mainly related to that of myocarditis, which is still the best-studied cause of dilated cardiomyopathy in HIV/AIDS. Myocarditis has been documented at autopsy in 40-52 per cent of patients who died of AIDS before the introduction of HAART [2] . Another important cause of cardiomyopathy in HIV/AIDS is drug cardiotoxicity. Zidovudine is associated with diffuse destruction of cardiac mi­tochondrial ultrastructure and inhibition of mito­chondrial DNA replication that may contribute to myocardial cell dys­function [3] . Doxorubicin (adria­mycin), which is used to treat AIDS-associated Kaposi's sarcoma and non-Hodgkin's lymphoma, has a dose-related effect on dilated cardiomyopathy [4] , as does foscarnet sodium when used to treat cyto­megalovirus oesophagitis [5] .

The introduction of HAART regimens, by preventing opportunistic infections and reduc­ing the incidence of myocarditis, has reduced the prevalence of HIV-associated cardiomyopathy by about 30 per cent in developed countries [6] . However, the median prevalence of HIV-associated cardiomyopathy is increasing in developing countries (about 32%), where the availability of HAART is scanty and greater is the pathogenetic impact of nutritional factors [7] . Nutritional deficiencies, in fact, are common in HIV-infected subjects living in developing countries and may contribute to ventricular dys­function independently of HAART [7] . Selenium, as a component of glutathione peroxidase, is involved in the antioxidant response in cells and tissues and is associated with congestive cardiomyopathy and skeletal-muscle disorders. Low levels of selenium have been described in African HIV-infected patients with cardiomyopathy and recognized as an independent factor associated with cardiomyopathy in multivariate analysis [7] . The selenium depletion in these patients may be responsible for the cardiotoxic effects of coxsackievirus B3 and for the ability of these viruses to enhance the toxic effects of zidovudine on skeletal and myocardial muscle [8] . HIV infection may also be as­sociated with altered levels of vitamin B12, carni­tine, growth hormone, and thyroid hormone, all of which have been associated with left ventricu­lar dysfunction [9] . A trend similar to that observed for cardiomyopathy has also been observed for pericardial effusion, the prevalence of which is reduced by 30-35 per cent after the introduction of HAART in developed countries, whereas in the developing countries, the prevalence of pericardial effusion is increased by 35-40 per cent, mostly related to Mycobacterium infections [10],[11] .

Endocarditis: The prevalence of infective endocarditis did not vary in HIV-infected patients who use intravenous drugs after the introduction of HAART even in the developed countries, being similar to that observed in HIV-uninfected intravenous drug addicts [1] .Among intravenous drug addicts, the tricuspid valve is most frequently affected and the most frequent agents are Staphylococcus aureus (>75% of cases), Streptococcus pneumoniae, Haemophilus influenzae, Candida albicans, Aspergillus fumigatus and Cryptococcus neoformans[2] . A virulent bacteria, as the HACEK group (Haemophilus species, Actinobacillus actinomycetemcomitans, Cardiobacterium hominis, Eikenella corrodens and Kingella kingae), which are often part of the endogenous flora of the mouth, can cause endocarditis in HIV-infected patients [12] . A prevalence of 3-5 per cent of non­bacterial thrombotic endocarditis, also known as marantic endocarditis was seen in AIDS patients, mostly with HIV-wasting syndrome, before the introduction of HAART [2] . Marantic endocarditis is now more frequently observed in developing countries with a high incidence (about 10-15%) and mortality for systemic embolization [10],[11] .

Pulmonary hypertension: The incidence of HIV-associated pulmonary hypertension is increased in HIV-infected patients after the introduction of HAART. It has been estimated in 1/200, much higher than 1/200,000 found in the general population [13] . A key pathogenetic role in this condition is played by pulmonary dendritic cells which are not sensitive to HAART and may hold HIV-1 on their surfaces for extended time periods. The infection of these cells by HIV-1 causes a chronic release of cytotoxic cytokines (e.g., endothelin-1, interleukin-6, interleukin-1 beta and TNF-alpha) contributing to vascular plexogenic lesions and progressive tissue damage and congestive heart failure, independently of opportunistic infections, stage of HIV disease and HAART regimens [13] . Endothelin-1 receptor antagonists, such as bosentan, may be useful, even in combination with HAART in the early stages of the disease [14],[15] . The use of phosphodiesterase-5 inhibitors (e.g., sildenafil), although promising, is still debated because of their interaction with protease inhibitors.

AIDS-associated neoplasms: The introduction of HAART reduced significantly the prevalence of cardiac involvement in AIDS-associated neoplasms. The prevalence of cardiac Kaposi's sarcoma in AIDS patients ranged from 12 to 28 per cent in retrospective autopsy studies performed in the pre-HAART era, with a lower prevalence for non-Hodgkin lymphoma [2] .The introduction of HAART led to a reduction by about 50 per cent in the overall incidence of cardiac involvement by Kaposi's sarcoma and non-Hodgkin lymphomas. The fall may be attributable to the improved immunologic state of the patients and the prevention of opportunistic infections (human herpes virus-8 and Epstein-Barr virus) known to play an aetiologic role in these neoplasms. On the contrary, an increased prevalence of cardiac involvement of AIDS-­associated tumours has been observed in developing countries in relation to the scanty availability of HAART [10] .

Vasculitis: A wide range of inflammatory vascular diseases including polyarteritis nodosa, Henoch-Schonlein purpura, and drug-induced hypersensitivity vasculitis may develop in HIV-infected individuals. Kawasaki-like syndrome [16],[17] and Takayasu's arteritis [18] have also been described. Some HIV-infected patients have a clinical presentation resembling systemic lupus erythematosus with arthralgias, myalgias, and autoimmune phenomena with a low titre positive antinuclear antibody, coagulopathy with lupus anticoagulant, haemolytic anaemia, and thrombocytopenic purpura [19] . Drug-induced hypersensitivity vasculitis is common in HIV-infected patients receiving HAART [19] .The vasculitis associated with drug reactions typically involves small vessels and has a lymphocytic or leukocytoclastic histopathology. Medical practitioners need to be especially aware of abacavir hypersensitivity reactions because of the potential for fatal outcomes. Hypersensitivity reactions of this type should always be considered as a possible aetiology for a vasculitic syndrome in an HIV-infected patient [19] .

Viral infection and coronary artery disease: The association between viral infection (cytomegalovirus or HIV-1 itself) and coronary artery lesions is not clear. HIV-1 sequences have been detected by in situ hybridization in the coronary vessels of an HIV-infected patient who died from acute myocardial infarction [20] . Po­tential mechanisms through which HIV-1 may damage cor­onary arteries include activation of cytokines and cell-adhesion molecules and alteration of major-histocompatibility-complex (MHC) class I molecules on the surface of smooth-muscle cells [20] . It is possible also that HIV-1-associated protein gp 120 may induce smooth-muscle cell apoptosis through a mitochondrion-controlled pathway by activation of inflammatory cytokines [21] .


   HIV-Associated Lipodystrophy Syndrome and Cardiovascular Risk Top


HIV-associated lipodystrophy or lipoatrophy, first described in 1998 [22] , after the introduction of HAART in 1996, is characterized by the presence of a dorso-cervical fat pad (also known as buffalo hump), increased abdominal girth and breast size, lipoatrophy of subcutaneous fat of the face, buttocks and limbs, and prominence of veins on the limbs. The overall prevalence of at least one physical abnormality is thought to be about 50 per cent in otherwise healthy HIV-infected patients receiving HAART, although reported rates range from 18 to 83 per cent [23],[24] . Among HIV-infected patients with lipodystrophy, increased serum total and low density lipoprotein cholesterol and triglyceride levels have been observed in about 70 per cent, whereas insulin resistance (elevated C-peptide and insulin) and type 2 diabetes mellitus have been observed in 8 to 10 per cent [23],[24] . The increased risk for cardiovascular events associated with lipodystrophy syndrome may be related both to a specific action of antiretroviral drugs, especially protease inhibitors, and to individual risk factors (e.g. smoking habit, and inheritated metabolic disease).

Coagulation disorders: HIV-infected patients receiving HAART, especially those with fat redistribution and insulin resistance, might develop coagulation abnormalities, including increased levels of fibrinogen, D-dimer, plasminogen activator inhibitor-1, and tissue-type plasminogen activator antigen, or deficiency of protein S [25] . For instance, protein S deficiency has been reported in up to 73 per cent of HIV-infected men [25] . These abnormalities have been associated with thromboses involving veins and arteries and seem to be related to HAART regimens that include protease inhibitors [26],[27] . Thrombocytosis has been reported in 9 per cent of patients receiving HAART, with cardiovascular complications in up to 25 per cent of cases [28] .

Systemic arterial hypertension and renal disease: The prevalence of systemic arterial hypertension in HIV infected individuals had been estimated to be about 20-25 per cent before the introduction of HAART [29] . Arterial hypertension, even in agreement with the Adult Treatment Panel-III guidelines [30] , is currently considered part of HIV-associated lipodystrophy syndrome [31] . It appears to be related to protease inhibitors-induced lipodystrophy [32] and metabolic disorders, especially to elevated fasting triglyceride and insulin resistance [31],[33] . HIV-associated endothelial dysfunction and injury, autoimmune reaction to viral infection (vasculitis), and renal disease have been also hypothesized in the aetiopathogenesis of HIV-associated hypertension. HIV-associated renal impairment can present as acute or chronic kidney disease [34] . It can be caused directly or indirectly by HIV-1 and/or by drug-related effects that are directly nephrotoxic or lead to changes in renal function by inducing metabolic vasculopathy and renal damage. Antiretroviral agents such as indinavir and tenofovir have been found to be associated with nephrotoxic effects that were reversible in most cases [34] .

Peripheral vascular disease: The risk for peripheral vascular disease in HIV-infected patients receiving HAART has been evaluated by surrogate markers of atherosclerosis, such as the measurement of carotid intima-media thickness (cIMT) [35],[36],[37],[38] . There is a unanimous consensus on the increased prevalence of subclinical atherosclerosis in HIV-infected patients compared to the general population. Presumably, both HIV infection and HAART may promote atherosclerosis through mechanisms involving endothelial cells, either directly or indirectly via metabolic disorders. However, HAART should be considered as a strong, independent predictor for the development of subclinical atherosclerosis in HIV-infected patients, regardless of known major cardiovascular risk factors and atherogenic metabolic abnormalities induced by this therapy [35],[36],[37],[38] . The increased use of lipid-lowering agents, protease inhibitors-free HAART regimens, and the reduction of smoking may decrease cIMT in HIV-infected patients over time [39] . Markers of subclinical atherosclerosis should be carefully assessed in HIV-infected patients receiving HAART, especially in those with lipodystrophy.

Coronary artery disease: Prevalence of coronary artery disease in HIV-infected patients receiving HAART is widely debated [40],[41],[42],[43],[44],[45] . Differences in the study design, in the selection of the patients and in the statistical analyses of data, might explain this disparity. However, longer exposure to HAART and/or protease inhibitors seems to increase the risk of myocardial infarction. The results of the Data Collection on Adverse Events of Anti-HIV Drugs study showed that HAART therapy is associated with a 26 per cent relative risk increase in the rate of myocardial infarction per year of HAART exposure [43] . A recent analysis of the risk for myocardial infarction in relation to the exposure to specific antiretroviral drugs has shown that indinavir, lopinavir-ritonavir, didanosine and abacavir are associated with a more significant risk [45] . However, as with any observational study, these findings must be interpreted with caution (given the potential for confounding) and in the context of the benefits that these drugs provide [45] .


   Cardiovascular Risk Stratification In HIV-Infected Patients on HAART Top


For patients on HAART, it may be important to evaluate the traditional vascular risk factors and to try to intervene on those that can be modified. Existing guidelines for the management of dyslipidaemias in the general population, such as those of the National Cholesterol Education Program [30] , currently represent the basis for therapeutic recommendations in HIV-infected individuals as well, such as those reported by the HIV Medicine Association of the Infectious Disease Society of America and Adult AIDS Clinical Trial Groups [46] and by the Pavia Consensus Statement [47] . New insights in defining the cardiometabolic risk in patients with HAART-associated metabolic syndrome have been provided recently by the echocardiographic measurement of the epicardial adipose tissue [48] . Epicardial adipose tissue is the true visceral fat of the heart and is significantly correlated with abdominal visceral fat measured by magnetic resonance imaging. Given its potential as an easy and reliable marker of visceral fat, epicardial fat has been recently evaluated in patients with HIV- associated lipodystrophy syndrome. In these patients, echocardiographic epicardial fat correlated with intra-abdominal visceral fat, cIMT, and clinical parameters of the metabolic syndrome (especially, waist circumference, blood pressure, fasting glucose, fasting insulin, and markers of fatty liver disease) [49],[50],[51] . Taken together, these findings suggest that echocardiographic assessment of epicardial fat may have the potential to be a simple and reliable marker of visceral adiposity and increased cardiovascular risk in patients with HIV-associated lipodystrophy syndrome.


   Conclusions Top


The introduction of HAART in the developed countries has significantly reduced the prevalence of cardiomyopathy and pericardial effusion, which heavily influenced the prognosis of HIV-infected patients living in these countries in the pre-HAART period, and still influences the prognosis of HIV-infected patients living in developing countries. However, HIV-associated lipodystrophy syndrome and related cardiovascular risk in developed countries is an increasingly recognized clinical entity. The multifactorial pathogenesis of HIV-associated lipodystrophy syndrome represents an intriguing field of future basic and clinical research. Careful cardiac screening for patients who are being evaluated for, or who are receiving HAART regimens, is warranted according to the current clinical guidelines, with a close collaboration between cardiologists and infectious disease specialists.

 
   References Top

1.Barbarini G, Barbaro G. Incidence of the involvement of the cardiovascular system in HIV infection. AIDS 2003; 17 : S46-S50.  Back to cited text no. 1
    
2.Barbaro G, Di Lorenzo G, Grisorio B, Barbarini G and the Gruppo Italiano per lo Studio Cardiologico dei pazienti affetti da AIDS Investigators. Cardiac involvement in the acquired immunodeficiency syndrome. A multicenter clinical-pathological study. AIDS Res Hum Retroviruses 1998; 14 : 1071-7.  Back to cited text no. 2
    
3.Lewis W, Grupp IL, Grupp G, Hoit B, Morris R, Samarel AM, et al. Cardiac dysfunction in the HIV-1 transgenic mouse treated with zidovudine. Lab Invest 2000; 80 : 187-97.  Back to cited text no. 3
[PUBMED]    
4.Bristow MR, Mason JW, Billingham ME, Daniels JR. Doxorubicin cardiomyopathy : evaluation by phonocardiography, endomyocardial biopsy and cardiac catheterization. Ann Intern Med 1978; 88 : 168-75.  Back to cited text no. 4
[PUBMED]    
5.Brown DL, Sather S, Cheitlin MD. Reversible cardiac dysfunction associated with foscarnet therapy for cytomegalovirus esophagitis in an AIDS patient. Am Heart J 1993; 125 : 1439-41.  Back to cited text no. 5
[PUBMED]    
6.Bijl M, Dieleman JP, Simoons M, Van Der Ende ME. Low prevalence of cardiac abnormalities in an HIV-seropositive population on antiretroviral combination therapy. J AIDS 2001; 27 : 318-20.  Back to cited text no. 6
    
7.Twagirumukiza M, Nikeramihigo E, Seminega B, Gasakure E, Boccara F, Barbaro G. Prevalence of dilated cardiomyopathy in HIV-infected african patients not receiving HAART: a multicenter, observational, prospective, cohort study in Rwanda. Curr HIV Res 2007; 5 : 129-37.  Back to cited text no. 7
    
8.Beck MA, Kolbeck PC, Shi Q, Rohr LH, Morris VC, Levander OA. Increased virulence of a human enterovirus (coxackievirus B3) in selenium-deficient mice. J Infect Dis 1994; 170 : 351-7.  Back to cited text no. 8
[PUBMED]  [FULLTEXT]  
9.Hoffman M, Lipshultz SE, Miller TL. Malnutrition and cardiac abnormalities in the HIV-infected patients. In: Miller TL, Gorbach S, editors. Nutritional aspects of HIV infection. London: Arnold; 1999. p. 33-9.  Back to cited text no. 9
    
10.Nzuobontane D, Blackett KN, Kuaban C. Cardiac involvement in HIV-infected people in Yaounde,Cameroon. Postgrad Med J 2002; 78 : 678-81.  Back to cited text no. 10
[PUBMED]  [FULLTEXT]  
11.Ntsekhe M, Hakim J. Impact of human immunodeficiency virus infection on cardiovascular disease in Africa. Circulation 2005; 112 : 3602-7.  Back to cited text no. 11
[PUBMED]  [FULLTEXT]  
12.Klatt EC. Cardiovascular Pathology in AIDS. Adv Cardiol 2003; 40 : 23-48.  Back to cited text no. 12
[PUBMED]    
13.Barbaro G. Reviewing the clinical aspects of HIV-associated pulmonary hypertension. J Respir Dis 2004; 25 : 289-93.  Back to cited text no. 13
    
14.Sitbon O, Gressin V, Speich R, Mcdonald PS, Opravil M, Cooper DA, et al. Bosentan for the treatment of human immunodeficiency virus-associated pulmonary arterial hypertension. Am J Respir Crit Care 2004; 170 : 1212-7.  Back to cited text no. 14
    
15.Barbaro G, Lucchini A, Pellicelli AM, Grisorio B, Giancaspro G, Barbarini G. Highly active antiretroviral therapy compared with HAART and bosentan in combination in patients with HIV-associated pulmonary hypertension. Heart 2006; 92 : 1164-6.  Back to cited text no. 15
[PUBMED]  [FULLTEXT]  
16.Johnson RM, Little JR, Storch GA. Kawasaki-like syndromes associated with human immonodeficiency virus infection. Clin Infect Dis 2001; 32 : 1628-34.  Back to cited text no. 16
[PUBMED]  [FULLTEXT]  
17.Johnson RM, Barbarini G, Barbaro G. Kawasaki-like syndromes and other vasculitic syndromes in HIV-infected patients. AIDS 2003; 17 (S1):S77-S82.  Back to cited text no. 17
    
18.Shingadia D, Das L, Klein-Gitelman N, Chadwick E. Takayasu's arteritis in a human immunodeficiency virus-infected adolescent. Clin Infect Dis 1999; 29 : 458-9.  Back to cited text no. 18
    
19.Barbaro G. Vasculitic syndromes in HIV-infected patients. Adv Cardiol 2003; 40 : 185-96.  Back to cited text no. 19
[PUBMED]    
20.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.  Back to cited text no. 20
[PUBMED]  [FULLTEXT]  
21.Twu C, Liu QN, Popik W, Bukrinsky M, Sayre J, Roberts J, et al. Cardiomyocytes undergo apoptosis in human immunodeficiency virus cardiomyopathy through mitochondrion and death receptor-controlled pathways. Proc Natl Acad Sci USA 2002; 99 : 14386-91.  Back to cited text no. 21
    
22.Carr A, Samaras K, Burton S, Law M, Freund J, Chisholm DJ, et al. A syndrome of peripheral lipodystrophy, hyperlipidaemia and insulin resistance in patients receiving HIV protease inhibitors. AIDS 1998; 12 : F51-F58.  Back to cited text no. 22
[PUBMED]  [FULLTEXT]  
23.Carr A. HIV lipodystrophy: risk factors, pathogenesis, diagnosis and management. AIDS 2003; 17 (S1) : S141-8.  Back to cited text no. 23
    
24.Grinspoon S, Carr A. Cardiovascular risk and body-fat abnormalities in HIV-infected adults. N Engl J Med 2005; 352 : 48-62.  Back to cited text no. 24
[PUBMED]  [FULLTEXT]  
25.Hadigan C, Meigs JB, Rabe J, D'Agostino RB, Wilson PW, Lipinska I, et al. Increased PAI-1 and tPA antigen levels are reduced with metformin therapy in HIV-infected patients with fat redistribution and insulin resistance. J Clin Endocrinol Metab 2001; 86 : 939-43.  Back to cited text no. 25
[PUBMED]  [FULLTEXT]  
26.Witz M, Lehmann J, Korzets Z. Acute brachial artery thrombosis as the initial manifestations of human immunodeficiency virus infection. Am J Hematol 2000; 64 : 137-9.  Back to cited text no. 26
[PUBMED]  [FULLTEXT]  
27.Sullivan PS, Dworkin MS, Jones JL, Hooper WC. Epidemiology of thrombosis in HIV-infected individuals. The Adult/Adolescent Spectrum of HIV Disease Project. AIDS 2000; 14 : 321-4.  Back to cited text no. 27
[PUBMED]  [FULLTEXT]  
28.Miguez-Burbano MJ, Burbano X, Rodriguez A, Lecusay R, Rodriguez N, Shor-Posner G. Development of thrombocytosis in HIV+ drug users: impact of antiretroviral therapy. Platelets 2002; 13 : 183-5.  Back to cited text no. 28
[PUBMED]  [FULLTEXT]  
29.Aoun S, Ramos E. Hypertension in the HIV-infected patient. Curr Hyperten Rep 2000; 2 : 478-81.  Back to cited text no. 29
    
30.National Cholesterol Education Program (NCEP) Expert Panel on Detection EaToHBCiAATPI. Third Report of the National Cholesterol Education Program (NCEP) Expert Panel on Detection, Evaluation, and Treatment of High Blood Cholesterol in Adults (Adult Treatment Panel III) final report. Circulation 2002; 106 : 3143-421.  Back to cited text no. 30
    
31.Gazzaruso C, Bruno R, Garzaniti A, Giordanetti S, Fratino P, Sacchi P, et al. Hypertension among HIV patients: prevalence and relationship to insulin resistance and metabolic syndrome. J Hypertens 2003; 21 : 1377-82.  Back to cited text no. 31
[PUBMED]  [FULLTEXT]  
32.Crane H, Van Rompaey S, Kitahata M. Antiretroviral medications associated with elevated blood pressure among patients receiving highly active antiretroviral therapy. AIDS 2006; 20 : 1019-26.  Back to cited text no. 32
    
33.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.  Back to cited text no. 33
[PUBMED]  [FULLTEXT]  
34.Roling J, Schmid H, Fischereder M, Draenert R, Goebel FD. HIV-associated renal diseases and highly active antiretriviral therapy-induced nephropathy. Clin Infect Dis 2006; 42 : 1488-95.  Back to cited text no. 34
    
35.Maggi P, Serio G, Epifani G, Fiorentino G, Saracino A, Fico C, et al. Premature lesions of the carotid vessels in HIV-1-infected patients treated with protease inhibitors. AIDS 2000; 14 : F123-8.  Back to cited text no. 35
[PUBMED]  [FULLTEXT]  
36.Depairon M, Chessex S, Sudre P, Rodondi N, Doser N, Chave JP, et al. Premature atherosclerosis in HIV-infected individuals: focus on protease inhibitor therapy. AIDS 2001; 15 : 329-34.  Back to cited text no. 36
[PUBMED]  [FULLTEXT]  
37.Hsue PY, Lo JC, Franklin A, Bolger AF, Martin JN, Deeks SG, et al. Progression of atherosclerosis as assessed by carotid intima-media thickness in patients with HIV infection. Circulation 2004; 109 : 1603-8.  Back to cited text no. 37
[PUBMED]  [FULLTEXT]  
38.Currier JS, Kendall MA, Zackin R, Henry WK, Alston-Smith B, Torriani F, et al. Carotid artery intima-media thickness and HIV infection: traditional risk factors overshadow impact of protease inhibitor exposure. AIDS 2005; 19 : 927-33.  Back to cited text no. 38
    
39.Thiebaut R, Aurillac-Lavignole V, Bonnet F, Ibrahim N, Cipriano C, Neau D, et al. Change in atherosclerosis progression in HIV-infected patients: ANRS Aquitane Cohort, 1999-2004. AIDS 2005; 19 : 729-31.  Back to cited text no. 39
    
40.Barbaro G, Di Lorenzo G, Cirelli A, Grisorio B, Lucchini A, Hazra C, et al. An open-label, prospective, observational study of the incidence of coronary artery disease in patients with HIV receiving highly active antiretroviral therapy. Clin Ther 2003; 25 : 2405-18.  Back to cited text no. 40
[PUBMED]  [FULLTEXT]  
41.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.  Back to cited text no. 41
[PUBMED]  [FULLTEXT]  
42.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.  Back to cited text no. 42
[PUBMED]  [FULLTEXT]  
43.Friis-Moller N, Weber R, Reiss P, Thiebaut R, Kirk O, D'Arminio Monforte A, et al. Cardiovascular risk factors in HIV patients-association with antiretroviral therapy. Results from DAD study. AIDS 2003; 17 : 1179-93.  Back to cited text no. 43
    
44.Mary-Krause M, Cotte L, Simon A, Partisani M, Costagliola D and the 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.  Back to cited text no. 44
    
45.Worm SW, Sabin C, Weber R, Reiss P, El-Sadr W, Dabis F, et al. Risk of myocardial infarction in patients with HIV infection exposed to specific individual antiretroviral drugs from the 3 major classes: the data collection on adverse events of anti-HIV drugs (DAD) study. J Infect Dis 2010; 20 : 318-30.  Back to cited text no. 45
    
46.HIV Medicine Association of the Infectious Disease Society of America and the Adult AIDS Clinical Trial Groups. Guidelines for the Evaluation and Management of Dyslipidemia in Human Immunodeficiency Virus (HIV)-Infected Adults Receiving Antiretroviral Therapy: Recommendations of the HIV Medicine Association of the Infectious Disease Society of America and the Adult AIDS Clinical Trial Groups. Clin Infect Dis 2004; 37 : 613-27.  Back to cited text no. 46
    
47.Volberding P, Murphy R, Barbaro G, Barbarini G, Bruno R, Cirelli A, et al. The Pavia Consensus Statement. AIDS 2003; 17 (S1): S170-9.  Back to cited text no. 47
    
48.Barbaro G, Iacobellis G. Metabolic syndrome associated with HIV and highly active antiretroviral therapy. Curr Diab Rep 2009; 9 : 37-42.  Back to cited text no. 48
[PUBMED]    
49.Iacobellis G, Sharma AM, Pellicelli AM, Grisorio B, Barbarini G, Barbaro G. Epicardial adipose tissue is related to carotid intima-media thickness and visceral adiposity in HIV-infected patients with highly active antiretroviral therapy-associated metabolic syndrome. Curr HIV Res 2007; 5 : 275-9.  Back to cited text no. 49
[PUBMED]  [FULLTEXT]  
50.Iacobellis G, Pellicelli AM, Sharma AM, Grisorio B, Barbarini G, Barbaro G. Relation of subepicardial adipose tissue to carotid intima-media thickness in patients with human immunodeficiency virus. Am J Cardiol 2007; 99 : 1470-2.  Back to cited text no. 50
[PUBMED]  [FULLTEXT]  
51.Iacobellis G, Pellicelli AM, Grisorio B, Barbarini G, Leonetti F, Sharma AM, et al. Relation of epicardial fat and alanine aminotransferase in subjects with increased visceral fat. Obesity 2008; 16 : 179-83.  Back to cited text no. 51
[PUBMED]  [FULLTEXT]  



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    Abstract
   Introduction
    HIV-Associated C...
    HIV-Associated L...
    Cardiovascular R...
   Conclusions
    References

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