Cardiac diseases in AIDS pathophysiology

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]; Associate Editor(s)-in-Chief: Raviteja Guddeti, M.B.B.S. [2]

Overview

Many observational studies have shown that HIV-infected patients are at an increased risk for developing a variety of cardiac diseases. With the introduction of HAART, longevity of HIV-infected patients increased, in turn leading to increased prevalence of cardiac and allied diseases. Inflammation and immune regulation leading to atherogenesis, endothelial dysfunction and coagulation abnormalities have been proposed as the major factors in the pathogenesis of cardiovascular diseases in AIDS. Compared to age-matched uninfected controls, HIV-infected patients have a higher risk of myocardial infarction (MI) and cardiovascular death, even with effective anti-retroviral therapy. Concerns have been raised about HAART by itself is associated with increased risk of peripheral (PAD) and coronary artery disease (CAD) [1].

Pathophysiology

Atherogenesis

Many observational studies have demonstrated an increased prevalence of subclinical atherosclerosis in HIV-infected patients. The pathology of subclinical atherogenesis is multifactorial and involves inflammation and immune dysregulation along with traditional risk factors like smoking, hypertension, dyslipidemia and diabetes mellitus (DM). Observational studies have shown that compared with uninfected controls, HIV-infected patients have higher intima media thickness (IMT), intra-luminal arterial plaque and coronary artery calcification resulting in increased over-all plaque burden [2][3][4][5]. Contributing factors for atherogenesis in HIV-infected patients include:

  • Active inflammation [6]
    • HIV infection is linked to elevated levels of several inflammatory markers like C-reactive protein (CRP), interleukin-6 (IL-6) etc.
    • Many studies have shown that elevated CRP is associated with increased risk of cardiovascular events.
    • In a small study, it was found that patients with HIV infection and elevated CRP levels have a four fold increased risk of MI compared with patients who have neither of them.
    • Elevated IL-6 levels are associated with HIV RNA viremia, CV events and all-cause mortality.
  • Endothelial dysfunction, as evident by elevated plasma markers like sICAM-1, sVCAM-1, E-selectin, tPAI-1, MPO and MMP9 [7][8]
  • Chronic viral co-infections

HIV drives inflammatory response via direct action by HIV RNA [9] and HIV-associated proteins like Tat and gp120 [10][11]. These proteins are known to promote endothelial dysfunction and apoptosis. It is a known fact that HIV inhibits T-cell responses, however, recent data indicate that HIV, as well as other viruses, induce changes via the activation of T cells into an immunosenescent and more atherogenic phenotype. In a study of 93 HIV infected and 37 uninfected subjects it was found that HIV-infected subjects had thicker carotid IMT compared to controls. It was also found that HIV patients had higher T-cell activation, hs-CRP levels, and CMV-specific T-cell responses and CMV-specific T-cell responses were independently associated with carotid intima media thickness [12][13].

Another mechanism by which HIV accelerates atherosclerosis is by causing alterations in cholesterol metabolism, resulting in redirection of cholesterol to extrahepatic tissues and impairment of cholesterol efflux from macrophages. This leads to accelerated foam cell formation, a characteristic feature of atherosclerosis [14].

Coagulation Abnormalities

Plasma levels of endothelial cell products like von Willebrand factor and soluble thrombomodulin, and D-dimer have been observed to be elevated in HIV-infected patients suggesting an increased risk of thrombosis [15][16]. A review of medical records involving 42,935 HIV patients stated that among HIV-infected individuals, clinically detected thrombosis is more common in those who have opportunistic illnesses, for whom megestrol acetate or indinavir have been prescribed, who have been hospitalized, and who are aged 45 years or older [17]. However, a recent study of 278 HIV-infected patients found that HIV infection is associated with decreased thrombin generation, as measured by the endogenous thrombin potential, and an increased antithrombin level [18].

These findings suggest an unclear association between HIV infection and increased propensity towards clotting.

Cardiac Diseases in AIDS

Cardiac manifestations of AIDS include:

Pericarditis

Pericardial disease is the most common clinical manifestation of cardiovascular disease in patients with AIDS with Mycobacterium tuberculosis being the major infectious cause [19][20]. However, majority of the cases of pericarditis are of unknown etiology. Other causes of pericarditis in AIDS include [21][22][23][24]:

Majority of the cases of pericarditis manifest as asymptomatic pericardial effusions. Larger effusions result in cardiac tamponade.

Myocardial Diseases

Major forms of myocardial diseases in patients with AIDS include [25][26]:

Focal myocarditis is more of an autopsy finding [27][28] and is caused by opportunistic infections like Cytomegalovirus, Coxsackie virus, Epstein-Barr virus [28], bacterial, fungal and protozoal infections. Since the introduction of HAART for AIDS the incidence of myocarditis has reduced considerably [29].

Clinical dilated cardiomyopathy is seen in 1-3% of patients with AIDS. It was proposed that HIV-associated cardiomyopathy may be related either to a direct action of HIV on the myocardial tissue or to an autoimmune process induced by HIV even in association with other cardiotropic viruses. In a prospective echocardiographic study in 296 HIV infected adults it was found that dilated cardiomyopathy was strongly associated with a CD4 cell count of < 100 x 10(6)/l [30]. In a study to assess the frequency of circulating cardiac specific autoantibodies in HIV positive patients with and without echocardiographic evidence of left ventricular dysfunction, it was found that anti-alpha myosin autoantibody (cardiac-specific antibody) concentrations were greater in HIV positive patients than in HIV negative controls, regardless of cardiac status [31]. This finding supports the role of cardiac autoimmunity in the pathogenesis of HIV related heart muscle disease.

Other factors that contribute to LV dysfunction and cardiomyopathy include [32][25]:

Freiberg et al. conducted a population-based, retrospective cohort study of HIV-infected and HIV-uninfected veterans enrolled in the Veterans Aging Cohort Study Virtual Cohort (VACS-VC) and the 1999 Large Health Study of Veteran Enrollees (LHS) to determine whether HIV infection is a risk factor for incident heart failure (HF). Data from the study suggested that ongoing viral replication is associated with a higher risk of developing HF [37].

Endocardial and Valvular Heart Diseases

Common endocardial diseases in patients with AIDS include:

  • Marantic endocarditis: Marantic endocarditis consists of sterile vegetations and is diagnosed at autopsy. The vegetations consist of platelets within a fibrin mesh with few inflammatory cells. It is clinically silent but may occasionally cause systemic embolization.
  • Infective endocarditis: Infective endocarditis (IE) in AIDS is almost always exclusively due to intravenous (IV) drug abuse. The most common culprit organism is Staphylococcus aureus and the most common valve involved is tricuspid valve [38] followed by mitral valve. Other causes include Streptocococcus pneumoniae, Haemophilus influenzae, Enterococci, gram negative rods, Candida albicans, Aspergillus fumigatus, Cryptococcus neoformans and other less common organisms [39].

With the introduction of HAART the incidence of both marantic endocarditis and infective endocarditis declined drastically and no cases of marantic endocarditis in AIDS patients have been reported since 1989.

Coronary Artery Disease

Many observational studies have shown that HIV infection is associated with increased risk of coronary artery disease (CAD) [40][41]. HIV infection by itself along with anti-retroviral regimens containing protease inhibitors have been stated to contribute to this increased risk [42][43]. Recent data from a large cohort study, to investigate whether HIV is associated with an increased risk of acute MI, suggest that HIV infection is associated with 50% increased risk of AMI [44].

Also, traditional risk factors like smoking, diabetes, dyslipidemia, obesity and sedentary lifestyle are common in patients with AIDS. Other possible causes include polyarteritis nodosa, Henoch-Schönlein purpura, drug-induced hypersensitivity vasculitis, Kawasaki-like syndrome and Takayasu arteritis [45][46].

Studies have shown that HAART regimens containing protease inhibitors are frequently associated with the development of lipid disorders. Protease inhibitors prevent viral replication by selectively binding to viral proteases (e.g. HIV-1 protease) and blocking proteolytic cleavage of protein precursors that are necessary for the production of infectious viral particles. Possible explanation for the development of lipid disorders is that the catalytic region of HIV-1 protease is homologous with regions of two human proteins that regulate lipid metabolism and administration of protease inhibitors leads to interference with these proteins resulting in lipid abnormalities [47][48]. Also, lipodystrophy (abnormal fat redistribution with lipoatrophy and/or lipohypertrophy) [49] and metabolic syndrome [50][51][52], that are seen commonly in HIV-infected patients, further contribute to increased risk of CAD.

Mechanisms by which HIV may promote CAD include:

Pulmonary Hypertension

Primary pulmonary hypertension is known to occurs in less than 0.5% of patients with HIV infection. Plexogenic arteriopathy has been described in most of these patients [59]. IV drug abusers are particularly prone to develop pulmonary hypertension [60][61][62]. HIV-related pulmonary hypertension should be suspected in any HIV-infected patient with unexplained dyspnea [63].

Hypertension

Elevated blood pressure (hypertension) has been reported frequently in patients with HIV infection and the frequency increased significantly after the introduction of HAART. HAART related metabolic syndrome is one possible explanation [64].

Arrhythmias

Long QT syndrome has been documented frequently in patients with AIDS, even in the absence of anti-retroviral therapy and the possible mechanisms include:

Cardiac Tumors

Tumors that involve the heart in patients with AIDS include:

Kaposi's sarcoma of the heart can involve the myocardium or the pericardium and can cause effusions. Large and severe effusions lead to tamponade. Autopsy findings may include extensive plaques, nodules or multilobular masses [65][66][21].

Cradiac lymphomas can be either secondary or primary, the former being more common than the latter [67]. Primary cardiac lymphoma, a type of non-Hodgkin lymphoma, is an extremely rare condition, although its incidence is more in immunosuppressed states like AIDS. The tumor is diffusely infiltrative and forms nodules and intracavitary masses [68][69]. These primary cardiac lymphomas usually involve the right atrium and can present with conduction disturbances[70], arrhythmias, superior vena cava obstruction or heart failure.

Aneurysms

HIV-infected and AIDS patients are predisposed to aneurysms, especially aortic and cerebral vasculature. Causes include HIV itself or opportunistic infections like CMV and tuberculosis. Aneurysms due to HIV virus are usually atypical and multiple [71].

References

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  2. ↑ Grunfeld C, Delaney JA, Wanke C; et al. (2009). "Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study". AIDS (London, England). 23 (14): 1841–9. doi:10.1097/QAD.0b013e32832d3b85. PMC 3156613. PMID 19455012. Unknown parameter |month= ignored (help)
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  55. ↑ Riddler SA, Smit E, Cole SR; et al. (2003). "Impact of HIV infection and HAART on serum lipids in men". JAMA : the Journal of the American Medical Association. 289 (22): 2978–82. doi:10.1001/jama.289.22.2978. PMID 12799406. Unknown parameter |month= ignored (help)
  56. ↑ Fisher SD, Miller TL, Lipshultz SE (2006). "Impact of HIV and highly active antiretroviral therapy on leukocyte adhesion molecules, arterial inflammation, dyslipidemia, and atherosclerosis". Atherosclerosis. 185 (1): 1–11. doi:10.1016/j.atherosclerosis.2005.09.025. PMID 16297390. Unknown parameter |month= ignored (help)
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  62. ↑ Pétureau F, Escamilla R, Hermant C, Mourlanette P, Berjaud J, Krempf M (1998). "[Pulmonary artery hypertension in HIV seropositive drug addicts. Apropos of 10 cases]". Revue Des Maladies Respiratoires (in French). 15 (1): 97–102. PMID 9551521. Unknown parameter |month= ignored (help)
  63. ↑ Le Houssine P, Karmochkine M, Ledru F; et al. (2001). "[Primary pulmonary hypertension in human immunodeficiency virus infection. Study of 9 cases amd review of the literature]". La Revue De Médecine Interne / Fondée ... Par La Société Nationale Francaise De Médecine Interne (in French). 22 (12): 1196–203. PMID 11794890. Unknown parameter |month= ignored (help)
  64. ↑ Sattler FR, Qian D, Louie S; et al. (2001). "Elevated blood pressure in subjects with lipodystrophy". AIDS (London, England). 15 (15): 2001–10. PMID 11600829. Unknown parameter |month= ignored (help)
  65. ↑ Stotka JL, Good CB, Downer WR, Kapoor WN (1989). "Pericardial effusion and tamponade due to Kaposi's sarcoma in acquired immunodeficiency syndrome". Chest. 95 (6): 1359–61. PMID 2721281. Unknown parameter |month= ignored (help)
  66. ↑ Chyu KY, Birnbaum Y, Naqvi T, Fishbein MC, Siegel RJ (1998). "Echocardiographic detection of Kaposi's sarcoma causing cardiac tamponade in a patient with acquired immunodeficiency syndrome". Clinical Cardiology. 21 (2): 131–3. PMID 9491957. Unknown parameter |month= ignored (help)
  67. ↑ Ioachim HL, Cooper MC, Hellman GC (1985). "Lymphomas in men at high risk for acquired immune deficiency syndrome (AIDS). A study of 21 cases". Cancer. 56 (12): 2831–42. PMID 3863692. Unknown parameter |month= ignored (help)
  68. ↑ Little RF, Gutierrez M, Jaffe ES, Pau A, Horne M, Wilson W (2001). "HIV-associated non-Hodgkin lymphoma: incidence, presentation, and prognosis". JAMA : the Journal of the American Medical Association. 285 (14): 1880–5. PMID 11308402. Unknown parameter |month= ignored (help)
  69. ↑ Constantino A, West TE, Gupta M, Loghmanee F (1987). "Primary cardiac lymphoma in a patient with acquired immune deficiency syndrome". Cancer. 60 (11): 2801–5. PMID 3677014. Unknown parameter |month= ignored (help)
  70. ↑ Nishikawa Y, Akaishi M, Handa S; et al. (1991). "A case of malignant lymphoma simulating acute myocardial infarction". Cardiology. 78 (4): 357–62. PMID 1889055.
  71. ↑ Nair R, Robbs JV, Naidoo NG, Woolgar J (2000). "Clinical profile of HIV-related aneurysms". European Journal of Vascular and Endovascular Surgery : the Official Journal of the European Society for Vascular Surgery. 20 (3): 235–40. doi:10.1053/ejvs.2000.1169. PMID 10986021. Unknown parameter |month= ignored (help)


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