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De novo presentation of cardiovascular disease in HIV-infected patients

HIV affects a multitude of organ systems and tissues, and is known to upregulate inflammatory response pathways, particularly in patients who do not have access to combination anti-retroviral therapy (ART) [1]. For example, HIV-infected individuals often have lower protein C levels and elevated levels of markers for endothelial activation[2]. Protein C is a known anti-inflammatory, and anti-coagulant molecule; therefore, low levels may indicate an individual is at greater risk for cardiovascular disease and thrombosis[3]. Similarly, upregulation of endothelial activating factors is associated with increased risk of atherosclerosis and therefore increased risk of cardiovascular disease (CVD), and myocardial infarction (MI)[4]. Endocrine disruption is also associated with HIV infection, and may contribute to de novo manifestations of CVD1. Yet studies have also shown that prolonged use of highly active anti-retroviral therapy (HAART) also contributes to increased risk for coronary artery disease and MI [5],[6]. Use of combination anti-retroviral therapy, consisting of protease inhibitor drugs such as Indinavir, and nonnucleoside reverse-transcriptase inhibitor (NNRTI) drugs such as Nevirapine may increase lipid levels and LDL cholesterol levels[7]. Overtime, patients taking combination therapy may be at increased risk for developing atherosclerotic plaques, or experiencing an MI or stroke4. For example, researchers calculated a relative rate for MI of 1.16 per year of therapy, indicating a doubled risk of MI per five-year exposure[8]. The risk of HAART-associated CVD is highest in developed countries, since treatment is more widely available, and patients are surviving for longer periods of time[9]. Lengthened survival time is associated with a greater risk for developing co-morbidities such as vascular disease, diabetes, and/or overweight or obesity related syndromes[10]. However, several prevention methods exist to either reduce the incidence of CVD in HIV positive patients, or to improve disease-management. Lifestyle interventions along with pharmaceutical interventions are often preferred, although it depends on the health status of the patient and disease severity[11]. Diet and exercise are two of the most benign interventions, although individuals who have taken HAART for prolonged periods of time may also be placed on lipid-lowering drugs such as statins[12]. In contrast, HIV positive patients in the developing world often experience cardiac abnormalities that are characteristic of non-adherence to ARV therapy, and resulting infectious-disease syndromes. HIV-related cardiovascular disease in the developing world predominantly presents itself in the form of pericardial effusion, Pericarditis, and/or HIV-related cardiomyopathy[13]. HIV in South Africa alone affects more than 5 million people, and most are not able to receive combination therapy or HAART[14]. De novo presentations of CVD in developing countries of sub-Saharan Africa are therefore related either to HIV infection, or to cardiovascular manifestations of opportunistic infections[15]. One of the most common opportunistic infections is tuberculosis, which often results in pericardial effusion among moderate to severe cases[16]. Patients who are not prescribed HAART have high viral loads, and low CD4 counts, effectively increasing susceptibility to co-infection6. Individuals generally recover if combination therapy and appropriate antibiotics are administered[17]. While overall, HIV-related cardiomyopathies represent a low proportion of total cases of heart disease in the developing world, greater understanding is needed on the role of prolonged HAART and the risk of CVD[18]. As access improves in the developing world, and ARV medication is more readily prescribed, public health practionners and clinicians may observe an increase in HIV-related co-morbidities that are reflective of cases in developed nations[19].

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  1. ^ Ntsekhe, Mpiko and Bongani M. Mayosi (2009) Cardiac manifestations of HIV infection: an African Perspective Nature Clinical Practice Vol. 6 No. 2
  2. ^ Ntsekhe, Mpiko and Bongani M. Mayosi (2009) Cardiac manifestations of HIV infection: an African Perspective Nature Clinical Practice Vol. 6 No. 2
  3. ^ Vetrano, Stefania et al. (2011) Unexpected role of anticoagulant protein C in controlling epithelial barrier integrity and intestinal inflammation PNAS 10.1073 pp. 1-6.
  4. ^ Ross, Allison C. et al. (2009) Relationship between Inflammatory Markers, Endothelial Activation Markers, and Carotid Intima-Media Thickness in HIV-Infected Patients Receiving Antiretroviral Therapy HIV/AIDS Vol. 49 pp. 1119-11127.
  5. ^ Ntsekhe, Mpiko and Bongani M. Mayosi (2009) Cardiac manifestations of HIV infection: an African Perspective Nature Clinical Practice Vol. 6 No. 2
  6. ^ The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group (2007) Class of Antiretroviral Drugs and the Risk of Myocardial Infarction The New England Journal of Medicine Vol. 356 pp. 1723-1725.
  7. ^ The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group (2007) Class of Antiretroviral Drugs and the Risk of Myocardial Infarction The New England Journal of Medicine Vol. 356 pp. 1723-1725.
  8. ^ The Data Collection on Adverse Events of Anti-HIV Drugs (DAD) Study Group (2007) Class of Antiretroviral Drugs and the Risk of Myocardial Infarction The New England Journal of Medicine Vol. 356 pp. 1723-1725.
  9. ^ Jones-Parker, Hazel (2011) Primary, Secondary, and Tertiary Prevention of Cardiovascular Disease in Patients with HIV Disease: A Guide for Nurse Practitioners Journal of the Association of Nurses in AIDS Care pp. 1-10.
  10. ^ Jones-Parker, Hazel (2011) Primary, Secondary, and Tertiary Prevention of Cardiovascular Disease in Patients with HIV Disease: A Guide for Nurse Practitioners Journal of the Association of Nurses in AIDS Care pp. 1-10.
  11. ^ Jones-Parker, Hazel (2011) Primary, Secondary, and Tertiary Prevention of Cardiovascular Disease in Patients with HIV Disease: A Guide for Nurse Practitioners Journal of the Association of Nurses in AIDS Care pp. 1-10.
  12. ^ Jones-Parker, Hazel (2011) Primary, Secondary, and Tertiary Prevention of Cardiovascular Disease in Patients with HIV Disease: A Guide for Nurse Practitioners Journal of the Association of Nurses in AIDS Care pp. 1-10.
  13. ^ Sliwa, Karen et al. (2011) Contribution of the human immunodeficiency virus/acquired immunodeficiency syndrome epidemic to de novo presentations of heart disease in the Heart of Soweto Study cohort European Heart Journal Vol. 398 pp. 2-9.
  14. ^ Sliwa, Karen et al. (2011) Contribution of the human immunodeficiency virus/acquired immunodeficiency syndrome epidemic to de novo presentations of heart disease in the Heart of Soweto Study cohort European Heart Journal Vol. 398 pp. 2-9.
  15. ^ Sliwa, Karen et al. (2011) Contribution of the human immunodeficiency virus/acquired immunodeficiency syndrome epidemic to de novo presentations of heart disease in the Heart of Soweto Study cohort European Heart Journal Vol. 398 pp. 2-9.
  16. ^ Man Kim, Jong et al. (2011) Cardiac tamponade caused by tuberculosis Pericarditis in renal transplant recipients Journal of the Korean Surgical Society Vol. 80 pp. S40-S42.
  17. ^ Man Kim, Jong et al. (2011) Cardiac tamponade caused by tuberculosis Pericarditis in renal transplant recipients Journal of the Korean Surgical Society Vol. 80 pp. S40-S42.
  18. ^ Sliwa, Karen et al. (2011) Contribution of the human immunodeficiency virus/acquired immunodeficiency syndrome epidemic to de novo presentations of heart disease in the Heart of Soweto Study cohort European Heart Journal Vol. 398 pp. 2-9.
  19. ^ Sliwa, Karen et al. (2011) Contribution of the human immunodeficiency virus/acquired immunodeficiency syndrome epidemic to de novo presentations of heart disease in the Heart of Soweto Study cohort European Heart Journal Vol. 398 pp. 2-9.