Cardiac diseases in AIDS pathophysiology: Difference between revisions
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** [[Hepatitis C virus]] | ** [[Hepatitis C virus]] | ||
HIV drives inflammatory response via direct action by HIV RNA and HIV-associated proteins like Tat and gp120. These proteins are known to promote endothelial dysfunction and apoptosis. | HIV drives inflammatory response via direct action by HIV RNA <ref name="pmid16224540">{{cite journal |author=Beignon AS, McKenna K, Skoberne M, ''et al.'' |title=Endocytosis of HIV-1 activates plasmacytoid dendritic cells via Toll-like receptor-viral RNA interactions |journal=[[The Journal of Clinical Investigation]] |volume=115 |issue=11 |pages=3265–75 |year=2005 |month=November |pmid=16224540 |pmc=1253628 |doi=10.1172/JCI26032 |url=}}</ref> and HIV-associated proteins like Tat and gp120. These proteins are known to promote endothelial dysfunction and apoptosis. | ||
===Coagulation Abnormalities=== | ===Coagulation Abnormalities=== | ||
Revision as of 22:10, 29 June 2013
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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.
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 [1][2][3][4]. Contributing factors for atherogenesis in HIV-infected patients include:
- Active inflammation [5]
- 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 [6][7]
- Chronic viral co-infections
HIV drives inflammatory response via direct action by HIV RNA [8] and HIV-associated proteins like Tat and gp120. These proteins are known to promote endothelial dysfunction and apoptosis.
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 [9][10]. 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 [11].
These findings suggest an unclear association between HIV infection and increased propensity towards clotting.
Cardiac Diseases in AIDS
Cardiac manifestations of AIDS include:
- Pericarditis
- Myocardial diseases (myocarditis, cardiomyopathy)
- Valvular heart disease
- Arrhythmias
- Coronary artery disease
- Cor pulmonale and pulmonary hypertension
References
- ↑ 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) - ↑ Lo J, Abbara S, Shturman L; et al. (2010). "Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men". AIDS (London, England). 24 (2): 243–53. doi:10.1097/QAD.0b013e328333ea9e. PMC 3154841. PMID 19996940. Unknown parameter
|month=ignored (help) - ↑ Fitch KV, Lo J, Abbara S; et al. (2010). "Increased coronary artery calcium score and noncalcified plaque among HIV-infected men: relationship to metabolic syndrome and cardiac risk parameters". Journal of Acquired Immune Deficiency Syndromes (1999). 55 (4): 495–9. doi:10.1097/QAI.0b013e3181edab0b. PMC 2974783. PMID 20720497. Unknown parameter
|month=ignored (help) - ↑ Pereyra F, Lo J, Triant VA; et al. (2012). "Increased coronary atherosclerosis and immune activation in HIV-1 elite controllers". AIDS (London, England). 26 (18): 2409–12. doi:10.1097/QAD.0b013e32835a9950. PMID 23032411. Unknown parameter
|month=ignored (help) - ↑ Subramanian S, Tawakol A, Burdo TH; et al. (2012). "Arterial inflammation in patients with HIV". JAMA : the Journal of the American Medical Association. 308 (4): 379–86. doi:10.1001/jama.2012.6698. PMID 22820791. Unknown parameter
|month=ignored (help) - ↑ Kristoffersen US, Kofoed K, Kronborg G, Giger AK, Kjaer A, Lebech AM (2009). "Reduction in circulating markers of endothelial dysfunction in HIV-infected patients during antiretroviral therapy". HIV Medicine. 10 (2): 79–87. doi:10.1111/j.1468-1293.2008.00661.x. PMID 19200170. Unknown parameter
|month=ignored (help) - ↑ Neuhaus J, Jacobs DR, Baker JV; et al. (2010). "Markers of inflammation, coagulation, and renal function are elevated in adults with HIV infection". The Journal of Infectious Diseases. 201 (12): 1788–95. doi:10.1086/652749. PMC 2872049. PMID 20446848. Unknown parameter
|month=ignored (help) - ↑ Beignon AS, McKenna K, Skoberne M; et al. (2005). "Endocytosis of HIV-1 activates plasmacytoid dendritic cells via Toll-like receptor-viral RNA interactions". The Journal of Clinical Investigation. 115 (11): 3265–75. doi:10.1172/JCI26032. PMC 1253628. PMID 16224540. Unknown parameter
|month=ignored (help) - ↑ Seigneur M, Constans J, Blann A; et al. (1997). "Soluble adhesion molecules and endothelial cell damage in HIV infected patients". Thrombosis and Haemostasis. 77 (4): 646–9. PMID 9134636. Unknown parameter
|month=ignored (help) - ↑ Armah KA, McGinnis K, Baker J; et al. (2012). "HIV status, burden of comorbid disease, and biomarkers of inflammation, altered coagulation, and monocyte activation". Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 55 (1): 126–36. doi:10.1093/cid/cis406. PMID 22534147. Unknown parameter
|month=ignored (help) - ↑ Hsue PY, Scherzer R, Grunfeld C; et al. (2012). "HIV infection is associated with decreased thrombin generation". Clinical Infectious Diseases : an Official Publication of the Infectious Diseases Society of America. 54 (8): 1196–203. doi:10.1093/cid/cis014. PMC 3309887. PMID 22438347. Unknown parameter
|month=ignored (help)