Cardiac diseases in AIDS pathophysiology: Difference between revisions
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===Atherogenesis=== | ===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 <ref name="pmid19455012">{{cite journal |author=Grunfeld C, Delaney JA, Wanke C, ''et al.'' |title=Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study |journal=[[AIDS (London, England)]] |volume=23 |issue=14 |pages=1841–9 |year=2009 |month=September |pmid=19455012 |pmc=3156613 |doi=10.1097/QAD.0b013e32832d3b85 |url=}}</ref>. Contributing factors for atherogenesis in HIV-infected patients include: | 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 <ref name="pmid19455012">{{cite journal |author=Grunfeld C, Delaney JA, Wanke C, ''et al.'' |title=Preclinical atherosclerosis due to HIV infection: carotid intima-medial thickness measurements from the FRAM study |journal=[[AIDS (London, England)]] |volume=23 |issue=14 |pages=1841–9 |year=2009 |month=September |pmid=19455012 |pmc=3156613 |doi=10.1097/QAD.0b013e32832d3b85 |url=}}</ref><ref name="pmid19996940">{{cite journal |author=Lo J, Abbara S, Shturman L, ''et al.'' |title=Increased prevalence of subclinical coronary atherosclerosis detected by coronary computed tomography angiography in HIV-infected men |journal=[[AIDS (London, England)]] |volume=24 |issue=2 |pages=243–53 |year=2010 |month=January |pmid=19996940 |pmc=3154841 |doi=10.1097/QAD.0b013e328333ea9e |url=}}</ref>. Contributing factors for atherogenesis in HIV-infected patients include: | ||
* Active inflammation | * Active inflammation | ||
** HIV infection is linked to elevated levels of several inflammatory markers like C-reactive protein (CRP), [[interleukin]]-6 (IL-6) etc. | ** HIV infection is linked to elevated levels of several inflammatory markers like C-reactive protein (CRP), [[interleukin]]-6 (IL-6) etc. | ||
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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]. Contributing factors for atherogenesis in HIV-infected patients include:
- Active inflammation
- 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
- Chronic viral co-infections
Coagulation Abnormalities
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)