Abstract
The development of HIV related pulmonary arterial hypertension (PAH) reduces the probability of survival by half as compared with HIV-infected individuals without HIV related PAH. HIV infected patients have a greater incidence of PAH compared to general population and have a 2500-fold increased risk of developing PAH. It is therefore important to have a recent overview of the problem in Africa, the most HIV affected part of the world (70 % of all HIV infection in the world). First, we discussed the epidemiology of HIV-related PAH in Africa. Second, the current understanding of the HIV-related PAH pathogenesis has been covered. Third, role of highly active antiretroviral therapy on HIV-related PAH has been revisited. There are few data concerning epidemiology of HIV related pulmonary hypertension in Africa leading to necessity to conduct further prospective large studies. The prevalence of PAH among HIV infected people in Africa varies from 5 to 13 %. The prevalence of HIV-related PAH in Africa is notably high compared to those in developed countries and in general population. The pathogenesis of PAH is clearly complex, and probably results from the interaction of multiple modulating genes with environmental factors. The physiopathology includes cytokines secretion increase which induces dysregulation of endothelial and vascular smooth muscle cell growth and imbalance of endogenous vasodilators and constrictors; HIV viral proteins which induces vascular oxidative stress, smooth myocyte proliferation and migration, and endothelial injury and genetic predisposition due to some major histocompatibility complex alleles, particularly HDL-DR6 and HLA-DR5. Histologically, HIV related PAH has the same characteristics with other types PAH. Antiretroviral therapy have a beneficial effect on the outcome of HIV related pulmonary hypertension, but it lacks evidence from large prospective studies.
Highlights
Pulmonary hypertension (PH) is defined as mean pulmonary arterial pressure ≥25 mmHg on right heart catheterization at rest [1]
The mechanism is not directly due to the action of the virus because attempts to localize the virus in the vascular lesions or endothelial cells of affected patients have been unsuccessful [15], suggesting that a direct role of the virus is unlikely, and indicating that the underlying mechanism in pulmonary arterial hypertension associated with human immunodeficiency virus (HIV) is related to the indirect action of infection, possibly through the action of viral proteins and chronic inflammation cytokines mediated due to HIV infection
As demonstrated in a cross sectional study, detectable plasma HIV-RNA was associated with the risk to develop pulmonary arterial hypertension (PAH) [11]. This suggests that the use of highly active antiretroviral therapy (HAART), whose aim is to prevent the multiplication of HIV and make undetectable viral load; could reduce the risk of developing PAH in patients infected with HIV
Summary
Pulmonary hypertension (PH) is defined as mean pulmonary arterial pressure (mPAP) ≥25 mmHg on right heart catheterization at rest [1]. The classification of PH involves five groups: pulmonary arterial hypertension (PAH) which includes human immunodeficiency virus (HIV) related PH, PH due to left heart diseases,. As demonstrated by a study, echocardiographic assessment of pulmonary arterial pressure was inaccurate in 19.7 % of patients compared to right heart catheterization [14]. The mechanism is not directly due to the action of the virus because attempts to localize the virus in the vascular lesions or endothelial cells of affected patients have been unsuccessful [15], suggesting that a direct role of the virus is unlikely, and indicating that the underlying mechanism in pulmonary arterial hypertension associated with HIV is related to the indirect action of infection, possibly through the action of viral proteins and chronic inflammation cytokines mediated due to HIV infection. These growth factors and cytokines can lead to dysregulation of endothelial and vascular smooth muscle cell growth and imbalance of endogenous
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