The Spectrum of Atherosclerotic Coronary Artery Disease in HIV Patients

Abstract

The incidence of HIV is on the rise. With the advent of antiretroviral therapy, the average life expectancy of HIV patients has increased by several decades, but the increasing life expectancy has shifted the spectrum of HIV-associated morbidity and mortality away from opportunistic infections and toward chronic medical conditions. In fact, coronary artery disease has become the leading cause of mortality in patients with HIV. The pathophysiology of atherosclerosis in patients with HIV is very complex, including direct endothelial damage from viremia, a heightened overall state of inflammation from immune activation, higher prevalence and contribution from traditional atherosclerotic risk factors, and direct effects from antiretroviral therapy itself. This review focuses on the patterns, predictors, and pathophysiology of atherosclerotic disease in patients with HIV. In addition, the risks and benefits of evidence-based highly active antiretroviral therapy are critically evaluated.

Analysis of the effects of HIV‐1 Tat on the survival and differentiation of vessel wall‐derived mesenchymal stem cells

“…Interestingly, the formation of atherosclerotic lesions can be accelerated by treatment with protease inhibitors (PIs) suggesting a complex scenario of atherosclerosis development in HIV-positive subjects [Carr et al, 1999]. Although the relationship between HIV infection and atherosclerosis enhancement is well understood [Hakeem et al, 2010], the mechanisms involved have not been clearly elucidated, although chronic inflammation and endothelial layer impairment have been related to atherosclerosis induction during the course of HIV infection. Indeed, HIV elicits chronic immune activation and systemic inflammation along with a disruption of the regulation of different cytokines [Barqasho et al, 2009] including IL-1, IL-6, M-CSF, IL-10, TNF-a, and RANKL that may affect the atherosclerosis genesis.…”

Early Atherosclerosis in HIV Infected Subjects on Suppressive Antiretroviral Treatment: Role of Osteoprotegerin

“…Cardiovascular disease (CVD) is an emerging and significant cause of morbidity and mortality in HIV-infected patients [1]. HIV itself and antiretroviral drugs may contribute to the increased risk of CVD.…”

The HIV-1 protease inhibitor nelfinavir activates PP2 and inhibits MAPK signaling in macrophages: a pathway to reduce inflammation

“…Although sCD14 levels remain significantly elevated compared with uninfected individuals [14], initiation of cART before decline in CD4 ϩ T cells below 25% reduces the extent of monocyte/macrophage activation in the post-therapy patient [14]. Despite suppression of plasma viral levels by cART, inflammation-associated comorbidities, including HIV-associated neurocognitive impairment [15][16][17][18][19][20], cardiovascular disease/coagulopathy [21][22][23][24], endothelial dysfunction [25], and cancer [26,27], continue to develop.…”