Pathophysiology and management of HIV-associated atherosclerotic cardiovascular disease

Schematic representation of the effects of HIV infection (in rounded rectangles) and the available strategies (in rectangles), as well as approaches under investigation (in octagons), for reducing the risk of atherosclerotic cardiovascular disease (ASCVD) and chronic inflammation in this patient population. In the setting of HIV infection, the increased microbial translocation from the gut, the continued HIV viral replication and the HIV-induced immunodeficiency, along with traditional ASCVD risk factors, contribute to immune cell activation and chronic inflammation. HIV-specific interventions to reduce the risk of ASCVD include strategies targeted at co-infections (such as Cytomegalovirus [CMV] infection), use of newer antiretroviral therapies (ARTs) and intensification of ART. Strategies aimed at eradicating the HIV infection are under investigation. Treatments targeting traditional ASCVD risk factors, such as hypertension, diabetes mellitus, smoking and metabolic syndrome, are also critical for reducing the risk of ASCVD in patients with HIV infection. Use of anticoagulants, beta-blockers, angiotensin-converting enzyme (ACE) inhibitors and LDL cholesterol (LDL-C)-lowering agents (such as statins and PCSK9 inhibitors) reduce the risk of ASCVD in patients with cardiovascular disease without HIV infection and might, therefore, be useful in reducing the risk of HIV-associated ASCVD. Finally, strategies to lower inflammation, such as canakinumab, which has been reported to reduce cardiovascular events significantly in a non-HIV patient population, might also reduce the risk of HIV-associated ASCVD.