Abstract
Heart and vascular complications now rank among the leading health threats facing individuals with HIV, a reality that continues even when modern drug regimens successfully silence viral replication. Sustained immune system overdrive and persistent low-grade systemic inflammation appear central to this heightened vulnerability. This narrative review integrates current understanding of how inflammatory signaling molecules, particularly interleukins, connect to heightened cardiovascular danger in HIV-positive populations, while exploring mechanistic underpinnings, cohort-derived evidence, and prospective treatment possibilities. Elevated concentrations of proinflammatory messengers such as IL-6 and IL-18, alongside indicators of myeloid cell activation including sCD14 and sCD163, characterize the HIV-positive state and independently forecast arterial disease progression, clinical cardiac events, and shortened survival. Notably, this inflammatory signature endures despite pharmacologically induced viral quiescence. Disturbances in protective lipoprotein function, heightened clotting propensity, and leakage of gut-derived bacterial components into the bloodstream each amplify vascular injury. Inflammatory cytokines occupy a central position in HIV-associated cardiovascular pathobiology, serving dual roles as disease predictors and candidate treatment targets. Importantly, recent evidence from the REPRIEVE randomized clinical trial demonstrated that pitavastatin therapy reduced major adverse cardiovascular events by approximately 35% in people living with HIV receiving antiretroviral therapy, highlighting inflammation-modulating strategies as a new foundation of cardiovascular prevention in this population.