The article discusses the impact of HIV on cardiovascular disease (CVD), particularly atherosclerotic cardiovascular disease (ASCVD). People living with HIV (PLWH) have a 1.5- to 2-fold increased risk of developing CVD, despite effective antiretroviral therapy (ART). Chronic inflammation, driven by factors such as viral persistence, coinfections, and microbial translocation, contributes to this increased risk. Macrophages, which harbor latent HIV, play a crucial role in the inflammatory process by secreting cytokines like IL-6 and TNF-α, leading to endothelial dysfunction and immune cell recruitment. HIV also activates the NLRP3 inflammasome, enhancing IL-1β expression, and inhibits cholesterol efflux through ABCA1, promoting foam cell formation and plaque progression. The article highlights the role of both innate and adaptive immune cells, including monocytes, macrophages, T cells, and B cells, in the pathogenesis of ASCVD. It also discusses the impact of HIV-related factors such as clonal hematopoiesis of indeterminate potential (CHIP) and the potential of trained immunity in reprogramming innate immune cells. The review emphasizes the need for further research to understand and mitigate the residual inflammation and improve cardiovascular outcomes in PLWH.The article discusses the impact of HIV on cardiovascular disease (CVD), particularly atherosclerotic cardiovascular disease (ASCVD). People living with HIV (PLWH) have a 1.5- to 2-fold increased risk of developing CVD, despite effective antiretroviral therapy (ART). Chronic inflammation, driven by factors such as viral persistence, coinfections, and microbial translocation, contributes to this increased risk. Macrophages, which harbor latent HIV, play a crucial role in the inflammatory process by secreting cytokines like IL-6 and TNF-α, leading to endothelial dysfunction and immune cell recruitment. HIV also activates the NLRP3 inflammasome, enhancing IL-1β expression, and inhibits cholesterol efflux through ABCA1, promoting foam cell formation and plaque progression. The article highlights the role of both innate and adaptive immune cells, including monocytes, macrophages, T cells, and B cells, in the pathogenesis of ASCVD. It also discusses the impact of HIV-related factors such as clonal hematopoiesis of indeterminate potential (CHIP) and the potential of trained immunity in reprogramming innate immune cells. The review emphasizes the need for further research to understand and mitigate the residual inflammation and improve cardiovascular outcomes in PLWH.