Persistent Organic Pollutants (POPs) are a group of toxic chemicals that persist in the environment and accumulate in living organisms, posing significant risks to human health. Among these pollutants, polychlorinated biphenyls (PCBs), dioxins, polybrominated diphenyl ethers (PBDEs), and per- and polyfluoroalkyl substances (PFAS) have been identified as major contributors to cardiovascular diseases (CVD). These compounds, primarily entering the human body through food, water, and consumer products, cause adverse effects by inducing oxidative stress, inflammation, and endocrine disruption. Oxidative stress and inflammation are key mechanisms underlying cardiovascular damage, leading to conditions such as hypertension, atherosclerosis, and ischemic heart disease. Additionally, these pollutants interfere with lipid metabolism and alter gene expression, further exacerbating cardiovascular risk. Epidemiological studies have highlighted the link between POP exposure and CVD, although the long-term, cumulative effects remain poorly understood, especially regarding PFAS. The molecular mechanisms by which different POPs affect the cardiovascular system are still under investigation, with particular focus on how they disrupt lipid metabolism and hormone signaling. Despite significant progress in understanding their individual effects, the combined impact of multiple POPs, as well as their interaction with genetic and other environmental factors, is less explored. Future research should prioritize longitudinal studies to clarify causal relationships and explore potential synergistic effects of POPs mixtures. Improved regulatory measures and safer alternatives to POPs-containing products are essential to mitigate the health risks associated with these persistent pollutants.