Cellular senescence and the Senescence-Associated Secretory Phenotype (SASP) play both physiological and pathological roles in the cardiovascular system. While transient senescence aids regeneration, chronic accumulation of senescent cells promotes endothelial dysfunction, arterial stiffening, and maladaptive cardiac remodeling. This review elucidates the pivotal role of the immune system in senescent cell clearance and explores how immunosenescence drives systemic low-grade inflammation. Significant emphasis is placed on emerging pharmacological strategies, specifically senolytics and senomorphics, assessing their capacity to restore cardiac function and attenuate atherosclerosis. Additionally, the utility of molecular biomarkers and diverse in vitro and in vivo models is analyzed in the context of therapeutic efficacy. Ultimately, this article asserts that a comprehensive understanding of senescent-immune interactions is fundamental to the development of targeted, personalized interventions for age-related cardiovascular pathologies.