Obesity, a chronic inflammatory disease, is the most prevalent modifiable risk factor for cardiovascular disease. The mechanisms underlying inflammation in obesity are incompletely understood. Recent developments have challenged the dogma of immunological memory occurring exclusively in the adaptive immune system and show that the innate immune system has potential to be reprogrammed. This innate immune memory (trained immunity) is characterized by epigenetic and metabolic reprogramming of myeloid cells following endogenous or exogenous stimulation, resulting in enhanced inflammation to subsequent stimuli. Trained immunity phenotypes have now been reported for other immune and non-immune cells. Here, we provide a novel perspective on the putative role of trained immunity in mediating the adverse cardiovascular effects of obesity and highlight potential translational pathways. Obesity, a chronic inflammatory disorder, is the most prevalent modifiable risk factor for cardiovascular disease throughout the life-course; long-term outcomes following lifestyle interventions have generally been disappointing.Inhibition of inflammation has been shown to decrease cardiovascular risk in patients with a residual inflammatory risk.Recent studies have demonstrated that the innate immune system can adopt a long-term memory (trained immunity) after a previous encounter with a stimulus, resulting in an increased response upon secondary stimulation. Monocytes from patients with atherosclerosis have a trained immune phenotype.In obesity, a state of dyslipidemia, endotoxemia, and increased plasma cytokines and adipokines is likely to induce trained immunity.Non-immune cells can also be trained, indicating a possible role for adipocyte memory in chronic inflammation.