Dilated cardiomyopathy (DCM) is a common cause of congestive heart failure and commonly occurs in the setting of autoimmune cardio-inflammatory processes. Consistent with this notion myocardial damage and dilatory remodeling consistent with DCM occurs upon adoptive transfer of T cell subsets reactive to self-antigens abundantly expressed in cardiac tissue. In this review we discuss etiologic mechanisms by which cardio-destructive T cells are generated during T cell ontogeny, and we review accumulated work identifying myocardial-derived T cell epitopes. Additionally, we describe several possible mechanisms whereby autoimmune T cell responses are sustained during chronic DCM. Epitope spreading, intra-cardiac persistence of pathogen-derived proteinaceous determinants, and generation of long-lived memory T cells are discussed as putative processes operative in the chronic maintenance of DCM.