T lymphocytes are increasingly recognized as central regulators of cardiac inflammation, contributing to both tissue repair and disease progression across conditions such as myocardial infarction, heart failure, and myocarditis. While traditionally viewed as transient responders to injury, emerging evidence indicates that cardiac T cell responses are often antigen-driven, clonally expanded, and sustained over time. In particular, α-myosin heavy chain (α-MyHC, encoded by MYH6) has emerged as a dominant cardiac autoantigen capable of eliciting pathogenic T cell responses in both experimental models and human disease. In parallel, tissue-resident memory T cells (Trm) have been established as a distinct population of memory T cells that persist within non-lymphoid tissues and provide rapid, localized responses upon antigen re-exposure. Although extensively studied in non-lymphoid and barrier tissues, Trm are now increasingly implicated in chronic inflammatory and autoimmune diseases, where they can act as long-lived reservoirs of antigen-experienced T cells. Here, we propose that cardiac injury seeds antigen-specific T cell populations that acquire tissue-resident phenotypes within the myocardium, thereby linking acute immune activation to chronic, relapsing inflammation. We first review the role of T cells in cardiac homeostasis, aging, and disease, highlighting features of antigen specificity, persistence, and local adaptation. We then outline the defining characteristics and developmental pathways of Trm and integrate emerging evidence for their presence and function in the heart. Particular emphasis is placed on α-MyHC-specific Trm as potential drivers of cardiac autoimmunity and immune-related adverse events of cancer immunotherapies, including immune checkpoint inhibitor-associated myocarditis. Finally, we discuss the implications of this framework for understanding chronic cardiac inflammation and for developing therapeutic strategies targeting tissue-resident immune populations.