Myocardial inflammation can lead to lethal acute or chronic heart failure (HF). T lymphocytes (T cells), have been reported in the inflamed heart in different etiologies of HF, and more recent studies support that different T-cell subsets play distinct roles in the heart depending on the inflammation-triggering event. T cells follow sequential steps to extravasate into tissues, but their specific recruitment to the heart is determined by several factors. These include differences in T-cell responsiveness to specific chemokines in the heart environment, as well as differences in the expression of adhesion molecules in response to distinct stimuli, which regulate T-cell recruitment to the heart and have consequences in cardiac remodeling and function. This review focuses on recent advances in our understanding of the role T cells play in the heart, including its critical role for host defense to virus and myocardial healing postischemia, and its pathogenic role in chronic ischemic and nonischemic HF. We discuss a variety of mechanisms that contribute to the inflammatory damage to the heart, as well as regulatory mechanisms that limit the magnitude of T-cell-mediated inflammation. We also highlight areas in which further research is needed to understand the role T cells play in the heart and distinguish the findings reported in experimental animal models and how they may translate to clinical observations in the human heart.