Traumatic brain injury (TBI) is increasingly recognized as a systemic disorder with consequences that extend beyond the central nervous system (CNS) to include clinically relevant cardiac dysfunction. Clinical and experimental evidence indicate that TBI is associated with arrhythmias, myocardial injury, autonomic imbalance, and impaired cardiac performance, even in the absence of primary cardiac disease. These observations support the concept of a brain-heart axis through which neural injury influences cardiovascular regulation. Current evidence shows that multiple interacting mechanisms contribute to cardiac abnormalities following TBI. Acute autonomic dysregulation, particularly sympathetic overactivation, is strongly supported as an early driver of cardiovascular instability, while neuroimmune and neuroendocrine responses may modulate the persistence and severity of downstream effects. Emerging evidence further suggests that cerebrovascular dysfunction may act as a modifier of neurocardiac vulnerability, although direct clinical evidence remains limited. At the myocardial level, processes including inflammatory signaling, oxidative stress, and mitochondrial dysfunction are associated with electrophysiologic instability and impaired contractile function. However, much of the mechanistic understanding derives from experimental models, and translation to human populations remains incomplete. Accordingly, cardiac involvement after TBI is best understood as a multifactorial and heterogeneous process rather than the consequence of a single dominant pathway. This review synthesizes current clinical and experimental evidence within an integrated framework, emphasizing the interplay among autonomic, immune, and vascular mechanisms. Improved understanding of these interactions may enhance risk stratification and support the development of targeted strategies to mitigate cardiovascular complications after TBI.