Myocardial inflammation comes of age

Life expectancy has steadily increased over the past century, as has the occurrence of age-related diseases, most notably myocardial diseases. Aging is often accompanied by increased low-grade chronic inflammation, accumulation of terminally differentiated T-cells poised with proinflammatory phenotypes, and clonal hematopoiesis. These systemic alterations have been consistently shown to impact myocardial physiology, individual susceptibility to heart diseases and long-term heart disease prognosis. In recent years, progress has been made in understanding the interindividual (cross-sectional) and intraindividual (longitudinal) variability in the global immunosenescence profile, and novel immune-aging metric-based scoring systems bearing potential to predict cardiovascular events have emerged. We herein suggest that monitoring the patients’ individual immunosenescence trajectories, in addition to the classic cardiological work-up, could provide valuable diagnostic/prognostic information. Similarly, we propose that basic research in cardio-immunology could attain a deeper mechanistic understanding of age-related diseases and a more meaningful translational impact if the ‘aging context’ was embraced more systematically.