King's College London

Acute myocarditis is an inflammatory condition of the heart characterised by cellular injury and the influx of leucocytes, including neutrophils, monocytes, macrophages and lymphocytes. While this response is vital for tissue repair, excessive scar deposition and maladaptive ventricular remodelling can result in a legacy of heart failure. It is increasingly recognised as a clinical phenomenon due, in part, to increased availability of cardiac magnetic resonance imaging in patients presenting with chest pain in the absence of significant coronary artery disease. Emerging epidemiological evidence has associated myocarditis with poor outcomes in the context of left ventricular impairment, and even when the left ventricle is preserved outcomes are less benign than once thought. Despite this, our understanding of the contribution of the inflammatory response to the pathophysiology of acute myocarditis lags behind that of acute myocardial infarction, which is the vanguard cardiovascular condition for inflammation research. We recently reviewed monocyte and macrophage phenotype and function in acute myocardial infarction, concluding that their plasticity and heterogeneity might account for conflicting evidence from attempts to target specific leucocyte subpopulations. Here, we revise our understanding of myocardial inflammation, which is predominantly derived from myocardial infarction research, review experimental evidence for the immune response in acute myocarditis, focusing on innate immunity, and discuss potential future directions for immunotherapy research in acute myocarditis.