Inflammatory cardiomyopathy is a condition that is characterised by the presence of inflammatory cells in the myocardium, which can lead to a significant deterioration in cardiac function. The etiology of this condition involves multiple factors, both infectious and non-infectious causes. While it is primarily associated with viral infections, other potential causes include bacterial, protozoal, or fungal infections, as well as a wide variety of toxic substances and drugs, and systemic immune-mediated pathological conditions. In spite of comprehensive investigation, the presence of inflammatory cardiomyopathy accompanied by left ventricular dysfunction, heart failure or arrhythmia is indicative of an unfavourable outcome. The reasons for the occurrence of either favourable outcomes, characterised by the absence of residual myocardial injury, or unfavourable outcomes, marked by the development of dilated cardiomyopathy, in patients afflicted by the condition remain to be elucidated. The relative contributions of pathogenic agents, genomic profiles of the host, and environmental factors in disease progression and resolution remain subjects of ongoing discourse. This includes the determination of which viruses function as active inducers and which merely play a bystander role. It remains unknown which changes in the host immune profile are critical in determining the outcome of myocarditis caused by various viruses, including coxsackievirus B3 (CVB3), adenoviruses, parvoviruses B19 and SARS-CoV-2. The objective of this review is unambiguous: to provide a concise summary and comprehensive assessment of the extant evidence on the pathogenesis, diagnosis and treatment of myocarditis and inflammatory cardiomyopathy. Its focus is exclusively on virus-induced and virus-associated myocarditis. In addition, the extant lacunae of knowledge in this field are identified and the extant experimental models are evaluated, with the aim of proposing future directions for the research domain. This includes differential gene expression that regulates iron and lipid and metabolic remodelling. Furthermore, the current state of knowledge regarding the cardiovascular implications of severe acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infection is also discussed, along with the open questions that remain to be addressed.