From an aetiological standpoint, viral cardiomyopathy represents an uncommon subtype of non-inflammatory dilated cardiomyopathy. The most common aetiologic agents are enteroviruses, adenoviruses and erythroviruses. Pathogenesis depends on the causative virus. Enteroviruses and adenoviruses infect and injure the cardiomyocyte through cytopathic effect and immune-mediated damage leading to cardiac remodelling, myocarditis and ultimately cardiomyopathy. Erythroviruses infect and injure the vascular endothelial cells resulting in macrovascular dysfunction. Typical clinical presentation is heart failure, arrhythmias and chest pains. Clinical diagnosis requires the presence of electrocardiographic abnormalities, markers of myocardial necrosis or evidence of functional/structural ventricular abnormalities accompanied by at least one physical sign or clinical symptom. However, endomyocardial biopsy remains the reference standard but increased risks of complications and the need for highly experienced operators limits its widespread use. The available clinical management strategies are standard heart failure medication for the management of cardiac dysfunction and antiarrhythmic drugs for those with ventricular arrhythmias. Patients with refractory symptoms greater than six months despite optimal medical therapy and with biopsy-proven virus negative myocardium may benefit from supplementary immunosuppressive therapy. However, largescale and long-term prospective randomized clinical trials are warranted to determine long-term benefits of immunosuppression.