Acute viral myocarditis is the main cause of cardiac failure in young patients and accounts for up to 60% of "idiopathic" dilated cardiomyopathy. The clinical course of viral myocarditis is mostly insidious with limited cardiac inflammation and dysfunction. However, overwhelming inflammation may occur in a subset of patients, leading to fulminant cardiac injury, whereas others develop chronic heart failure due to autoimmune myocarditis. Today, little effective treatment exists for patients, apart from general supportive therapy and antifailure regimens. Urokinase-type plasminogen activator (u-PA) and matrix metalloproteinases (MMP) have been implicated in cardiac inflammation, matrix remodeling, and wound healing after cardiac injury. The present review will assess the mechanism by which these proteinases mediate cardiac dilatation, fibrosis, and dysfunction after cardiac stress or injury, in order to understand how inhibition of proteinases may provide a novel therapeutic tool to prevent cardiac dilatation and failure during viral myocarditis.