Acute myocarditis: a diagnostic dilemma.

Myocarditis, an inflammatory process affecting the myocardium, may be caused by any bacterial, viral, rickettsial, mycotic, or parasitic organism. In Europe and in the United States, however, most cases of acute myocarditis seem to be caused by viruses. It is often difficult to prove the viral aetiology in cases of myocarditis and such cases are often referred to as idiopathic myocarditis. The Coxsackie B enterovirus is especially cardiotropic in man, although Coxsackie pericarditis is thought to be more common than Coxsackie myocarditis. Coxsackie virus infections commonly appear as epidemics, particularly in the summer and autumn. Coxsackie virus types BI to 5 and A4 and 16 are the strains most commonly implicated. The echovirus group of enteroviruses, especially types 9, 11, and 22, can also cause acute myopericarditis. Even when a causative organism is isolated it is often not known whether direct invasion and tissue damage by the infectious agent or a toxic, allergic, or hypersensitivity response to this agent is responsible for the clinical, electrophysiological, haemodynamic, and morphological manifestations of myocarditis.' Although raised titres of neutralising antibody in the serum may suggest viral myocarditis they are not necessarily diagnostic. Also viral particles have never been seen unequivocally in the myocardium except cytomegalovirus in immunocompromised hosts. The clinical diagnosis of myocarditis is difficult, if not impossible. For this reason, the incidence and course of the disease have not been established. Some published reports suggest that myocarditis improves when immunosuppressive agents are given; however, others suggest that steroid treatment may increase the adverse effects of myocarditis or even accelerate its course. If treatment is to be attempted accurate diagnosis