HIV-associated myocarditis may be defined as ‘‘a process characterized by a lymphocytic infiltrate of the myocardium with necrosis and/or degeneration of adjacent myocytes not typical of the ischemic damage associated with coronary artery disease in subjects infected by HIV with or without evidence of opportunistic infective agents’’ [1,2]. Myocarditis has been documented at autopsy in 40% to 52% of patients who died of AIDS before the introduction of highly active antiretroviral therapy (HAART). According to a 5-year clinical echocardiographic study performed by the Gruppo Italiano per lo Studio Cardiologico dei pazienti affetti da AIDS (GISCA) [1], involving 952 HIV-infected patients, myocarditis had a prevalence of 8% (76 of 952) with an annual incidence of left ventricular dysfunction of 1.5%. In the GISCA autopsy series histologic diagnosis of myocarditis was made in 30 (37%) of 82 patients with cardiac involvement [2]. Of 12 autopsy patients with dilated cardiomyopathy, 10 (83%) had active myocarditis at histologic examination [2]. These data are in agreement with those previously reported by Herskowitz and coworkers [3], who detected myocarditis in endomyocardial biopsy specimens from 15 (40%) of 37 patients with symptomatic left ventricular dysfunction. Although there is no evidence from prospective studies to suggest that HAART has a beneficial effect on HIV-associated myocarditis, some retrospective studies suggest that by improving the immunologic state of the patients and reducing the incidence of opportunistic infections, HAART might reduce the incidence of myocarditis by about 33% [4,5]. The median incidence of HIV-associated myocarditis is increasing in developing countries (about 32%), however, where the availability of HAART is limited and the pathogenetic impact of nutritional factors is greater [6]. Pathology