LAUSR

Myocarditis is an inflammatory disease of the heart that is most commonly caused by a viral infection of the heart. Infections with cardiotropic viruses result in lymphocytic myocarditis (LM), characterized by infiltration in majority of lymphocytes into the heart, that can be accompanied by cardiomyocyte death, through virulence and/or the ensuing immune response.1 The pathological findings in autopsied hearts of LM patients are commonly subtle, with a patchy lymphocytic infiltrate and most often limited myocyte necrosis,2 and myocardium that has an overall normal morphological appearance. Knowledge regarding whether and how the viable morphologically normal myocardium is affected in LM is limited. We previously observed an increased presence of the stress response protein clusterin in the hearts of acute myocardial infarction patients.3 Herein, clusterin was not only present in necrotic cardiomyocytes but also in viable morphologically normal cardiomyocytes in the noninfarcted myocardium. Clusterin is a highly conserved glycoprotein found in most mammalian tissues and body fluids and has many biological functions, including chaperonelike functions,4 complement inhibition5 and apoptosis regulation.6 Moreover, cardiomyocytes were shown to express clusterin in response to ischemia and hypertrophic stimuli. Notably, the expression of clusterin was shown before in the hearts of mice with myosininduced autoimmune myocarditis.7 The aim of this study was to analyse the presence of clusterin in the hearts of LM patients with a special focus on the morphologically normal myocardium, and in the heart in time after during Coxsackievirus B3 (CVB3)induced myocarditis in mice.