Myocarditis and pericarditis--old questions and new answers

Old questions in diagnosis, pathophysiology, aetiology, pathogenesis and treatment of inflammatory heart diseases are manyfold. However, with the availability of the new techniques and tools from molecular biology, immunology and virology many of the basic questions should be revisited e.g.: 1. Which is the role of the aetiopathogenetic agent, most probably a cardiotropic virus, in the initiation of myocarditis? 2. Which is the role of DNA-viruses and cytomegalovirus in particular in the initiation and progression of myocardial disease? Are there connections to small vessel alterations or myocarditis? 3. What is the role in the chronic state, when it can no longer be recovered as an active viral particle from myocardial tissue but may be still detectable by in situ-hybridization possibly as a defective virus or mutant? 4. Is autoreactive heart muscle disease still an attractive hypothesis by which one can explain the development of dilated heart muscle disease as its end-stage manifestation? Which role can be attributed to T cells, granulocytes and macrophages that we detect by monoclonal antibodies in the endomyocardial or epicardial biopsies of patients with suspected myocarditis or perimyocarditis? Which role can be attributed to autoreactive anticardiac antibodies, whose cytotoxic or cytolytic properties we can assess in vitro? 5. Are there new investigative tools available apart from those listed above to permit a better classification of pericardial disease in particular? 6. Should our therapeutic repertoire not be supplemented by drugs, that interfere directly with the pathogenetic inflammatory mechanisms, that we can identify today, apart from conventional antiphlogistic therapy or steroid treatment? Today to all these questions a positive answer can be given.(ABSTRACT TRUNCATED AT 250 WORDS)