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HISTORY AND CLINICAL FINDINGS Two days before admission a 22-year-old woman developed general fatigue, nausea, headache and retrosternal pain. Physical examination was unremarkable. INVESTIGATIONS Erythrocyte sedimentation rate was increased to 20/48, C-reactive protein to 3.3 mg/dl, and there was evidence of myocardial damage (creatine kinase 609 U/l, creatine kinase-MB 42 U/l, troponine T 8.39 ng/ml); ST-segment elevations in I, II, III, aVF and V-V6 of the ECG. Echocardiography revealed clearly thickened myocardium, moderate but haemodynamically not significant pericardial effusion, as well as impaired left ventricular function. Antimyosin scintigraphy was very abnormal. Cardiac catheterization confirmed the left ventricular dysfunction, rise of left ventricular enddiastolic pressure to 17 mm Hg, and a markedly reduced cardiac output of 2.4 l/min. Myocardial biopsy showed severe myocarditis with marked myocytolysis and considerable lymphocytic infiltrations. Enteroviral RNA was demonstrated in the myocardium by polymerase chain reaction. TREATMENT AND COURSE The haemodynamics became normal within only 3 days. Myocardial biopsy after 6 months was unremarkable histologically and immunohistologically, and left ventricular function was also normal. However, while after a further 12 months myocardial biopsy remained normal and no virus was demonstrated, there was definite, though moderate, impairment in left ventricular function, indicating a dilated cardiomyopathy. INTERPRETATION Even when histological and immunohistological evidence of healing of an acute viral myocarditis has been achieved, with complete normalization of left ventricular function, a dilated cardiomyopathy may subsequently develop. The pathophysiological mechanism of this occurrence remains unknown.

Grundproblematik und Fragestellung: Die Ergebnisse der routinemasig eingesetzten Laboruntersuchungen zum Nachweis eines Myokardschadens sind bei Patienten mit klinischem Verdacht auf Myokarditis haufig negativ. Mit der vorliegenden Studie wurde untersucht, ob durch Bestimmung von kardialem Troponin T (cTnT) bei diesen Patienten ein myokardialer Zelluntergang sensitiv nachgewiesen werden kann, inwieweit dies mit den Befunden der Endomyokardbiopsate ubereinstimmt und ob durch eine cTnT-Bestimmung eine nicht-invasive Verlaufskontrolle der Myokarditis moglich ist. Patienten und Methodik: Es wurden 80 Patienten (52 Manner, 28 Frauen) mit dem klinischen Verdacht auf eine Myokarditis konsekutiv untersucht. Als klinisch fuhrende Symptome bestanden bei den Patienten eine Herzinsuffizienz (n = 45), Angina pectoris (n = 25) oder Herzrhythmusstorungen (n = 10). Die Symptomatik hatte sich bei der Mehrzahl der Patienten in zeitlichem Zusammenhang mit einem viralen Infekt entwikkelt. Eine koronare Herzkrankheit war bei allen Patienten durch eine Koronarangiographie ausgeschlossen worden. Die vom interventrikularen Septum entnommenen Endomyokardbiopsate wurden histologisch und immunhistologisch aufgearbeitet. cTnT wurde mit einem hochsensitiven Sandwich-Immunoassay bestimmt. Ergebnisse: Erhohte cTnT-Spiegel (> 0,1 ng/ml) wurden bei 28/80 Patienten (35 %) nachgewiesen. Histologisch konnte nur bei funf Patienten eine Myokarditis diagnostiziert werden, immunhistologisch zeigte sich jedoch eine Myokarditis bei 26/28 (93 %) Patienten mit erhohtem cTnT-Spiegel sowie ebenfalls bei 23/52 (44 %) Patienten mit normalen cTnT-Spiegeln. Bei Patienten einer Myokarditis mit nur kurzer Anamnesedauer war der cTnT-Spiegel haufiger erhoht als bei Patienten mit einer langeren Anamnesedauer. Nach 6 Monaten waren die cTnT-Spiegel nur noch bei vier von 28 Patienten mit einer Myokarditis erhoht, die Myokardbiopsate zeigten jedoch eine persistierende Myokarditis bei 14 Patienten. Folgerungen: Durch Bestimmung von cTnT ist sehr sensitiv ein Nachweis einer myokardialen Zellschadigung bei Patienten mit klinischem Verdacht auf eine Myokarditis moglich. Durch die immunhistologische Analyse der Myokardbiopsate kann hierbei haufig auch bei histologisch unauffalligem Befund eine Myokarditis diagnostiziert werden. Die Sensitivitat der cTnT-Bestimmung fur die Diagnostik einer Myokarditis ist am hochsten, wenn die Patienten bereits kurz nach Beginn der Symptomatik untersucht werden. Background and objective: Results of routine laboratory tests for demonstrating myocardial damage in patients suspected of having myocarditis are often negative. This study was undertaken to ascertain (1) whether measuring Tropinin T (cTnT) in these patients can sensitively determine myocardial cell death, (2) to what extent this correlates with the findings of endomyocardial biopsy, and (3) whether measurement of cTnT can provide noninvasive assessment of the course of myocarditis. Patients and methods: 80 consecutive patients (52 men, 28 women) with clinically suspected myocarditis were investigated. The main clinical symptoms were heart failure (n = 45), angina pectoris (n = 25) or cardiac arrhythmias (n = 10). In most patients the symptoms had developed in temporal relation to a viral infection. Coronary heart disease was excluded in all by coronary angiography. Interventricular septal endomyocardial biopsies were examined histologically and immunohistologically. cTnT was measured with a highly sensitive sandwich-Immunoassay. Results: An increased level of cTnT (> 0.1 ng/ml) was demonstrated in 28 of the 80 patients (35 %). Myocarditis was diagnosed histologically in only 5 patients, but immunohistologically in 26 of 28 (93 %) with a raised cTnT level and in 23 of 52 (44 %) with a normal cTnT level. The cTnT level was more frequently elevated in patients with a brief rather than a long history of myocarditis. After 6 months the cTnT level was elevated in only 4 of 28 patients with myocarditis, but the myocardial biopsy showed persisting myocarditis in 14 patients. Conclusion: Measurement of cTnT is a very sensitive way of demonstrating myocardial cell damage in patients clinically suspected of having myocarditis. Immunohistological analysis can often provide positive results even if the histological findings are unremarkable. The sensitivity in diagnosing of cTnT is greatest when the patient is tested shortly after the onset of symptoms.

History and clinical findings A 28-year-old woman was admitted after syncope which had been preceded by several flulike episodes. There was no history of any other serious disease. Physical examination was unremarkable. Heart sounds were regular and normal, there were no murmurs. Investigations White cell count was 9400/microliter, with a normal differential count. Erythrocyte sedimentation rate and C-reactive protein were also normal. Virus serology revealed no abnormality. The electrocardiogram (ECG) showed complete (third degree) atrioventricular (AV) block with an idioventricular rhythm of 38 beats/min and right bundle branch block pattern. Treatment and course A temporary transvenous pacemaker was inserted on the first hospital day. As myocarditis was suspected a right ventricular endomyocardial biopsy was obtained. Histological and immunohistological examinations demonstrated no unequivocal findings. But molecular-biological tests revealed. Coxsackie-B3 virus genome. The pacemaker was removed on the 6th day, when the ECG had shown intermittent second degree AV block. Regular sinus rhythm with a PR interval of 0.18 s was recorded on day 12, and 24-hour ECG monitoring for several days until her discharge on the 18th day confirmed this rhythm throughout. Conclusion In aetiologically undetermined disease molecular-biological techniques can be indispensable for the exact diagnosis and may be decisive for administering specific treatment.