The pathology of cardiomyopathies. A critical analysis.
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We describe the first sets of identical and nonidentical twins with right ventricular cardiomyopathy (RVC). Pair A: A 12-year-old boy was referred because of palpitation and syncope. Clinical and instrument examinations revealed an enlarged and depressed right ventricle (end-diastolic volume = 110 ml/m2; ejection fraction = 44%), spontaneous ventricular tachycardia, and fatty-fibrous infiltrates in the biopsy specimens. His asymptomatic, monozygotic twin showed localized involvement of the right ventricle with isolated, ventricular extrasystoles. Pair B: These 18-year-old nonidentical twin boys showed diffuse right ventricular involvement (end-diastolic volume = 110 ml/m2 and 114 ml/m2; ejection fraction = 30% and 24%, respectively), induction of sustained and nonsustained ventricular tachycardia, respectively, and fibrosis on endomyocardial biopsy. One of the boys died suddenly at rest after documented ventricular fibrillation. These cases support the hypothesis of a genetic etiology with a minor role for genotype and point to the important influence of environmental factors in determining the clinical features of the disease.
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Twenty dogs were studied to characterize the anatomic, hemodynamic and pathologic effects of catheter-delivered cardioversion (CDCV) in the left ventricle. Five dogs each received 1 CDCV of either 50, 100, 200 or 300 J at the left ventricular apex. The injury occurred at the posteroinferior apex. Structural integrity of the ventricle remained intact. Energy doses of 50 and 100 J resulted in focal subendomyocardial injury. Higher energy levels resulted in localized transmural injury. There was a linear dose-related correlation between the volume of injury and delivered energy. Electrocardiographic changes were seen immediately in all dogs. Fifteen dogs had acute, transient ventricular arrhythmias. One dog died with refractory arrhythmias. Minimal hemodynamic changes were associated with the CDCV. Unique histopathologic changes were observed. Thus, local tissue destruction can be produced with CDCV. The extent of injury is dose-related and is associated with minimum hemodynamic changes. The lesion may be acutely arrhythmogenic.
The distribution of gross myocardial lesions and the relative density of the inflammatory cells in various myocardial locations (subepicardial and subendocardial halves of the left ventricular free wall, right ventricular and left ventricular halves of the ventricular septum, and the right ventricular free wall) were studied in 14 patients (11 male [79%], 8 black [57%], aged 7 months to 65 years [median 16 years]) who died suddenly of acute mononuclear-cell myocarditis. Grossly visible myocardial lesions were present in 8 patients, and preferentially involved the subepicardial regions of the left ventricular free wall. The highest mean number of mononuclear cells were seen in the subepicardial regions of the left ventricular free wall (193 cells per high-power field) and the lowest in the right ventricular one half of the ventricular septum (92 cells per high-power field, p < 0.001). Thus the predominant location of the gross myocardial lesions in acute mononuclear-cell myocarditis is the subepicardial region of the left ventricular free wall. A relatively low density of mononuclear cells are found in the right ventricular half of the ventricular septum, the main location of endomyocardial biopsies.
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