To study the histopathology of the myocardium in Kawasaki Disease (KD) with various coronary angiographic fmdings, right endomyocardial biopsy specimens were evaluated on 20 boys and 16 girls with this disorder. KD with coronary artery lesions (CAL) showed various histopathological abnormalities, such as myocellular hypertrophy in 44%, degeneration in 61%, interstitial fibrosis in 44% and endomyocardial changes in 22%. KD without CAL revealed myocellular hypertrophy in 44%, degeneration in SO%, disarray in 28% and interstitial fibrosis in 6%. As in patients with long-standing KD, more than three years after onset, myocardial changes such as myocellular hypertrophy, disarray and interstitial fibrosis persisted, it is suggested that cardiomyopathy may develop in some patients with KD. (Acta Paediatr Jpn 1989; 3 1 : 706 -7 1 1) References Kawasaki T. Acute febrile mucocutaneous syndrome with lymphoid involvement with specific desquamation of the fingers and toes. Jpn J Allergy 1967; 16: 178-222 (in Jpn). Kato H, lchinose E, Yoshioka F et al. Fate of coronary aneurysm in Kawasaki disease: serial coronary angiography and long-term follow-up study. Am J Cardiol 1982; 49: 1758-1766. Nakano H. Ueda K, Saito A et al. Repeated quantitative angiograms in coronary arterial aneurysm in Kawasaki disease. Am J Cardiol 1985; 56: 846-851.
Whether the abnormalities were due to direct myocardial injury, chronic ischaemia, repeated small-vessel thrombosis, or other problems associated only with biopsies, is difficult to determine. However, this subgroup had residual abnormal lesions in the myocardium. Follow-up should be more aggressive in this group of patients to identify myocardial damage that could be asymptomatic.
To determine whether myocardial changes in patients with supraventricular tachycardia (SVT) are primary or secondary to persistent tachycardia, 11 patients with SVT were studied. These patients were divided into 2 groups with respect to the type of SVT. Group I consisted of 5 patients with incessant SVT and one with multifocal atrial tachycardia, while group II consisted of 4 patients with paroxysmal supraventricular tachycardia and one with short-run supraventricular premature contraction. All of the patients underwent electrophysiological study and endomyocardial biopsy from the right ventricle following routine cardiac catheterization. In group II, there were no significant abnormalities in the clinical and hemodynamic parameters. In group I, 3 patients had clinical features of dilated cardiomyopathy including abnormal ECG, chest X-ray and hypokinesis on left ventriculography. Induction and termination of SVT were possible in 2 patients in group I and in 4 of the 5 patients in group II. The only significant histologic difference between group I and group II was fibrosis. A high incidence of histopathological abnormalities, such as hypertrophy, degeneration, interstitial fibrosis and disarray was observed in both groups. The incidence of significant pathology was higher in group I than in group II. Almost all of the patients were given antiarrhythmic drugs. One patient underwent a successful surgical procedure and normal cardiac function returned after resection of the foci of the right atrium. Our present results suggest that patients with SVT who have incessant or recurrent SVT should undergo not only intracardiac electrophysiologic study but also endomyocardial biopsy for the evaluation of myocardial damage, since SVT might be the initial sign of cardiomyopathy.
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