Reversible left ventricular dysfunction with coronary stenotic or obstructive lesions in Kawasaki disease

Few studies have been reported on the prognosis or reversibility of ischemic myocardial lesions in Kawasaki disease. In this study, the pathophysiologic causes of reversible left ventricular dysfunction were evaluated in seven children with severe stenotic coronary lesions caused by Kawasaki disease.

The clinical process and the changes of coronary lesions in the repeated angiography were retrospectively evaluated in seven children. The ages of the seven patients (six boys and one girl) ranged from 7 to 15 years (mean, 10.4 +/- 2.6 y); the duration from the onset of Kawasaki disease to the last angiographic study ranged from 6 to 15 years (mean, 9.6 +/- 3.0 y).

During the acute stage, an acute myocardial infarction was detected clinically in two patients, transient ST depression in two, and deep Q waves without any symptoms in the remaining three patients. In the first angiographic study (2 mo to 6 y after the onset of Kawasaki disease), significant left ventricular dysfunction was observed in the posterior or inferior wall in all patients. In the right coronary arteries, giant aneurysms (> or = 8 mm in diameter) were angiographically detected in two patients, localized stenosis (> or = 95%) in one, and recanalization in four. In a recent angiographic study, the left ventricular dysfunction had normalized in all seven patients. Recanalization was observed, even in two patients with giant aneurysms and in one with localized stenosis. Collateral circulation was detected in five patients in this study. Abnormal deep Q waves on ECG were detected in only one patient, and no abnormal findings on ECG were seen in the remaining six. Upon 201TI myocardial scintigraphy, no reduction of 201TI uptake was observed in any of the seven patients at the site of the abnormal wall motion on the first angiography.

The regional left ventricular dysfunction in the seven patients may have been induced by severe acute ischemia due to a transient right coronary obstruction or by severe chronic ischemia due to coronary lesions. Eventually, left ventricular wall motion normalized after an improvement in the blood flow supply as a result of early recanalization and development of collateral circulation.