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Association of sinus node dysfunction, atrioventricular node conduction abnormality and ventricular arrhythmia in
Naokata Sumitomo1, Kensuke Karasawa, Kazuo Taniguchi
1Department of Pediatrics and Pediatric Health, Nihon University School of Medicine, 30-1Oyaguchi Kamimachi, Itabashi-ku, Tokyo 173-8610, Japan. naokata@med.nihon-u.ac.jp
Insights
Kawasaki disease (KD) patients show a higher incidence of abnormal sinus node and atrioventricular node function. These arrhythmias may stem from myocarditis or microcirculation issues, potentially leading to malignant ventricular events.
Area of Science:
- Pediatric Cardiology
- Electrophysiology
- Rheumatology
Background:
- Kawasaki disease (KD) is a critical pediatric illness.
- Cardiac involvement in KD, particularly arrhythmias, requires further investigation.
Purpose of the Study:
- To investigate the incidence of arrhythmias in patients with Kawasaki disease (KD).
- To assess electrophysiologic parameters in KD patients with coronary artery disease.
Main Methods:
- Electrophysiologic studies (EPS) were conducted on 40 KD patients.
- Analysis included sinus node function, atrioventricular nodal pathways, and conduction times.
Main Results:
- Clinical arrhythmias were observed in 4 patients.
- Abnormalities in sinus node recovery time and sino-atrial conduction were noted in several patients.
- Dual atrioventricular nodal pathways were identified in 3 patients.
Conclusions:
- KD patients exhibit a higher prevalence of abnormal sinus node and atrioventricular node function.
- Myocarditis or microcirculatory disturbances may underlie these functional abnormalities.
- Myocardial ischemia in some patients could precipitate malignant ventricular arrhythmias.
Background:
This study was performed to investigate the incidence of arrhythmias in patients with Kawasaki disease (KD).
Methods And Results:
Electrophysiologic studies (EPS) were performed in 40 patients (mean age: 10.3+/-5.1 years; 30 males, 10 females) with KD who had severe to moderate coronary artery disease. Clinical arrhythmias were documented in 4 patients (premature ventricular contractions, ventricular tachycardia, atrioventricular block, and ventricular fibrillation). Dual atrioventricular nodal pathways were demonstrated in 3 patients. Nonsustained atrial fibrillation was induced in 1 patient. The AH interval was prolonged in 2 patients. The Wenckebach rate was 164+/-37 beats/min, and 4 of the patients had a decreased Wenckebach rate. The maximum and corrected sinus node recovery times were 997+/-257 ms and 281+/-130 ms, respectively, and 7 patients were thought to be abnormal. The sino-atrial conduction time was 108+/-64 ms, and 2 patients had prolonged conduction times.
Conclusions:
Although there was no relationship between coronary stenosis or obstruction and the EPS parameters, the incidence of abnormal sinus node and atrioventricular node function is apparently higher in KD patients than in the normal population. These functional abnormalities may possibly be caused by myocarditis or an abnormal microcirculation in the sinus node and atrioventricular node artery. In some patients, myocardial ischemia may provoke malignant ventricular arrhythmia.
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