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Atrioventricular interval optimisation is important in patients with dual-chamber pacing, especially with heart failure. In patients with CHD, especially in those with Fontan circulation, the systemic atrial contraction is supposed to be more important than in patients without structural heart disease.
We retrospectively evaluated two patients after Fontan procedure with dual-chamber pacemaker with a unique setting of optimal sensed atrioventricular interval.
The optimal sensed atrioventricular interval determined by echocardiogram was extremely short sensed atrioventricular interval at 25 and 30 ms in both cases; however, the actual P wave and ventricular pacing interval showed 180 and 140 ms, respectively. In both cases, the atrial epicardial leads were implanted on the opposite site of the origin of their own atrial rhythm. The time differences between sensed atrioventricular interval and actual P wave and ventricular pacing interval occurred because of the site of the epicardial atrial pacing leads and the intra-atrial conduction delay.
We need to consider the origin of the atrial rhythm, the site of the epicardial atrial lead, and the atrial conduction delay by using electrocardiogram and X-ray when we set the optimal sensed atrioventricular interval in complicated CHD.
Eosinophilic myocarditis is rare in children, and consequently, it is difficult to diagnose eosinophilic myocarditis rapidly. We report the clinical course of acute eosinophilic myocarditis with pericarditis in two adolescent boys and their associated electrocardiograms. The two patients, 13- and 14-year-old boys, developed cardiomegaly and chest pain with vomiting. On examination by two-dimensional echocardiography, thickening of the ventricular septum and a pericardial effusion were detected. The eosinophil count had increased by the pericardial effusion. Acute eosinophilic myocarditis often complicates a moderate to severe pericardial effusion owing to acute pericarditis. A cellular fraction analysis of the pericardial effusion is easy and useful for the diagnosis of eosinophilic myocarditis. Some serial changes in the electrocardiogram occur during each stage of acute eosinophilic myocarditis. They are induced by eosinophilic granules, which are capable of inducing tissue damage and dysfunction, and those changes in the electrocardiogram resemble the changes after an acute myocardial infarction. It is important to know the characteristics of eosinophilic myocarditis in order to prevent lethal complications.
Severe valvulitis owing to acute Kawasaki disease leading to severe mitral regurgitation is a rare event in infants. Further, there is less information about underlying ruptured mitral chordae tendineae causing severe mitral regurgitation. We encountered ruptured mitral chordae tendineae in three female patients after Kawasaki disease. The age at the onset of Kawasaki disease ranged from 3 to 8 months, and detection of ruptured mitral chordae tendineae was from 24 to 90 days. Two patients had acute heart failure, and one was asymptomatic. One patient underwent mitral annuloplasty, and the others responded to medication. These ruptured mitral chordae tendineae occurred after the remission of the initial acute Kawasaki disease, in the early course and the convalescent of acute Kawasaki disease. Further, the recurrent fever was also detected in them. The ruptured mitral chordae tendineae in an infant within 6 months can be detected by systolic heart murmur around the convalescent stage of acute Kawasaki disease, although the prevalence is very low.
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