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In a series of over 6000 patients referred for fetal echocardiography during an eight year period, 37 fetuses were found to have complete heart block. There were 16 cases of isolated heart block and 21 cases associated with structural heart disease. All mothers of fetuses with isolated complete heart block had evidence of circulating syndrome Sjogren A antibody (Ro). Only one mother had clinical evidence of connective tissue disease. In the 21 cases associated with structural heart disease there were 17 cases of atrioventricular septal defect, one case of secundum atrial and perimembranous ventricular septal defects, two cases of tetralogy of Fallot, and one case of pulmonary stenosis. All fetuses with atrioventricular septal defects and complete heart block had left atrial isomerism. Additional abnormalities of the great arteries were often found in this group; these were double outlet right ventricle, transposition of the great arteries, pulmonary atresia, coarctation of aorta, and stenosis of the pulmonary or aortic valves. Intrauterine congestive heart failure was a feature of four cases in the group with isolated complete heart block and 11 cases of the group with associated structural heart disease. The outcome in the fetuses with isolated complete heart block was better than in those with heart disease: 12 of the 16 fetuses are alive, two of them have a pacemaker. But only three of the group of 21 fetuses with cardiac malformation are alive, and two of them have a pacemaker.

We present clinical and electrophysiological data on 9 patients with paroxysmal reciprocating sinus tachycardia (PRST) of whom only 6 described palpitations. Sinus node disease was present in 5 and cardiac ischemia and/or hypertension in another 3; the remaining case had apparently coincidental Wolff-Parkinson-White (WPW) syndrome. PRST could be initiated in all cases, and terminated in the 4 in whom it was sustained, by suitably timed atrial premature beats over a zone that was dependent on the effective atrial extrastimulus coupling interval (A1-A2) in the high right atrium (HRA). The sequence of atrial depolarization during PRST was similar to that of sinus beats although minor changes in both the P wave and the configuration of the HRA electrogram were observed in half the cases. During paroxysms, cycle length variation and sensitivity to alterations in vagal tone were common. In 6, paroxysms could be initiated by moderately rapid atrial pacing. Repetitive attacks were usually initiated by increases in the sinus rate and not be an antecedent premature atrial extrasystole. Verapamil suppressed sinus node reentry in 5 patients while small doses of atropine favored initiation in 3. PRST was seen in association with AV reentry tachycardias in the patient who had the WPW syndrome.

In 9 patients with paroxysmal supraventricular tachycardia the effects of tilting the body on the blood pressure and on responses during tachycardia or pacing revealed important effects that could influence the clinical presentation and the treatment required. Assessment of these reflex responses adds a major dimension to the understanding of the patient with supraventricular tachycardia.

A 67-year-old man with Wolff-Parkinson-White syndrome type A presented with second degree atrioventricular block in anomalous pathway and complete infra-Hisian block in the His-Purkinje pathway. He had increasingly frequent attacks of dizziness not related to exercise. A permanent ventricular demand pacemaker was successfully implanted following intracardiac electrophysiological studies.