Right bundle branch block with periods of alternating left anterior and left posterior hemiblock. Clinical evidence of incomplete fascicular block.

The case presented had an electrocardiographic pattern of complete right bundle branch block with alternating periods of left anterior hemiblock and left posterior hemiblock. During one of the periods of alternating hemiblock, an His bundle electrogram was recorded and the His Purkinje (H-V interval) conduction time was within normal limits. In a second episode of alternating hemoblock, periods of Mobitz type II second-degree A-V block were noted. It is postulated that this case provides clinical evidence that incomplete block of a fascicle may occur in spite of an electrocardiographic pattern of complete fascicular block. It is thought that the periods of alternating hemiblock result from a changing relationship between conduction velocity and refractory period.

Conduction disturbances in patients with mitral valve prolapse.

The electrocardiograms (ECGs) of 55 patients with mitral valve prolapse were analyzed. Twelve of these demonstrated conduction abnormalities. Five patients had first degree heart block. Three had the classic ECG changes of the Wolff-Parkinson-White syndrome. Two patients had left anterior hemiblock, one of whom also had incomplete right bundle branch block. One patient had episodes of advanced atrioventricular block and periods of sinus arrest, which resulted in recurrent syncopal attacks. One patient had incomplete left bundle branch block. The presence of conduction disturbances points to the diffuse nature of the myocardial abnormality in mitral valve prolapse.

The natural history of trifascicular disease following permanent pacemaker implantation. Significance of continuing changes in atrioventricular conduction.

Seventy-two patients with trifasicular disease were followed for an average of 40 months following permanent pacemaker insertion. The indications for pacemaker insertion were either electrocardiographic evidence of complete heart block with a wide QRS escape complex or a pattern of bifasicular block with either periods of Mobitz type II atrioventricular (A-V) block or a documented history of syncope. The patients were then divided into three groups depending on subsequent change in A-V conduction. There were 31 (43%) patients with no change in A-V conduction, 17 (24%) with increasing A-V block, and 24 (33%) with decreasing A-V block. The characteristics of these three groups, including age and sex distribution, were compared and found to be similar. The incidence of previous transmural myocardial infarction as determined by electrocardiographic criteria was higher in the group with decreasing block. Survival curves showed a significantly decreased probablity of surviving for those with decreasing block compared to both those with increasing block and those with no charge in conduction (P less than 0.03). We conclude that the probability of long-term survival was less in the group with decreasing block. This finding may be related to the greater prevalence of coronary heart disease in the patients.

Incidence and description of accelerated ventricular rhythm complicating acute myocardial infarction.

One hundred and nineteen episodes of accelerated ventricular rhythm (less than 125/min) were noted in 37 patinets with acute myocardial infarction during a 1 year period. The incidence was 12.7 per cent. Twenty-seven episodes of fast ventricular tachycardia (less than 125/min) were noted in 16 of these patients. Eighteen patients had anterior myocardial infarction and 19 inferior myocardial infarction. The mechanism of onset of accelerated ventricular rhythm was classified as escape in 65 episodes. Ventricular premature beats were noted close to episodes of accelerated ventricular rhythm in 31 patients and fast ventricular tachycardia in 14 patients. The morphology of accelerated ventricular rhythm was similar to the ventricular premature beats in 27 patients and similar to the fast ventricular tachycardia in 12. In 11 patinets the morphology of ventricular premature beats, accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm and fast ventricular tachycardia were all the same. In six patients the coupling time of the ventricular premature beats and the onset of the accelerated ventricular rhythm were the same. In seven patients the morphology of the accelerated ventricular rhythm and fast ventricular tachycardia were the same, and the rate of the accelerated ventricular rhythm was exactly half that of the fast ventricular tachycardia. There were three deaths due to shock and heart failure. Three episodes of fast ventricular tachycardia progressed to ventricular fibrillation and were successfully cardioverted. It is concluded that accelerated ventricular rhythm is a relatively common complication of both anterior and inferior myocardial infarction. The high incidence of concomitant fast ventricular tachycardia, the frequency of ventricular premature beats with similar morphology and coupling time, and the instances of two arrhythmias having common rate multiples, suggest that at least in some instances accelerated ventricular rhythm may represent an ectopic focus with exit block.