William H. Bernstein
University of Miami
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Featured researches published by William H. Bernstein.
American Heart Journal | 1966
Philip Samet; Cesar A. Castillo; William H. Bernstein
Abstract Comparison of the effects of atrial, ventricular, and sequential atrioventricular pacing in a group of patients with rheumatic heart disease and in a group with pulmonary emphysema has demonstrated that the absence of synchronized atrioventricular activity rather than aberrant ventricular depolarization is primarily responsible for the hemodynamic difference between atrial and ventricular pacing.
American Journal of Cardiology | 1965
Philip Samet; William H. Bernstein; David A. Nathan; Alfredo Lopez
Abstract Cardiac output studies were performed in 6 patients with complete heart block during four kinds of ventricular rhythm. These include ventricular or His-bundle pacing at the control rate, right ventricular outflow tract catheter electrode pacing, and both synchronous and atrial synchronous pacing by means of a Cordis Synchrocor unit. The latter two rhythms are defined as those with P wave, ventricular stimulus and QRS complex sequences, and atrial stimulus, P wave, ventricular stimulus and QRS complex sequences, respectively. Thirty-four paired observations were made during equal atrial and ventricular pacing rates in these patients. The importance of atrial systole for maintenance of cardiac output is clearly demonstrated by these data.
American Journal of Cardiology | 1965
Philip Samet; William H. Bernstein; Sydney Levine
Abstract The contributions of atrial systole to ventricular filling are emphasized by analyses of pressure curve data in (1) patients with complete heart block studied by right and left heart catheterization, (2) patients with sinus rhythm and atrial fibrillation and (3) sinus rhythm and ventricular premature beats. The level of systolic and diastolic right and left heart pressures varies with the temporal relation between the P and QRS complexes in patients with complete heart block. Peak pressures are recorded when there is a normal temporal relation between the P and QRS complexes. The rate of rise of the systemic arterial pressure curve is also at a maximum when the normal P-QRS relation is maintained. Comparison of left ventricular and systemic arterial pressures during sinus rhythm and ventricular premature beats demonstrates higher systolic peak pressures during sinus rhythm with normal atrioventricular conduction; of equal importance is the observation that left ventricular end-diastolic pressures are higher during sinus rhythm than during a series of ventricular premature beats. One subject was studied during both atrial fibrillation and normal sinus rhythm in the course of left heart catheterization. Left ventricular. systolic and end-diastolic pressures were higher during normal sinus rhythm than during atrial fibrillation. The development of mitral regurgitation during ectopic ventricular beats is also illustrated. These data demonstrate the physiologic importance of maintaining the normal temporal sequence of atrioventricular activity.
American Journal of Cardiology | 1968
Philip Samet; Cesar A. Castillo; William H. Bernstein
Abstract The hemodynamic sequelae of sequential atrioventricular pacing were compared to those of atrial and ventricular pacing and analyzed. The results clearly demonstrate that aberrant ventricular depolarization per se is of relatively minor hemodynamic import but that sequential atrial and ventricular activity is essential for optimal ventricular function even in the normal subject.
Circulation | 1968
John W. Lister; Lawrence S. Cohen; William H. Bernstein; Philip Samet
In 10 patients, 24 episodes of supraventricular tachycardia were treated by rapid electrical stimulation of the right atrium. One episode of sinus tachycardia, eight episodes of atrial tachycardia, two episodes of atrial flutter, and 13 episodes of A-V junctional tachycardia occurred. In each case the diagnosis of the arrhythmia was documented by obtaining unipolar and bipolar intra-atrial electrograms.In three cases of supraventricular tachycardia the ventricular rate was slowed as a result of an increased atrial rate. The increased atrial rate caused an increase of the functional refractory period of the A-V junction, and thus, fewer atrial impulses were transmitted to the ventricles.In seven cases, 21 episodes of supraventricular tachycardia were terminated by rapid atrial stimulation. In six of these cases the tachycardia was converted to normal sinus rhythm either during or shortly after atrial stimulation. In one case, 12 episodes of A-V junctional tachycardia were converted to rhythms varying between normal sinus rhythm and a slow A-V junctional rhythm. In this case, after termination of the last episode of A-V junctional tachycardia, the rhythm was stabilized by atrial pacing.
The American Journal of Medicine | 1965
Philip Samet; William H. Bernstein; Sydney Levine; Alfredo Lopez
Abstract The hemodynamic effects of right atrial and ventricular bipolar catheter pacing were investigated in fifty-four subjects in sinus rhythm. Right and left heart pressures were measured, and cardiac outputs determined by the indicator dilution method, at both control sinus rates and during atrial and ventricular tachycardias at varying rates above the control sinus rate, induced by atrial and ventricular catheter electrodes. The results of this study clearly demonstrate that, in intact man, ventricular pacing, at ventricular rates similar to those induced by atrial pacing, result in decrements in cardiac output and in systemic arterial pressures, together with atrioventricular regurgitation. The application of these data to synchronous or idioventricular pacing in patients in complete heart block seems evident.
American Journal of Cardiology | 1966
Philip Samet; Cesar A. Castillo; William H. Bernstein
Abstract The results of atrial and ventricular pacing upon cardiovascular dynamics in 20 subjects with normal cardiovascular systems have been analyzed. The average cardiac index during atrial pacing was 3.17 L./min., M. 2 compared to 2.66 during ventricular pacing. Similar conclusions were possible by analysis of the data at varying heart rates of 60 to 89,90 to 109 and 110 to 140. It is concluded that the atrial contribution to ventricular function is significant even in normal subjects.
American Journal of Cardiology | 1964
Philip Samet; William H. Bernstein; Aaron Medow; David A. Nathan
Abstract Evidence is presented, both from a review of the literature and from original observations in this laboratory during cardiac catheterization in man, to demonstrate that the cardiac output in the majority of patients with complete heart block can be increased with increments in ventricular rate. These data, especially when considered in conjunction with the demonstrated importance of synchronous as opposed to asynchronous atrioventricular contraction, strongly suggest that synchronous P-wave pacemakers, such as the one developed by our group, are physiologically and clinically superior to idioventricular pacemakers of either the fixed or variable rate types.
American Journal of Cardiology | 1963
Philip Samet; Warren Jacobs; William H. Bernstein; Ronald Shane
Abstract Systemic arterial and right heart pressure curves are reviewed in 3 patients with complete heart block. In all three the ventricles were driven by ventricular pacemakers so that the normal sequence of atrioventricular contraction was absent. Some of the hemodynamic consequences of such idioventricular pacemaking are reviewed, and the important role played by atrial systole in ventricular filling is emphasized.
American Heart Journal | 1960
Philip Samet; William H. Bernstein; Jack Widrich
Abstract Two cases of primary pulmonary hypertension are presented, and the results of right heart catheterization are given. Infusion of acetylcholine caused large decreases in pulmonary arterial pressure in one subject, both at rest and during exercise. In the second subject, infusion of acetylcholine resulted in a lesser but still significant decrease in pulmonary arterial pressure. The criteria that must be met before conclusions are drawn as to the existence of vasodilation or vasoconstriction in the pulmonary vascular bed are discussed.