John W. Lister

Atrioventricular conduction in man: Effect of rate, exercise, isoproterenol and atropine on the P-R interval☆

Abstract Atrioventricular conduction was studied in 14 patients. A bipolar electrode catheter was placed in the right atrium, and the heart rate was controlled by atrial pacing. Increases in the sinus heart rate were associated with decreases in atrioventricular conduction time. When the heart rate was increased by atrial pacing, there were progressive increases in atrioventricular conduction time. Exercise, isoproterenol and atropine shortened atrioventricular conduction time. In those cases where atrioventricular conduction block occurred during atrial pacing, there was a 1:1 atrioventricular response during exercise at the same paced heart rate. Stimuli which increase the rate of discharge of the sinus pacemaker also enhance atrioventricular conduction. It is concluded that there is a fine balance between heart rate and A-V conduction. When the heart rate is increased by neurohumoral stimuli, there is a corresponding enhancement of A-V conduction. When the heart rate is increased by artificial stimulation of the atria and neurohumoral effects are not altered, there is a progressive increase in conduction time and eventual blockage of conduction at the A-V nodal region.

The Relation of Heart Rate to Cardiovascular Dynamics Pacing by Atrial Electrodes

Hemodynamic studies were carried out as heart rates were controlled by atrial pacing on 10 normal patients at rest and during exercise. Each patient served as his own control. In both states tested the cardiac index, left ventricular work, and peripheral resistance were not significantly altered by changes in heart rate. The stroke index and mean systolic ejection rate decreased linearly with heart rate. During exercise the cardiac index increased up to 98% and again remained constant at all paced heart rates tested. At comparable heart rates the tension-time index, left ventricular work, stroke index, and mean systolic ejection rate were higher during exercise than at rest. At comparable heart rates[see figure in the PDF file]peripheral resistance was 38% lower during exercise than at rest. Myocardial oxygen consumption, as inferred from the tension-time index, increased with heart rate in both states.

Efficacy of procainamide on ventricular tachycardia: Relation to prolongation of refractoriness and slowing of conduction

The effect of procainamide on intraventricular conduction and refractoriness, and the prevention of induction of ventricular tachycardia (VT) were studied in 29 patients who had remote myocardial infarction and inducible sustained monomorphic VT. AFter intravenous administration of 15 mg/kg procainamide, induction of VT was suppressed in seven (24%) patients (responders), while in 22 (76%) VT was still inducible (nonresponders). The percent change in paced QRS duration at a cycle length (CL) of 400 msec produced by procainamide was significantly less in responders than in nonresponders: 29.8 +/- 3.9% versus 38.9 +/- 10.8% (p = 0.0020). The percent change in the right ventricular effective refractory period (ERP) at CLs of 600 and 400 msec was significantly greater in responders than in nonresponders: 14.6 +/- 6.9% versus 7.9 +/- 7.3% (p = 0.0414) for ERP at a CL of 600 msec and 15.1 +/- 7.0% versus 8.0 +/- 7.4% (p = 0.0386) for ERP at a CL of 400 msec. Stepwise discriminant analysis showed that greater percent increase in ERP at a CL of 400 msec and lesser percent increase in paced QRS duration at a CL of 400 msec were significantly independent markers for the responders. These findings suggest that lesser slowing of conduction and greater prolongation of refractoriness by procainamide tend to abolish reentry within the reentrant circuit. Greater slowing of conduction and lesser prolongation of refractoriness tend to stabilize a reentrant circuit, and promote the continued induction of VT.

Susceptibility of infarcted canine hearts to digitalis-toxic ventricular tachycardia

The susceptibility to the toxic arrhythmogenic effects of digitalis was studied in 10 normal dogs (group 1) and in 15 dogs with healed myocardial infarction (group 2) 26 ± 5 days after coronary artery ligation. The dose of ouabain required to cause stable digitalis-toxic ventricular tachycardia was 25% less in the group 2 dogs than in the group 1 control dogs (70 ± 21 versus 93 ± 16 μg/kg, probability [p] These findings are consistent with healed infarcted myocardium serving as a site of predilection for the origin of digitalis-toxic ventricular tachycardia. Our observations add to a growing body of information suggesting that hearts with healed myocardial infarction have an enhanced susceptibility to digitalis intoxication.

Atrial pacing and atrioventricular conduction in anomalous atrioventricular excitation (Wolff-Parkinson-White syndrome)

Abstract A comparative study of atrioventricular conduction was made by single atrial pacing in normal subjects and in patients with the Wolff-Parkinson-White phenomenon. In those with the WPW phenomenon the atrial impulse, by a functional bypass of the A–V node, is not subjected to a physiologic delay at the A–V nodal region. Data are presented which lead us to conclude that the WPW beat is not a fusion beat as postulated by others. We suggest that the delta wave represents conduction through the accessory pathway and depolarization of a portion of ventricular myocardium, and that the terminal (normal) portion of the QRS represents conduction through the normal pathways below the A–V node, probably by entry of the impulse in this region, and depolarization of the remainder of the ventricles. We further suggest that an atrial impulse traverses either the normal A–V nodal route or takes the accessory pathway, but it does not traverse both pathways simultaneously.

Heart block: A method for rapid determination of causes of pacing failure in artificial pacemaking systems☆

Abstract The causes of pacing failure in transvenous and implanted pacemaker systems have been reviewed, and a method for the rapid determination of the cause of failure has been described. In all instances of pacing failure in patients with bipolar pacemaker circuits, except when both wires to the heart were broken, pacing was restored without thoracotomy or replacement of the transvenous pacemaker catheter. In instances of pulse generator failure, the batteries or pulse generator were replaced. In cases of malposition, the catheter was repositioned. In cases of wire breaks or short circuits, a unipolar circuit was established; and in cases of increased impedance or threshold for myocardial stimulation, the output of the pulse generator was increased. The exact delineation of the defect in a malfunctioning pacemaker system markedly facilitated the rapidity and ease of restoration of pacing and minimized trauma to the patient. In the early phases of transvenous pacemaker development there was a high incidence of pacemaker failure in our series. In the last 60 cases with transvenous pacemakers, the incidence of pacemaker malfunction has been less than 20 per cent. In the 45 patients with implanted pacemakers there has been a 33 per cent incidence of pacemaker malfunction.

The hemodynamic effect of slowing the heart rate by paired or coupled stimulation of the atria

Abstract The effect on cardiac output and arterial pressure of slowing the heart rate below the sinus rate by paired and coupled stimulation of the atria, and of increasing the heart rate above the sinus rate by single pacing of the atria, was tested in 11 patients. When the heart rate was slowed by coupled or paired stimulation of the atria, the second of each of a pair of atrial impulses was blocked at the A-V node and ventricular activation was unaltered. In patients with sinus rhythm, coupled and paired stimulation of the atria is a safe method for slowing the heart rate. There was no significant change in the external work performed by the heart when the heart rate was decreased below the sinus rate as much as 45 per cent or increased above the sinus rate as much as 50 per cent.

Preexcitation and Tachycardias in Wolff-Parkinson-White Syndrome, Type B: A Case Report

Electrophysiologic events in a 52-year-old man with Wolff-Parkinson-White (W-P-W) syndrome, type B, recurrent supraventricular tachycardias, and coronary artery disease were studied during cardiac catheterization and at open-heart surgery.During cardiac catheterization reciprocal tachycardias were repeatedly initiated by premature atrial beats and terminated by rapid right atrial pacing. Our results confirm that the tachycardia usually seen in the W-P-W syndrome is reciprocal tachycardias with orthograde conduction to the ventricles through the normal atrioventricular conduction system and retrograde conduction to the atria via the Kent bundle.The epicardial surface of the ventricles was “mapped’ at surgery. The earliest site of excitation was the posterior base of the left ventricle near the crux of the heart. Kent bundle conduction was temporarily ablated with lidocaine (Xylocaine) hydrochloride.This is the first case of W-P-W syndrome, type B, in which the anomalous A-V bundle entered the left ventricle. Our results indicate that the analysis of the electrocardiogram in localizing an abnormal A-V connection cannot be relied upon completely.

Bradycardia Dependent Ventricular Tachycardia Facilitated by Myopotential Inhibition of a VVI Pacemaker

Bradycardia‐dependent ventricular tachycardia was facilitated by long asystolic pauses caused by myopotential inhibition of a VVI pacemaker. Increasing the pacemaker rate by reprogramming temporariiy eliminated the problem. This case demonstrates that myopotential inhibition can result in serious clinical ventricular tachyarrhythmias

Rhythm anomalies in contemporary demand pacing

Abstract A change in pacemaker rate, a slightly erratic rate, and even the apparent failure to detect a spontaneous beat are not necessarily indications of pacemaker unit failure. Each rhythm must be examined in the context of accurate knowledge of the particular pacemaker, its parameters and perhaps its history.