PubMed Health⌕ Search

Biomedical subjects

R W Wald

Publications and source records attributed to R W Wald.

At least 19 recordsLinked to original sources
PubMed1990

The mechanism of flutter interval alternans.

The mechanism of atrial flutter alternans was investigated by observing the effects of ventricular systole on flutter intervals in a patient with atrioventricular dissociation. Interval measurements were made both from atrial electrograms recorded from an esophageal electrode, and from surface ECG recordings. Flutter cycle intervals that occurred during a well-defined period subsequent to ventricular systole were consistently prolonged by up to 30 msec relative to the baseline flutter cycle interval. This prolongation was observed in two vastly different electrode configurations, implying that motion artifact was not predominantly responsible. We concluded that, by altering the characteristics of the flutter reentry circuit, transient increases in atrial volume and/or pressure arising during ventricular systole were responsible for the lengthening of the flutter cycle intervals.

Adult↗
PubMed1989

Isoproterenol induction of vasodepressor-type reaction in vasodepressor-prone persons.

The ability of isoproterenol to induce symptoms and laboratory findings of a vasodepressor reaction was tested in 48 patients, ages 17 to 74, divided into 4 groups according to the reason for their referral. Group 1 comprised 12 patients with vasodepressor syncope, group 2 had 8 patients with syncope of unknown origin, group 3 included 11 patients with syncope due to seizures in 2 and ventricular tachycardia in 9, group 4 had 17 patients with various arrhythmias not associated with syncope. Isoproterenol boluses were administered starting at 2 micrograms and increased in 2-micrograms steps to a maximum of 8 micrograms at 0 degree and +60 degrees. The responses at 0 degrees were all normal. At +60 degrees a vasodepressor reaction consisting of syncope or near syncope, hypotension and bradycardia was produced by isoproterenol (mean dose 6.0 +/- 0.26 micrograms) in 8 patients from group 1 (66.6%), 4 from group 2 (50%), 0 from group 3 and 4 from group 4 (23.5%). Three of the 4 patients in group 4 had a remote history of classic vasodepressor syncope. The overall sensitivity and specificity of the test were 73 and 85%, respectively, while the predictive accuracy of a test with positive or negative outcome were 69 and 89%, respectively. Muscarinic receptor blockade with atropine in 4 patients prevented isoproterenol-induced bradycardia but not hypotension or symptoms of fainting. Beta-adrenergic receptor blockade with propranolol inhibited all aspects of the isoproterenol-induced faint. Thus, the administration of isoproterenol during a passive upright tilt may identify persons who suffer from or are prone to a vasodepressor reaction.

Adult↗
PubMed1989

The protective effect of vagus nerve stimulation on catecholamine-halothane-induced ventricular fibrillation in dogs.

Parasympathetic neural activity modulates some ventricular arrhythmias in man. Therefore, a canine model of arrhythmias produced by the interaction of halothane and catecholamines was used to study the effects of vagal stimulation on the induction of ventricular fibrillation. The dose of catecholamine required to induce ventricular fibrillation was determined during a constant heart rate. Vagal stimulation reversibly raised the norepinephrine dose that produced ventricular fibrillation from 16.4 +/- 2.4 to 30.0 +/- 3.8 micrograms (p less than 0.001, n = 10), and the epinephrine dose from 15.5 +/- 2.0 to 22.5 +/- 2.6 micrograms (p less than 0.001, n = 5). Following atropine, vagal stimulation failed to raise the threshold dose of norepinephrine (16.8 +/- 2.4 vs. 18.3 +/- 3.3 micrograms, nonsignificant, n = 6) or epinephrine (15.5 +/- 2.0 vs. 16.0 +/- 2.3 micrograms, nonsignificant, n = 5). Ligation of the cervical vagus nerves did not affect the epinephrine threshold dose (16.3 +/- 3.3 vs. 17.5 +/- 2.7 micrograms, nonsignificant, n = 5). Following elevation of basal vagal tone by morphine premedication, the norepinephrine threshold of 53.0 +/- 9.2 micrograms declined by a nonsignificant amount to 46.5 +/- 11.5 micrograms after vagotomy (nonsignificant, n = 5). Thus resting vagal tone does not prevent catecholamine-halothane-induced ventricular fibrillation, whereas increasing vagal tone by electrical stimulation substantially protects against this arrhythmia. The protection is mediated through a muscarinic cholinergic receptor.

Animals↗
PubMed1983

Self-conversion of drug resistant ventricular tachycardia by rapid atrial pacing.

A 523-year-old man with recurrent ventricular tachycardia two months post myocardial infarction is described. The tachycardia resulted in low output and heart failure at the time of presentation. Following electrocardioversion of ventricular tachycardia, sinus rhythm would last for only a few seconds, and ventricular tachycardia could not be terminated or prevented by drugs, nor by overdrive pacing. Over a 20-hour period, asynchronous right ventricular pacing at 30/min resulted in repeated random interruption of successive paroxysms of ventricular tachycardia, resulting in maintenance of sinus rhythm about 60 to 70% of the time. This produced marked hemodynamic improvement and a decrease in the frequency of paroxysms of tachycardia which, however, continued to recur once every few days. Despite their reduced frequency, these paroxysms continued to be resistant to drugs and had to be terminated by cardioversion. At this point it was discovered that rapid atrial pacing was able to terminate the patient's tachycardia reliably and reproducibly. A permanent right atrial externally activated radio frequency pacemaker device was inserted and over the ensuing eighteen-month period the patient self-terminated over fifty discrete episodes of ventricular tachycardia.

Anti-Arrhythmia Agents↗
PubMed1983

Interactions between the autonomic nervous system and tachycardias in man.

We have endeavoured to present an integrated and dynamic overview of the interaction between the autonomic nervous system and cardiac arrhythmias. Our purpose was not to be comprehensive, detailed, or all inclusive but to present a clinically relevant summary of some of the areas where autonomic tone may be pertinent. Clearly, most arrhythmias are not the result of a primary autonomic nervous system disorder. However, subtle and overt alterations in autonomic tone, interacting with rate, pressure, cardiac volume, contractility, and the intrinsic myocardial electrophysiologic properties likely exert a critical influence on many cardiac arrhythmias. We wish to emphasize that autonomic effects may be temporarily concealed or overwhelmed during certain states or by the administration of drugs. However, the modulating role of neural tone and neurotransmitters is almost always present, contributing significantly to the outcome of therapy.

Anti-Arrhythmia Agents↗
PubMed1982

Reflex mechanisms responsible for early spontaneous termination of paroxysmal supraventricular tachycardia.

The incidence and possible mechanism of early spontaneous termination of paroxysmal supraventricular tachycardia was studied in 20 consecutive patients. Episodes of induced tachycardia that terminated spontaneously within the 1st minute after initiation were included. Tachycardias ending spontaneously were associated with a reproducible course of hypotension at the onset followed by blood pressure recovery above control levels and termination. Spontaneous termination of tachycardias occurred within the A-V node 18 to 45 seconds (mean +/- standard error of the mean 27.9 +/- 5.3) after their onset. In the supine position (0 degrees) 9 (45 percent) of 20 patients showed spontaneous termination in 36 (16 percent) of 219 episodes of tachycardia. In the head-dependent position (-20 degrees) only 1 (8 percent) of 13 patients manifested spontaneous termination in 2 (4 percent) of 54 episodes. In the head up position (+60 degrees) only 1 (6 percent) of 18 patients exhibited termination in 2 (2 percent) of 102 episodes. After partial cholinergic blockade with intravenous hyoscine butylbromide, 20 mg, or atropine, 0.6 mg, none of five patients showed spontaneous termination in 25 episodes. After beta adrenergic blockade with 10 mg of propranolol intravenously, none of 16 patients showed spontaneous termination in 87 episodes of tachycardia. We conclude that the initial hypotension during tachycardia evokes a sympathetic response that increases blood pressure and this increase in turn causes a rise in vagal tone that breaks the tachycardia.

Adrenergic beta-Antagonists↗
PubMed1981

Depression of distal AV conduction following ventricular pacing.

A 61-year-old man presented with symptomatic 2 degree Mobitz II AV block in association with bifascicular block. Ventricular pacing resulted in temporary depression of AV conduction. The extent of pacing-induced AV block varied directly with the duration and rate of ventricular pacing. Intracardiac recordings proved that the site of spontaneous and pacing-induced AV block was distal to the His bundle. Possible mechanisms by which this phenomenon may arise and several implications of practical importance are discussed.

Cardiac Pacing, Artificial↗
PubMed1981

Continuous on-line beat-to-beat analysis of AV conduction time.

A simple analog circuit is described which is capable of measuring on a beat-to-beat basis P-R, R-P, P-P, and R-R intervals during sinus rhythm and paroxysmal supraventricular tachycardia. In addition the circuit will emit a pulse when the consecutively alternating P and R wave sequence is interrupted thereby signalling a trigger problem or a change in rhythm. The operation of the device requires proper P and R wave sensing and provides outputs which are linear over a range of rates which are applicable to the human heart.

Atrioventricular Node↗
PubMed1980

The effect of antiarrhythmic drugs on depressed conduction and unidirectional block in sheep Purkinje fibers.

We studied the effect of therapeutic concentrations of lidocaine, procainamide, quinidine, propranolol, and diphenylhydantoin on two models of depressed conduction and unidirectional block produced by asymmetric focal cooling and crushing in sheep Purkinje fibers. All drugs were shown to induce reversible deterioration of conduction. Unidirectional block was converted to bidirectional block with each drug. Improvement of conduction was rare and conversion of unidirectional block to bidirectional conduction never was observed. These experiments suggest that all five drugs may act by a uniform mechanism of action in some reentrant ventricular arrhythmias involving a zone of depressed conduction or unidirectional block within the Purkinje network.

Animals↗
PubMed1979

Management of intractable ventricular tachyarrhythmias after myocardial infarction.

Twenty-five patients with recent or old myocardial infarction were studied because they had life-threatening ventricular arrhythmias that required repeated cardioversions and were intractable to medical management. All patients had had a large anterior infarction a mean of 4.6 weeks before the emergence of the arrhythmias and all had severe left ventricular dysfunction. Cardiac catheterization or autopsy revealed a left ventricular aneurysm in 18 of 18 patients and obstruction of the left anterior descending coronary artery in 20 of 20 patients. Of 16 patients treated surgically with aneurysm resection or coronary bypass grafting, or both, 10 (62 percent) were alive after 3 to 39 (mean 26) months of follow-up. The perioperative mortality rate was 31 percent and only one patient died during the postoperative follow-up period 4 months after discharge from the hospital. By contrast, all nine medically treated patients died either in the hospital (four patients) or suddenly within 2 months of discharge (five patients). Ventricular fibrillation was documented as the cause of death in five of these patients. Surgical intervention was found to improve significantly the survival of these patients (P less than 0.02). The perioperative mortality rate was lower when at least 4 weeks had elapsed from acute infarction to surgery (10 versus 67 percent) and when the procedure included coronary bypass grafting (13 versus 50 percent), although these differences were not statistically significant (P greater than 0.05).

Adult↗
PubMed1979

Carotid sinus massage induced elimination of rate related bundle branch block during paroxysmal atrial tachycardia: a simple method of proving bypass tract participation in the tachycardia.

Four cases of paroxysmal atrial tachycardia are described in whom rate related left bundle branch block (LBBB) was often present which persisted indefintely and showed no signs of spontaneous disappearance. Transient slowing of the tachycardia by carotid sinus massage in each case eliminated LBBB and this led to tachycardia acceleration. The tachycardia acceleration was traceable to a shortening in ventriculoatrial conduction. These observations proved the participation of a left sided bypass tract in the tachycardia circuit in each of these cases.

Bundle-Branch Block↗
PubMed1978

Myocardial perfusion imaging with thallium-201: correlation with coronary arteriography and electrocardiography.

Myocardial perfusion imaging with thallium-201 and electrocardiography with the subject at rest and undergoing submaximal treadmill exercise were performed in 19 men and 3 women. Selective coronary arteriography and left ventriculography showed that 7 had normal coronary arteries and 15 had coronary artery disease.The 11 persons with electrocardiographic evidence of an old myocardial infarct (q waves) had a perfusion defect at rest in the area of the infarct and a segmental abnormality of wall motion apparent on the left ventriculogram corresponding to the perfusion defect.MYOCARDIAL PERFUSION IMAGING AND ELECTROCARDIOGRAPHY WERE EQUALLY SENSITIVE IN DETECTING CORONARY ARTERY DISEASE IN EXERCISING INDIVIDUALS: perfusion defects were noted in 7 of the 15 persons with coronary artery disease, and diagnostic ST-segment depression was present in 8 of the 15. Combination of the results of the two tests with exercise permitted the identification of 11 of the 15 persons and improved the sensitivity. Combination of the results of rest and exercise imaging and electrocardiography permitted the identification of 94% of the patients with coronary artery disease.Myocardial perfusion imaging with (201)TI in the subject at rest is a sensitive indicator of previous myocardial infarction. Imaging after the subject has exercised is a useful adjunct to conventional exercise electrocardiography, especially in those whose exercise electrocardiogram is non-interpretable.

Adult↗
PubMed1978

Demand pacemaker slowing: a simple bedside technique.

We present a simple noninvasive bedside technique to slow gradually any R-wave inhibited ventricular demand pacemaker up to one-half its original rate for indefinite periods of time. Gradual pacemaker slowing allows accurate diagnostic observations and therapeutic interventions in pacemaker-induced arrhythmias and may possibly be used in the management of unstable angina in patients with ventricular demand pacemakers.

Aged↗
PubMed1978

Self-conversion of supraventricular tachycardia by rapid atrial pacing.

The use of pacemakers in the treatment of tachycardias is one of the most exciting and rapidly expanding applications of cardiac pacing. One of the more recent developments in this field has been the use of patient-activated radio frequency transmitted rapid atrial stimulation (RAS) in the treatment of paroxysmal supraventricular tachycardia (PSVT). Based on the previously established ability of asynchronous atrial pacing to interrupt a variety of re-entrant supraventricular rhythm disturbances, this modality of treatment is gaining increasing applicability in patients with PSVT associated with debilitating symptoms or other severe cardiovascular consequences in whom standard pharmacological regimens have either failed or are impossible to maintain for indefinite periods. This report describes our experience with five patients who underwent implantation of RAS units. The detailed electrophysiological studies required to ensure success and avoid any possible future complications are described. Over a follow-up period of four months to four years (mean 16 months) very few problems arose in the use of these units which have immeasurably improved the quality of life of the recipients. Our experience with RAS units has led to a few suggestions for future improvement and these are outlined in this report. The excellent patient acceptance and the reliability of this technique in terminating episodes of PSVT should, in the future, render RAS the treatment of choice in certain selected patients suffering from this common disorder.

Adult↗
PubMed1978

Technetium-99m stannous pyrophosphate scintigraphy in patients with calcification within the cardiac silhouette.

Technetium-99m stannous pyrophosphate scintiscanning was performed in 22 patients with radiographically detected calcification within the cardiac silhouette. All but one of these scintigrams showed a localised area of increased activity similar to that ordinarily seen in acute myocardial infarction. Scintiscans in 3 patients after removal of the calcified aortic valve reverted to negative. It was concluded that this technique for acute infarct detection may yield false positive results in the presence of cardiac calcification.

Calcinosis↗