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Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

At least 127 records · Page 7Linked to original sources
PubMed1978

Studies on the mechanism of sinus node dysfunction in the sick sinus syndrome.

The intrinsic heart rate (IHR) was determined in 17 patients with symptomatic sinus bradycardia by administering atropine 0.04 mg/kg and propranolol 0.2 mg/kg, i.v. In this way, sick sinus (SSS) patients with intrinsic sinus node (SN) dysfunction could be distinguished from those patients with disturbed autonomic regulation of SN function. Sick sinus syndrome patients with normal corrected sinus node recovery time (SNRTC), adjusted for the magnitude and direction of autonomic chronotrophy, consistently had normal IHRs and therefore abnormalities of autonomic regulation. Sick sinus syndrome patients with abnormal adjusted SNRTC consistently had abnormal IHRs and therefore abnormalities of intrinsic SN function. We conclude that more than one pathophysiologic mechanism can produce the clinical manifestations of sick sinus syndrome and that abnormal prolongation of SNRTC is dependent upon the underlying mechanism of sinus node dysfunction.

Adolescent↗
PubMed1978

Elimination of the delta wave in the Wolff-Parkinson-White syndrome. A misleading indicator of therapeutic effectiveness.

A 66-year-old white woman with a greater than 20-year history of electrocardiographic evidence of the Wolff-Parkinson-White syndrome, including documented recurrent supraventricular tachycardias, was studied. Despite the disappearance of the delta wave after initiation of therapy with digoxin and quinidine sulfate, the patient continued to have frequent episodes of supraventricular tachycardia. At a time when the serum levels of digoxin and quinidine were in the therapeutic range, extensive electrophysiologic studies were performed. Supraventricular tachycardia at a rate of 160 beats per minute was initiated by induced atrial premature depolarizations. The circuit of tachycardia involved anterograde conduction through the pathway of the atrioventricular node and His bundle and retrograde conduction through the bypass tract. We concluded that elimination of the delta wave and other electrocardiographic characteristics of the Wolff-Parkinson-White syndrome cannot be relied upon to indicate successful pharmacologic prophylaxis for induction of tachyarrhythmia associated with this syndrome.

Aged↗
PubMed1977

Electrophysiologic effects of anterior septal arterial occlusion.

The effect of reduction in anterior septal arterial flow on the conduction system was studied in seven anesthetized dogs. After 2 hours of occlusion P-Q, A-H, and H-V intervals as well as atrioventricular nodal effective and functional refractory periods were significantly prolonged, sinoatrial conduction time was prolonged and the heart rate was decreased. The duration of the His bundle electrogram was significantly prolonged and the configuration altered. However, QRS duration did not prolong significantly. Fifteen minutes after reperfusion, A-H interval, duration of the His bundle electrogram, effective refractory period and functional refractory period returned toward control values. However, the H-V and QRS intervals as well as sinoatrial conduction time were unchanged after reperfusion. Thus, reduction of anterior septal arterial flow influences not only the distal but also the proximal portion of the conduction system; the most vulnerable part is probably the His bundle. The distal portion of the conduction system is directly influenced by ischemia itself, whereas the proximal portion is influenced through other mechanisms induced by reduction of anterior septal arterial flow.

Animals↗
PubMed1977

Comparative effects of overdrive on sinus and subsidiary pacemaker function.

Recent evidence has suggested a difference in response to overdrive pacing dependent on the location of the pacemaker within the A-V conduction system. To test this hypothesis, the effects of overdrive pacing were evaluated in five anesthetized dogs with experimentally induced A-V block and in seven patients with advanced A-V block. In the animals, sinoatrial node recovery times were studied over wide ranges of rates (130 to 210 beats per minute) and durations (30 to 180 seconds) of atrial pacing. All sinus node recovery times were less than 600 msec. with a mean maximum pause of 0.540+/-0.043 seconds (M.+/-S.E.M.). In contrast, after ventricular pacing (rates 90 to 150 beats per minute; durations 30 to 180 seconds), subsidiary pacemaker recovery times were significantly greater (p less than 0.025) with a mean maximum recovery time of 28.4+/-8.3 seconds. In the seven patients studied, all sinus node recovery times were less than 1,400 msecs. with a mean maximum pause of 0.954+/-0.051 seconds. As seen with the experimental animals, a significantly longer (p less than 0.025 mean maximum subsidiary pacemaker recovery time of 3.55+/-0.92 seconds was observed. The present studies in both experimental animals and in man without evidence of sinus node dysfunction showed that sinus node recovery time was independent of both rate and duration of atrial overdrive pacing. In contrast, subsidiary pacemaker recovery time was correlated with both rate and duration of ventricular overdrive pacing. In both experimental protocols, subsidiary pacemaker recovery time was shown to exceed sinus node recovery time at all rates and at all durations of pacing. Postrecovery sinus node acceleration was consistently observed after atrial overdrive pacing. In contrast, postrecovery subsidiary pacemaker "depression" characterized ventricular overdrive pacing. It is concluded that subsidiary pacemakers are significantly more susceptible to overdrive suppression than the sinoatrial node, a feature of substantial clinical significance.

Adolescent↗
PubMed1977

Lignocaine: a new technique for intravenous administration.

Current practices of intravenous lignocaine administration may result in a significant drop in blood level between the peak serum level from the initial bolus and the subsequent steady state from the constant infusion. This can cause a significant interval when plasma lignocaine levels are less than therapeutic, and ventricular ectopy may occur. To eliminate this subtherapeutic interval, a new therapeutic approach was devised. Seven patients were studied who had no evidence of congestive heart failure or liver disease. Lignocaine was infused at a rate of 25 mg/min; infusion dosages were selected by patient weight. The above therapeutic regimen eliminated the subtherapeutic hiatus and did not result in clinical toxicity. Therefore, this new infusion technique has significant clinical advantages in patients who require therapy with intravenous lignocaine.

Adult↗
PubMed1977

Characteristics of sinoatrial conduction in patients with coronary artery disease.

Electrophysiologic studies were performed in 32 patients with angiographically documented coronary artery disease (CAD). Group I was composed of ten patients (31%) with severe stenosis (greater than or equal to 75%) proximal to the origin of the sinus node artery (SNA); group II was composed of five patients (16%) with moderate (50--75%) proximal stenosis; and group III was composed of 17 patients (53%) with insignificant (0--50%) proximal stenosis. The mean sinoatrial conduction time (SACT) for group I was 119 +/- 18 msec; group II was 84+/- 16 msec; and group III was 72 +/- 5 msec. The SACT was significantly longer in group I than in group III (P less than 0.005). In conclusion 1) in patients with CAD, SACT greater than 72 +/- 5 msec is abnormal; 2) the results suggest a pathogenetic role of CAD in the development of sinus node dysfunction; 3) the SACT is a more sensitive indicator of subtle sinus node dysfunction in CAD patients than is heart rate, sinus node response to artrial extrastimuli, or sinus node recovery time; and 4) the ability to diagnose sinus node dysfunction in its early stages and recognition that coronary artery disease is an etiologic factor may allow for the elucidation of the natural history of the sick sinus syndrome.

Adult↗
PubMed1977

Relationship between the electrical (electrocardiographic) and mechanical (echocardiographic) events in Wolff-Parkinson-White syndrome.

Studies using epicardial mapping on patients with Wolff-Parkinson-White syndrome have demonstrated that the delta vector of the electrocardiogram is a detector of the location of at least one bypass tract. In order to relate the electrical activities (preexcitation) with the mechanical activity (septal and ventricular wall motion), echocardiographic strip-chart recordings were obtained in 22 patients with Wolff-Parkinson-White syndrome. Our studies indicated that in the majority of patients with Wolff-Parkinson-White syndrome, left ventricular and septal contraction is normal, suggesting that normal activation predominates and that the determinants of abnormal septal wall motion are (1) the location (right ventricular free lateral wall or septrum) and (2) the degree (duration of the QRS complex greater than 130 msec) of ventricular preexicitation.

Adolescent↗
PubMed1977

Wolff-Parkinson-White syndrome. Alterations in electrophysiologic characteristics of the bypass tract secondary to ischemia.

Accurate electrocardiographic diagnosis of myocardial ischemia or infarction is difficult in patients with the Wolff-Parkinson-White syndrome; however, myocardial ischemia may also have profound effects on the electrophysiologic characteristics of the bypass tract in these patients. Comparison of studies performed during and two months following an episode of significant myocardial ischemia demonstrated substantial prolongation of the refractoriness of the bypass tract during the period of ischemia. Bypass refractoriness was prolonged by 196 msec, yet atrioventricular nodal refractoriness was not significantly different from normal. These studies, therefore, suggest that, on occasion, the presence of acute myocardial ischemia may, in fact, obscure the electrocardiographic diagnosis of the Wolff-Parkinson-White syndrome.

Aged↗
PubMed1976

Cardiovascular effects of ajmaline.

Ajmaline, a rauwolfia derivative, has been found to possess potent antiarrhythmic effects. The present study has been designed to define the cardiovascular effects of this drug. Hemodynamic studies performed in anesthetized and conscious dogs demonstrated no significant changes in measured hemodynamic parameters at doses equal to or less than 2 mg. per kilogram. Studies in isolated papillary muscle demonstrated no negative inotropic effects until concentrations of 1 X 10(-4). Disparate results were obtained with regard to heart rate reflecting the state of autonomic tone. Electrophysiologic studies in both anesthetized and conscious dogs demonstrated a significant depression of intraventricular conduction with no significant effect on AV nodal conduction; ventricular automaticity was not affected. Ajmaline did not alter digitalis-induced AV nodal conduction prolongation. However, ajmaline dramatically altered or abolished ventricular arrhythmias secondary to acute ischemia. In conclusion, these studies demonstrate that ajmaline specifically depresses intraventricular conduction, suggesting that this drug would be particularly effective in the treatment of re-entrant ventricular arrhythmias.

Ajmaline↗
PubMed1976

Electrophysiological effects of ajmaline in isolated cardiac tissue.

The electrophysiological effects of increasing molar concentrations of ajmaline were studied in isolated cardiac tissue, including sino-atrial node and Purkinje fibre. Ajmaline produced significant shortening of the plateau of Purkinje fibre action potential associated with marked depression of dV/dt and directly measured conduction velocity. A negative chronotropic effect was noted both in the sinus node and in spontaneously beating Purkinje fibres. Ajmaline's major electrophysiological effect appears to be depression of Purkinje fibre conduction velocity.

Action Potentials↗
PubMed1976

Wenckebach phenomenon occurring in the distal conducting system in a young adult.

This report describes the case of a young man who presented with right bundle-branch block and second degree atrioventricular block; intermittent episodes of Wenckebach periods were recorded. His bundle electrograms demonstrated progressive prolongation of the HV interval followed by block occurring distal to His. This report emphasizes the fact that the Wenckebach phenomenon as a manifestation of the distal conducting system disease can occur in young adults. The observations lend credence to the concept that Lenègre's disease can occur in young people.

Adult↗
PubMed1976

Recurrent reciprocating tachycardias in the Wolff-Parkinson-White syndrome; control by the use of a scanning pacemaker.

Frequent episodes of arrhythmias in patients with the Wolff-Parkinson-White syndrome are sometimes unresponsive to medical management. Recent emphasis has been placed on the role of surgery as a means of effectively controlling these patients' tachyarrhythmias; however, in some patients the use of permanent pacing has been espoused as an effective means of controlling arrhythmias. This report documents the efficacy of a new pacemaker with rate-scanning features, which offers significant technical advantages. Subsequent follow-up has documented the efficacy of this unit in the management of a young woman with type-A Wolff-Parkinson-White syndrome and previously intractable arrhythmias.

Adult↗
PubMed1975

The effect of lidocaine on peripheral hemodynamics.

Lidocaine was given in increasing step-wise dose concentrations of 1, 2, 3, 4, and 5 mg/minute and the resulting serum concentrations correlated with the effect of this agent on the peripheral vasculature of seven patients. Lidocaine infusion causes an immediate sustained increase in mean calf venous capacitance but little effect on mean diastolic blood pressure. In high concentration levels this agent causes an increase in mean calf blood flow and systolic blood pressure. Its effect on calf vascular resistance is variable, but there is a tendency to reduce resistance, particularly at a high concentration level. The effect of lidocaine infusion rate on serum lidocaine levels was such that the greater the infusion rate, the higher the resultant serum lidocaine levels.

Adult↗