Biomedical subjects

W J Mandel

Publications and source records attributed to W J Mandel.

At least 145 records · Page 8Linked to original sources

PubMed1975

The Wolff-Parkinson-White syndrome: pharmacologic effects of procaine amide.

The effect of procaine amide, 10 mg. per kilogram via intravenous infusion, was studied in 13 patients with the WPW syndrome. The delta wave was eliminated by procaine amide in 10 and modified in three patients. This effect lasted between 30 minutes and 8 1/2 hours and was unrelated to the total dose administered. Anterograde A-V conduction was assessed by atrial pacing with increasing rates. More rapid atrial pacing rates with 1:1 A-V conduction were observed in patients who maintained rather than lost their delta wave during pacing. Ventriculoatrial conduction was assessed with ventricular pacing at increasing rates; ventricular conduction time was fixed regardless on the pacing rate. Procaine amide significantly prolonged V-A conduction time in six and blocked V-A conduction in one patient. In addition, A-V and V-A refractory periods were measured by the extrastimulus technique. Two types of responses were observed: (1) Type I or (2) line of identity. A-V nodal refractoriness was observed to be within the normal range. Procaine amide converted anterograde line of identity responses to Type I responses in all patients who had their delta waves eliminated. In this patient group, bypass refractoriness was shorter than A-V nodal refractoriness. Procaine amide was not observed to alter significantly normal A-V conduction as assessed by atrial pacing or A-V refractory period measurements. Furthermore, a significant disparity between the effects of procaine amide on anterograde and retrograde bypass refractoriness was observed. Tachycardias could be induced in nine of the 13 patients with a mean rate of 167.2 +/- 7.9 beats per minute; delta waves were abent during all episodes of tachycardia. Procaine amide prevented tachycardia induction in six of the none patients. Procaine amide therefore demonstrates electrophysiologic effects which would be beneficial for prevention or treatment of reciprocating tachycardias in the WPW syndrome. Moreover, procaine amide would be an ideal agent for the prevention of rapid ventricular rates in patients with the WPW syndrome and atrial fibrillation.

Adolescent↗

PubMed1975

Cardiorenal effects of lidocaine and procaine amide in the conscious dog.

Simultaneous measurements of hemodynamics, arterioventricular (AV) conduction, and renal functioner were obtained in conscious dogs. Catheters were implanted for the long-term measurement of central aortic, right ventricular, and pulmonary artery pressure. AV conduction was assessed following surgical implantation of multipolar electrode plaques in the area of the bundle of His, as well as on the epicardium of the right and left atria and ventricles. Renal function was assessed utilizing standard techniques. Following control measurements, lidocaine, 1 mg/kg, or procaine amide, 10 mg/kg, was administered intravenously. Subsequently, serial measurements were obtained for a 90-min period. No significant changes in hemodynamics were observed following either drug. Procaine amide produced a significant increase in heart rate and a minimal increase in QRS duration associated with a decrease in low right atrial to His bundle conduction time. However, no significant changes in cardiac conduction were observed after lidocaine administration. Renal function was unaffected by lidocaine but significantly depressed by procaine amide, as demonstrated by a decrease in GFR and effective renal flow. In summary, acute administration of procaine amide significantly alters renal function in the conscious dog with minimal effects on AV conduction and hemodynamics.

Aminohippuric Acids↗

PubMed1975

Atrioventricular nodal reentry in the Wolff-Parkinson-White syndrome.

Wolff, Parkinson, and White, in their initial description of the syndrome that bears their names, emphasized the association of tachycardias with the electrocardiographic abnormality. Subsequent investigations have identified, both anatomically and electrophysiologically, that dual pathways of atrioventricular (AV) conduction exist. Furthermore, experimental and clinical evidence has stressed that the mechanism of tachycardia production in the syndrome appears to reentry utilizing these dual pathways. However, recent studies have emphasized that other mechanisms of tachycardia production may be responsible for the arrhythmias seen in this syndrome. The present report identifies that AV nodal reentry may be the sole mechanism for tachycardia induction in the Wolff-Parkinson-White (WPW) syndrome. This finding may be of great clinical significance in light of the availability of surgical therapy for WPW patients with intractable arrhythmias.

Adolescent↗

PubMed1975

Prolongation of the tachycardia zone: a possible mechanism for medical failure in paroxysmal supraventricular tachycardia.

Paroxysmal supraventricular tachycardia in man has been considered to be due to either development of reentry utilizing AV junctional tissue or the presence of an ectopic pacemaker located within the atrium. Most contemporary information suggests that AV junctional reentry is the dominant mechanism for this arrhythmia in man. This present study identifies that the frequence of tachycardia episodes may be correlated with the width of a tachycardia zone as determined by the atrial extrastimulus technique. Moreover, pharmacological therapy directed toward the elimination of this arrhythmia can be assessed utilizing this atrial stimulation technique. Findings in this present study identify that, in patients with widened tachycardia zones, propranolol therapy may not be efficacious. This latter finding is no contrast to the previous observations suggesting that propranolol therapy is the drug of choice for reentrant arrhythmias in man.

Atrioventricular Node↗

PubMed1974