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A Munsif

Publications and source records attributed to A Munsif.

5 recordsLinked to original sources
PubMed1995

A technique for stable His-bundle recording and pacing: electrophysiological and hemodynamic correlates.

His-bundle electrograms recorded from intracardiac electrode catheters have been a mainstay of basic and clinical electrophysiology. However, consistent His-bundle pacing has not been as readily achieved. In 13 dogs anesthetized with sodium pentobarbital (30 mg/kg), we recorded leads II and aVR as well as the His-bundle electrogram from the aortic root. A deflectable tip multipolar catheter (4 rings, 5 mm apart) was introduced via the right jugular vein into the right ventricle (RV). In 7 dogs, using fluoroscopy, the tip was placed under the tricuspid septal leaflet. In the other 6, after thoracotomy, the same placement was made by palpation through the right atrial wall. Stable His-bundle and right bundle (Rb) branch recordings were made from distal and proximal electrode pairs, respectively. H-V intervals measured 35 +/- 6 ms from the aortic root and 33 +/- 5 ms from under the tricuspid leaflet (P = NS). Rb-V measured 25 +/- 4 ms. Consistent His-bundle pacing was accomplished from the aortic root with an average stimulus intensity of 6 +/- 10 mA and from the tricuspid leaflet at 16 +/- 8 mA (P < 0.05). In 7 anesthetized dogs we compared the hemodynamic effects of A-V sequential pacing at the same heart rates using the His-bundle recording site under the septal leaflet of the tricuspid valve (A-H pacing) or pacing from the RV apex (A-RV pacing). Under normal conditions there was a significant depression of mean blood pressure when A-RV pacing was compared with atrial pacing (AOO); but no difference was found between AOO and A-H pacing.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1994

Elucidation of Prinzmetal's variant form of preexcitation.

BACKGROUND: In 1952, Prinzmetal induced preexcitation in the normal dog heart using subthreshold stimulation (SS) delivered to the right ventricle. METHODS AND RESULTS: In 12 dogs we recorded ECG leads II, aVR, His (Hb) and proximal right bundle potentials with electrode catheters at the aortic root and a special electrode that was inserted through the right ventricular (RV) free wall. In 12 others, SS was delivered to the Hb area by a catheter placed under the septal leaflet of the tricuspid valve. During SS, the HV interval shortened from 35 +/- 4 milliseconds (mean +/- SD) to 19 +/- 7 milliseconds (P = .0001), but AH intervals were unchanged. The ECG showed delta waves with aberrant QRS complexes. Endocardial electrograms showed that the origin of activation in the preexcitation beats was localized to the muscle adjacent to the Hb or proximal right bundle. When vagal stimulation induced sudden AV block, no ventricular excitation was seen, confirming the subthreshold nature of the applied stimulation. By adjusting the levels of SS, latent forms of preexcitation could be induced, eg, early local septal muscle activation but no change in the ECG leads. Premature ventricular stimuli delivered to the RV apex or outflow tract could cause manifest preexcitation in the ECG leads or inhibit expression of latent preexcitation in endocardial recordings. CONCLUSIONS: SS delivered to the RV apex or Hb area causes ventricular preexcitation, as shown previously by Prinzmetal et al. SS delivered at the insertion sites of an accessory pathway may facilitate localization of such abnormal connections, particularly when preexcitation is concealed.

Animals↗
PubMed1993

Variant forms of AV and VA conduction in the canine heart.

In 19 pentobarbital anesthetized dogs subjected to right thoracotomy, plunge wire and catheter electrodes were positioned to record and pace from the high right atrium, coronary sinus os, aortic root (for His bundle electrograms), and the right ventricular outflow tract and apex. A deflectable-tip catheter electrode was placed under the septal tricuspid leaflet for pacing the right ventricular septal crest. Electrocardiographic leads II and aVR were also recorded during atrial and ventricular pacing in the control state and during low- and high-intensity left vagosympathetic trunk stimulation. Pacing from each A or V site in 12 dogs showed normal atrioventricular (AV) and ventriculoatrial (VA) conduction over a wide range of heart rates (120-360 beats/min) with progressive AV and VA delay at each heart rate until Wenckebach cycles occurred (AV Wenckebach cycle averaged 325 +/- 44 beats/min; VA Wenckebach cycle averaged 246 +/- 52 beats/min). In two dogs, pacing from the coronary sinus os showed a 30-beat/min difference in the Wenckebach cycle rate compared to high right atrium pacing, and the AH intervals for the former were relatively insensitive to vagosympathetic trunk stimulation compared with the latter. In five other dogs, retrograde VA and HA intervals showed little, if any, decrement over a wide range of heart rates, with no immediate response to low-intensity vagal stimulation. After 7-22 seconds of continuous vagal stimulation, VA intervals abruptly prolonged and/or blocked. In all, second-degree heart block occurred at ventricular pacing rates > or = 300 beats/min in the form of atypical Wenckebach cycles. In all cases, the earliest atrial activation, as measured by a close bipolar probing electrode, was in the posterior septum adjacent to the coronary sinus os. In one dog, VA block occurred as a Mobitz type II with paroxysmal complete VA block (sinus escape rhythm) during continuous ventricular pacing at 330 beats/min. After radiofrequency ablation of the earliest atrial activation site typical VA Wenckebach cycles, immediately responsive to vagal stimulation, was then observed at a ventricular pacing rate of 150 beats/min. These data suggest that AV and VA connections in some canine hearts show varying degrees of bypass of the AV node, similar to cases reported in the clinical literature.

Animals↗
PubMed1992

Mapping in the atrioventricular junction.

Ectopic conduction is defined as the premature exit of the cardiac impulse from the specialized conduction system across a damaged Purkinje-ventricular muscle interface. This anomalous form of atrioventricular (AV) conduction was induced in the dog heart by lidocaine injection of the His bundle-interventricular septum interface and by ischemic damage of the AV junction subsequent to anterior septal artery ligation in the dog heart. The electrocardiogram (ECG) manifestation of ectopic conduction is the loss of initial forces and replacement of the Q waves with delta waves. In order to verify these effects, the authors devised a multi-electrode, malleable plaque (63 electrode sites) that could be secured at the AV junction during venous occlusion in the open-chest, anesthetized dog. Preliminary maps indicated a dramatic change in activation that proceeded from apex to base of the heart in the control state and reversed after ischemic damage to the His bundle. In vitro, it was possible to induce ectopic conduction by lidocaine injection at the interface of the right bundle branch and septal muscle. Microelectrode studies demonstrated that foot potentials, for example, electrotonic, or subthreshold potentials mediated the connection from Purkinje to muscle in the damaged zone. In a recent set of experiments in vivo, subthreshold stimulation (STS) was delivered to simulate electrotonic potentials to the His bundle region, and right ventricular apex, using multipolar electrode catheters. In the normal heart, STS delivered as DC constant current or pulse trains (1000 Hz, 50 ms pulse duration) induced shortened P-R intervals and delta waves with or without bundle branch block patterns.(ABSTRACT TRUNCATED AT 250 WORDS)

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