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R J Sung

Publications and source records attributed to R J Sung.

At least 19 recordsLinked to original sources
PubMed1992

Negative dromotropism of adenosine under beta-adrenergic stimulation with isoproterenol.

Adenosine depresses atrioventricular (AV) nodal function by binding to specific A1 receptors which activate the acetylcholine, adenosine-regulated potassium current. In addition, adenosine can act to antagonize the effects of beta-adrenergic stimulation on AV nodal function. To assess the negative dromotropic effects of adenosine under beta-adrenergic stimulation, 15 patients were studied during clinical electrophysiologic study. During high right atrial pacing at a cycle length of 400 to 600 ms, adenosine was injected intravenously at an initial dose of 0.5 mg followed by a stepwise increment of 0.5 or 1.0 mg given at 5-minute intervals until a maximal dose of 12 mg was achieved or AV block developed. Intravenous isoproterenol (1 to 3 micrograms/min) was then infused to accelerate sinus rate by 20 to 30% during which intravenous injection of incremental doses of adenosine as described was repeated. The AV nodal conduction time (AH interval) was measured at each dose of adenosine. Dose-response curves of AV nodal conduction time (expressed as percent increase in AH interval) were studied during the control state and during isoproterenol infusion. The dose of adenosine required to produce AV nodal Wenckebach block, the increase in the AH interval by 50% (ED50) and the maximal response (Emax) were 3.4 +/- 0.9 mg, 1.8 +/- 0.9 mg and 60 +/- 4%, respectively, in the control state, and 3.7 +/- 0.8 mg, 2.0 +/- 0.7 mg and 56 +/- 4%, respectively, during isoproterenol infusion. No significant changes in ED50, Emax and the dose of adenosine yielding AV nodal Wenckebach block could be demonstrated between the control state and during isoproterenol infusion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenosine↗
PubMed1979

His bundle electrocardiography in digitalis-induced "atrioventricular junctional" Wenckebach periods with irregular H-H intervals.

His bundle electrograms were recorded during catheter insertion for prophylactic demand pacing in two patients with accelerated or nonaccelerated "atrioventricular (A-V) junctional" rhythms associated with A-V junctional Wenckebach periods. This appears to be the first published report of so-called A-V junctional Wenckebach periods in which the characteristic irregularities of the H-H intervals were recorded. Patient 1 had an additional area of "complete" anterograde A-V nodal (A-H) block. In Patient 2 the rate of impulse formation was consistent with nonparoxysmal A-V junctional tachycardia. The His bundle recordings were obtained in patients with digitalis toxicity and should be interpreted in the context. The integration of clinical and intracardiac findings with extrapolations from microelectrode and pharmacolic studies and with deductions from the clinical electrocardiograms suggests that the conduction disturbances probably occurred within the A-V node itself (in its AN region). This hypothesis implies that automaticity also originated in the A-V node because the site of impulse formation must have been proximal to the site of the Wenckebach periods. However, conclusive proof of of these postulates will require further studies with refined techniques.

Bundle of His↗
PubMed1979

The fast-slow form of atrioventricular nodal reentrant tachycardia in children.

An unusual form of atrioventricular (A-V) nodal reentry is described as the underlying mechanism for incessant tachycardia in two children. During tachycardia a fast pathway was utilized for anterograde conduction and a slow pathway for retrograde conduction. This is the reverse of the usual form of A-V nodal reentrant tachycardia, in which the slow pathway is utilized for anterograde conduction and the fast pathway for retrograde conduction. One patient had a smooth ventriculoatrial (V-A) conduction curve demonstrating exclusive utilization of the slow pathway for retrograde conduction. The other had a discontinuous V-A conduction curve demonstrating failure of retrograde fast pathway conduction with resultant slow pathway conduction. In both cases the retrograde effective refractory period of the fast pathway was longer than that of the slow pathway, resulting in the establishment of this unusual reentry circuit. Both patients had a superior P axis with a P-R interval shorter than the R-P interval during tachycardia, features described in a significant number of children with incessant tachycardia. This unusual form of reentrant tachycardia can be suggested by its electrocardiographic pattern and is another mechanism for reentrant tachycardia not previously documented in children.

Atrioventricular Node↗
PubMed1979

Right ventricular apical activation times in patients with conduction disturbances occurring during acute transmural myocardial infarction.

His bundle and right ventricular apical electrograms were recorded in 18 patients with acute transmural myocardial infarction in whom catheter insertion was considered necessary for clinical reasons. The V-RVA and H-V intervals were of normal duration (5 to 30 and 35 to 55 msec, respectively) in five patients (Group 1) with persistently narrow (less than 100 msec) QRS complexes. In contrast, 13 patients (Group 2) who manifested a "complete" right bundle branch block pattern within 96 hours after admission had prolonged V-RVA intervals (range 50 to 80 msec, mean 59.2 msec) and H-V intervals that were at the upper limits of normal or prolonged (range 55 to 90 msec, mean 63 msec). In 6 of these 13 patients, the duration of the V-RVA interval became normal when the "complete" right bundle branch block pattern disappeared and was replaced by a "complete" left bundle branch block pattern in three patients and by narrow QRS complexes in the three other patients. This study showed that transmural myocardial infarction in itself did not increase the duration of the V-RVA interval even when "complete" left bundle branch block was present. Moreover, a prolonged V-RVA interval coexsting with a "complete" right bundle branch block pattern was not due to distal right bundle branch block but resulted from a conduction disturbance located in the proximal portions of the right bundle, or perhaps, even within the His bundle itself.

Adult↗
PubMed1979

Ventricular tachycardia and ventricular fibrillation in patients with short P-R intervals and narrow QRS complexes.

Eleven patients with short P-R intervals and narrow QRS complexes had ventricular tachycardia due to organic heart disease: mitral valve prolapse with mitral insufficiency (2 patients); alcoholic (?) cardiomyopathy (2 patients); and coronary artery disease (7 patients). Intracardiac studies showed short A-H intervals during sinus rhythm in all cases. The onset of ventricular fibrillation (which, to our knowledge, has not been observed in patients having short P-R and A-H intervals coexisting with narrow QRS complexes) was documented in 4 cases. Only 1 patient (with quinidine syncope) had been premedicated. In the 3 other patients the episodes of ventricular fibrillation appeared during bouts of atrial fibrillation with rapid ventricular rates which could have been an exprerssion of the "enhanced A-V conduction" that had been manifested in sinus beats by short P-R and A-H intervals. In clinical settings and physiological conditions proven to be hemodynamically unstable (such as transient ischemia or acute myocardial infarction) these rapid ventricular rates could have led to ventricular fibrillation; directly because of the R-on-T phenomenon, and/or indirectly due to decreased coronary perfusion. Ventricular tachycardia and ventricular fibrillation due to organic heart disease probably occur more often than suggested by the few reported cases in the literature. Its significance, however, has to be clarified by further prospective studies.

Adult↗
PubMed1979

Mode of operation induced by rapid external chest wall stimulation in patients with normally functioning QRS-inhibited (VVI) pacemakers.

The effects of rapid external chest wall stimulation were evaluated in 10 patients with normally-operating unipolar, lithium-powered, QRS-inhibited pacemakers functioning in their control VVI (QRS-inhibited) mode. Stimuli delivered at slow rates resulted in the expected pacemaker inhibition. On the other hand, during rapid (greater than 900/min) external chest wall stimulation, 8 pacemakers reverted to a VOO mode, 1 to a VVI mode and 1 to either a VVI or VOO mode. No pacemaker was totally inhibited by rapid chest wall stimulation. In accordance with the manufacturer's specifications, the rate to which the implanted pacemakers reverted during the VOO modes produced by the fast external stimuli were the same as those of the VOO modes induced by proper application of an external magnet. Although rapid external chest wall stimulation proved to be a safe procedure, more studies are necessary to determine its usefulness in the follow-up of patients with implanted QRS-inhibited (VVI) pacemakers. At present, conclusions cannot be drawn regarding whether these pacemakers will revert to a mode of operation similar to that induced by rapid external chest wall stimulation when subjected to extrinsic sources of strong electromagnetic interference.

Cardiac Pacing, Artificial↗
PubMed1979

Antiarrhythmic drug therapy in survivors of prehospital cardiac arrest: comparison of effects on chronic ventricular arrhythmias and recurrent cardiac arrest.

We studied the long-term effects of membrane-active antiarrhythmic agents on chronic ventricular arrhythmias in patients who have survived prehospital cardiac arrest. Among 16 patients treated with a dose-adjusted, plasma level-monitored antiarrhythmic regimen, eight have survived for longer than 12 months and eight have had recurrent cardiac arrests (RCAs). Monthly Holter monitor tapes (HM) recorded during the 4 months before the eight RCAs were compared with monthly HM tapes matched for time of entry and duration of follow-up in the eight patients who did not have RCAs. Transient or persistent complex ventricular ectopic depolarizations (VEDs) have been recorded on 47 of the 63 monthly HM tapes (75%). The difference between VEDs in the RCA patients (mean 153 VEDs/hr, median 19 VEDs/hr) and VEDs in the patients who have not had RCA (mean 122 VEDs/hr, median 8 VEDs/hr) was not significant (p less than 0.2); nor was there a predictable relationship between therapeutic plasma levels of antiarrhythmic agents and the frequency and complexity of chronic asymptomatic VEDs (therapeutic levels--mean 104 VEDs/hr, median 6 VEDs/hr; subtherapeutic levels--mean 184 VEDs/hr, median 21 VEDs/hr). Differences were not significant (p greater than 0.1). In contrast, all eight RCA patients had unstable plasma levels (21 of 31 determinations subtherapeutic) while six of the eight patients who have not had RCA had consistently therapeutic levels (p less than 0.01). Thus, adequate plasma levels of antiarrhythmic agents may protect against RCA, despite failure to suppress VEDs predictably. The apparent dissociation between predictable suppression of chronic VEDs and protection against RCA suggests that clinical effectiveness of these agents may not be best measured by their effect on chronic VEDs.

Adult↗
PubMed1979

Programmed simultaneous biventricular stimulation in man, with special reference to its use in the evaluation of intraventricular reentry.

Programmed stimulation was alternatively performed exclusively from the right ventricular endocardium, exclusively from the left ventricular epicardium and simultaneously from both ventricles in 8 patients who did not have coronary artery disease or bundle branch block. A specially constructed QRS triggered pacemaker, (with a refractory period of 260 msec and an escape interval of 800 msec) connected to the right ventricular and left ventricular electrodes, was used to perform simultaneous biventricular stimulation. The latter had no untoward effects and was not more dangerous than exclusive right ventricular, or exclusive left ventricular, stimulation. In 3 patients, pacemaker-induced repetitive firing occurred during right and left ventricular pacing. Persistence of this phenomenon (in these 3 patients) during simultaneous biventricular stimulation is in keeping either with a microreentry occurring in the vicinity of the electrodes or with a macroreentry involving the bundle branches. A more precise evaluation of the reentry circuit requires that left ventricular pacing be performed from an endocardial (rather than from an epicardial) site. This study suggests that the pulse generator described in the present communication can be used to produce simultaneous atrial and ventricular activation (or pacing) by connecting one pole to an atrial electrode and the other pole to a ventricular electrode. This modality of stimulation can be effective in preventing or abolishing some types of reciprocating atrioventricular tachycardias.

Aged↗
PubMed1978

Multiple intracardiac recordings in evaluation of patterns occurring during attempted his bundle pacing in man.

The various patterns resulting from stimulation through the catheter electrodes recording His bundle activity were evaluated in 30 patients using intracardiac electrograms from the right ventricular apex (RVA), posterosuperior wall of the left ventricle (LV), high right atrium (HRA) and left atrium (LA) in the vicinity of the coronary sinus. His bundle pacing was characterized by a QRS complex and stimulus (St)-V, St-RVA and St-LV intervals that equated the QRS configuration, H-V, H-RVA and H-LV intervals of sinus beats. Right septal pacing produced pattern of "complete" left bundle branch block (with normal electrical axis) associated with St-V intervals of 0 msec, and St-RVA and St-LV intervals of different duration from that of the H-RVA and H-LV intervals recorded during sinus rhythm. Fusion beats resulting from simultaneous activation of His bundle and right septal muscle were characterized by St-V intervals of 0 msec and St-RVA or St-LV intervals of similar duration to that of the H-RVA or H-LV intervals of sinus beats. Fusion QRS configuration depended on the type of ventricular complex present during sinus rhythm. Analysis of the retrograde atrial activation intervals permitted differentiation among impulse initiation at the low right atrium, His bundle or right septal muscle. Simultaneous recording of multiple atrial and ventricular electrograms has enhanced understanding of the complex patterns observed during attempted His bundle pacing in man.

Bundle of His↗
PubMed1978

Second degree His-Purkinje block during his bundle pacing.

This report presents, for the first time, clear evidence supporting the occurrence of Wenckebach and 2:1 H-V block during His bundle pacing. The simultaneous recording of various intracardiac electrograms, as well as the comparison of the effects produced by selective His bundle pacing and high right atrial pacing at the same rates, permitted the identification of conduction disturbances located distal to the paced His bundle site. This could be done although one criterion usually required to diagnose selective His bundle pacing (namely, stimulus-V intervals of constant duration) was not present.

Bundle of His↗
PubMed1978

Exposure of concealed right bundle branch block in Wolff-Parkinson-White type B by pacing from the vicinity of the A-V node.

In two infants with Wolff-Parkinson-White type B, right bundle branch block was concealed during sinus rhythm and pacing from close to the atrial entrance of the right-sided accessory pathway. However, pacing from the vicinity of the A-V node, the A-V node itself, and the His bundle exposed the right bundle branch block by producing exclusive ventricular activation through the normal, A-V nodal His-Purkinje pathway. In addition, pacing from close to the A-V node also resulted in fusion beats characterized by absence of delta waves with (pseudo) normal QRS complexes and short H-V intervals. False patterns of tachycardia-dependent and bradycardia-dependent block in the accessory pathway also occurred. These dynamic phenomena were attributed to the (peri-A-V nodal) pacing-related, relatively early arrival of excitation at the ventricles through the normal pathways coexisting with delayed arrival of excitation via the accessory pathway. The latter in turn was due to the longer intra-atrial conduction time from paced (peri-A-V nodal) site to atrial entrance of the accessory pathway.

Atrioventricular Node↗
PubMed1978

Effects of proximal intra-atrial Wenckebach on distal atrioventricular nodal, and His-Purkinje, block with special reference to the theory of alternating Wenckebach periods.

Intra-atrial Wenckebach patterns of stimulus-to-response intervals coexisting with distal, A-V nodal, and His-Purkinje, blocks occurred in eight patients during high right atrial stimulation at rapid rates. In two patients with 2:1 St-H block and in two patients with 4:1 St-V block, an increase in the degree of block occurred when the proximal intra-atrial Wenckebach cycle was completed with the stimulus which otherwise would have been propagated to the distal levels. However, the degree of block did not increase when the intra-atrial Wenckebach terminated in distally blocked stimuli. In one patient progression of 4:1 into 5:1 St-V block was due to the association of intra-atrial Wenckebach with alternating 2:1 block at the A-V nodal, and His-Purkinje, levels. Contrasting with most reports dealing with the mechanisms of alternating Wenckebach in a single structure, this study permitted the determination of the boundaries between proximal and more distal levels. It also showed that alternating Wenckebach cycles (of St-H intervals) ending with two consecutively blocked stimuli could result from the association of proximal intra-atrial Wenckebach with distal, A-V nodal Wenckebach, or abortive AW, cycles. The electrophysiology of documented two, or three, level block in different structures has validated previously made assumptions regarding multilevel block in a single structure.

Atrioventricular Node↗