C.Pratap Reddy

Antegrade and retrograde conduction characteristics in three patterns of paroxysmal atrioventricular junctional reentrant tachycardia.

Abstract In 20 patients with PSVT without ventricular pre-excitation, the site of reentry and functional characteristics of Ant. and Ret. pathways were studied. Three distinct patterns of PSVT were observed. In 13 patients (group I) in whom A-V node was the site of reentry, the interval between the Ant. H bundle deflection and the following atrial echo response (H-Ae) measured 30 to 85 msec. and the Ae was partially or completely obscured by ventricular electrogram. The ratio between the H-Ae and the subsequent Ae-H interval ranged 1:3.1–17.3. In a majority of Group I patients (eight out of 13) the Ret. conduction was better than Ant. conduction, as the VACS sustained a 1:1 response at faster paced rates than AVCS. The FRP of the AVCS in Group I was determined by the A-V node in all patients and significantly exceeded the FRP of the VACS; the latter was determined by the HPS in 12 out of 13 patients. In four patients (Group II) a V-A AP silent antegradely was operative during PSVT. The H-Ae in Group II valued 145 to 200 msec. and the Ae clearly followed the ventricular electrogram, the H-Ae: Ae-H being 1:0.5–1.7. The V-A conduction in all Group II patients was better than the A-V conduction. A-V node determined the FRP of the AVCS, whereas AP determined the FRP of the VACS in Group II patients, and the former significantly exceeded the latter. Good correlation existed between PSVT, Ant. and Ret. conduction patterns in Group I and Group II patients. In three patients (Group III) the H-Ae measured 270 to 470 msec. with an H-Ae:Ae-H of 1:0.2–0.4, a relationship quite the opposite of Group I patients. No definite relationship existed between PSVT, Ant. and Ret. conduction patterns in Group III patients. The data in Group III patients were compatible with (1) A-V nodal reentry with reversal of conduction balance compared to Group I, (2) intra-atrial reentry, and (3) enhanced atrail automaticity. It is concluded (1) the site of reentry in patients with PSVT is variable, (2) a fair estimation of reentry site can be made from H-Ae and Ae-H relationship, (3) all patients with PSVT have intact V-A conduction and in most the V-A conduction is better than A-V conduction, and (4) in the majority of patients with PSVT refractoriness of the AVCS exceeds that of the VACS.

Ventricular septal motion and left ventricular dimensions during abnormal ventricular activation

To determine the effect of abnormal ventricular activation on ventricular septal motion, left ventricular endocardial motion and left ventricular dimensions, 12 patients with normal motion were studied with echocardiography during incremental pacing of the right ventricular apex, outflow and inflow regions. Three types of abnormal ventricular septal motion were seen: The type I pattern was characterized by an early rapid preejection posterior ventricular septal motion followed by another posterior systolic motion that lasted throughout ejection, both of which were associated with septal thickening. In the type II pattern an early rapid preejection posterior ventricular septal motion was followed by an anterior ejection motion; the latter was not accompanied by septal thickening. The type III pattern consisted of an early preejection posterior ventricular septal motion followed by a mid and late systolic posterior motion: the latter motion extended through diastole. During right ventricular apical pacing, 8 of 11 patients showed a type 1 pattern, 1 a type II pattern and 2 a normal septal motion. During right ventricular outflow pacing,seven of nine patients showed a type II pattern, one a type III pattern and one a type I pattern. During right ventricular inflow pacing, eight of nine patients showed a type II pattern and one a type III pattern. At faster pacing rates patterns of types I and III changed to a type II pattern (five patients). End-diastolic dimensions decreased significantly during incremental right ventricular pacing when compared with those during sinus rhythm. End-systolic dimensions decreased significantly only during right ventricular apical and outflow pacing at maximal rates. In the seven patients who had pacing from all three sites, the decrease in left ventricular dimensions did not significantly differ when the three pacing sites were compared. These findings suggest that (1) abnormal ventricular septal motion during right ventricular pacing (induced left bundle branch block patterns) is dependent on the sequence of ventricular activation; (2) ventricular septal motion during right ventricular outflow and inflow pacing is similar to that seen in spontaneous left bundle branch block, whereas the pattern of septal motion during right ventricular apical pacing is different from that of spontaneous left bundle branch block; and (3) changes in left ventricular dimension are dependent on ventricular pacing rate but independent of pacing site.

Effect of Procainamide on Reentry Within the His-Purkinje System in Man

Abstract The effects of a single intravenous infusion of 500 mg of procainamide on macro-reentry within the His-Purkinje system were assessed, in 10 patients using bundle of His electrograms and the ventricular extrastimulus method. Procainamide did not abolish reentry in any of the 10 patients and produced repetitive reentry (two or more consecutive reentrant beats) in 8 of 10 patients. On the average, procainamide caused reentry to be initiated at longer S 1 -S 2 intervals, widening the zone of reentry. In all but one patient reentry was manifest at significantly longer S 2 -H 2 intervals than control values. The H-V intervals of reentrant beats (H 2 -V 3 intervals) after procainamide were longer than control values at comparable S 2 -H 2 intervals. Procainamide shortened or abolished the retrograde gap zones thereby causing reentry to be present more frequently within the zone of reentry. No significant change was seen in effective refractory period of ventricular muscle. On the assumption that many clinically encountered ventricular arrhythmias that respond to procainamide result from micro-reentry, the observed differences between the effects of procainamide on macro- and micro-reentry may be explained on the basis of the relation between drug effect and size of the reentrant circuit. Procainamide may produce a greater increase in refractoriness in a micro-reentrant circuit than in macro-reentry, thereby producing bilateral block and abolishing reentry in the former; or if the degree of electrophysiologic changes produced by procainamide were the same in both types of circuits, then for a given change, the pathway in a micro-reentrant circuit may be too small to sustain reentry.

Electrophysiologic effects of procainamide in subtherapeutic to therapeutic doses on human atrioventricular conduction system

The effects of single intravenous infusions of 50 to 400 mg of procainamide on the functional properties of the atrioventricular (A-V) conduction system were studied in 36 patients and correlated with plasma concentrations. A 50 mg dose of procainamide resulted in a plasma concentration of less than 1.0 mug/ml and produced no electrophysiologic changes. Doses of 100, 200, 300 and 400 mg resulted in progresively increasing plasma concentrations (1.2, 1.8, 3.5 and 4.2 mug/ml, respectively). The effects of procainamide on the sinus rate were variable and not dose-related. The effects of doses of up to 300 mg on A-V nodal conduction were variable and not dose-related. Only in a dose of 400 mg did procainamide prolong A-V nodal conduction in six of seven patients. Whereas 100 mg had no effect on His-Purkinje system conduction, doses of 200, 300 and 400 mg prolonged His-Purkinje system conduction time by 6, 8 and 9 msec, respectively. Dose-related increases in atrial refractoriness started with a dose of 200 mg and became statistically significant with doses of 300 and 400 mg. The effects of procainamide on A-V nodal functional refractoriness were variable and not dose-related, but in doses of 100 to 400 mg, procainamide produced significant and progressively dose-related increases in His-Purkinje system refractoriness. Suppression of some types of ventricular arrhythmia by small doses of this drug may be explained by changes in refractoriness of the His-Purkinje system produced by doses of procainamide as small as 100 mg.

Characteristics and coexistence of two forms of ventricular echo phenomena

During the scanning of paced basic ventricular cycle lengths (V1V1) with extrastimulus method (V2) two forms of ventricular echo phenomena (Ve) were recognized. The Ve resulting from A-V nodal re-entry (VeAVN) occurred in 12 of 45 patients, from re-entry in the His-Purkinje system (Ve-HPS) in 20 of 45 patients, and simultaneous dual re-entry (Ve-AVN and Ve-HPS) occurred in five of 45 patients. The Ve-AVN (1) appeared at longer V1V2 intervals, (2) was dependent on retrograde A-V nodal conduction delay, (3) had normal QRS complexes and H-V intervals, and (4) did not occur when V2 blocked in the A-V node. (5) Ve-AVN had aberrant QRS complexes when preceded by Ve-HPS. The Ve-HPS (1) appeared at shorter V1V2 intervals, (2) was dependent upon retrograde conduction delay in the HPS, (3) its QRS morphology and axis orientation resembled V2, i.e., left bundle branch block pattern, when right ventricular apex was the site of stimulation, (4) persisted when V2 blocked in the A-V node and was abolished when V2 blocked below the bundle of His, and (5) rarely occurred in patients with pre-existing right bundle branch block. It is concluded that (1) at least two forms of Ve can result from induced premature ventricular beats, (2) Ve-HPS is more common than Ve-AVN in the presence of normal QRS complexes, and (3) coexistence of Ve-AVN and Ve-HPS can give rise to complex ECG pattern mimicking multiple multifocal premature ventricular beats.

Idiopathic long QT syndrome: Association of ventriculartachycardia with alternating left and right bundle branch block

A case of sporadic long QT syndrome with ventricular tachycardia characteristic of torsades de pointes is presented. The ECG revealed sinus rhythm with marked prolongation (less than 140%) of QT interval and alternating periods of left and right bundle branch block. The onset of ventricular tachycardia was associated with alternating left and right bundle branch block and the disappearance of bundle branch block coincided with the resolution of ventricular tachycardia. This observation suggests the possibility that heterogeneous repolarization of the bundle branch system contributed to ventricular tachycardia either alone or in combination with dispersion of refractoriness of the ventricular myocardium.

Study of the temporal effects on conduction and refractoriness of the His-Purkinje system in man

Temporal effects on refractoriness within the His-Purkinje system (HPS) were studied in 14 patients in whom effective refractory period (ERP) of HPS could be determined, using His bundle electrograms, incremental atrial pacing, and atrial extrastimulus method. His-Purkinje conduction times (H-V interval) and relative (R), effective (E), and functional (F) refractory periods (RP) of HPS were measured during the control period and repeat measurements were made after a 30 minute interval. H-V intervals were unchanged from control in all patients. Although changes of the magnitude of 5 to 25 msec. in either direction from control values commonly occurred, on the average, no statistically significant changes were seen in RRP, ERP, or FRP of HPS. The results of the present study confirm the stability of refractoriness of HPS over a 30 minute period and provide baseline data for future investigations of cardiovascular drugs which act primarily on the distal part of the A-V conduction system.

Asystole during treatment with amiodarone in a patient with persistent atrial tachycardia

During treatment with amiodarone, digoxin and nadolol, asystole occurred repeatedly in a patient with chronic persistent automatic atrial tachycardia. Asystole did not occur after discontinuation of drug therapy, and rechallenge with amiodarone alone produced marked overdrive suppression of all pacemakers resulting in asystole. Amiodarone serum level was within therapeutic range. The possible electrophysiologic mechanisms by which amiodarone might suppress both normal and abnormal pacemakers are discussed. The occurrence of asystole at therapeutic serum concentration of amiodarone suggests that this drug should be used with caution.

Paroxysmal ventricular tachycardia in Wolff-Parkinson-White syndrome: case report and review of the literature.

A case with Type A Wolff-Parkinson-White pattern and recurrent sustained ventricular tachycardia is presented. Because of ventricular pre-excitation, electrocardiographic clues suggestive of ventricular tachycardia were ignored and the diagnosis of supraventricular tachycardia with conduction to the ventricles over the accessory pathway was made during each admission to the hospital. Ventricular tachycardia was suspected only when programmed stimulation studies performed twelve years after initial presentation and many hospitalizations failed to induce a tachycardia with a QRS pattern similar to that of spontaneously occurring tachycardia. The diagnosis of ventricular tachycardia was later confirmed by intracardiac recordings made during a spontaneous episode of tachycardia. Tachycardia was unresponsive to all conventional antiarrhythmic agents but was controlled with amiodarone. The differential diagnosis of wide QRS complex tachycardia in patients with Wolff-Parkinson-White syndrome, the implications of correctly diagnosing the tachycardia, and the usefulness of intracardiac electrophysiologic studies in differentiating supraventricular tachycardia with aberrant conduction from ventricular tachycardia are discussed.

Intra His Purkinje gap phenomenon during retrograde conduction in man

Ventricular refractory period studies were performed in 24 patients using the ventricular extrastimulus (V2) method at a basic ventricular drive (V1V1). Gap phenomenon confined to the His-Purkinje system (V-H gap) during retrograde conduction was observed in six of 24 patients. In this form of gap, the premature impulse (V2) is initially blocked in the His-Purkinje system (HPS) as recognized by the absence of retrograde His bundle deflection (H2) and atrial depolarization (A2) following V2. At closer V1V2 intervals, V2 resumed conduction to the bundle of His (H2) but not to the atria. The mechanism of this form of gap is similar to the one proposed for the previously described gap phenomena in ventriculoatrial (V-A) conduction and involves proximal delay allowing more time for distal recovery. At shorter V1V2 intervals, V2 resumes conduction to the bundle of His because it encounters sufficient delay in some region below the His bundle. However, this delay may be insufficient to allow recovery of excitability at the A-V node and hence resumption of conduction to the atria is not an integral part of V-H gap. The relation of V-H gaps to the occurrence of reentry within the HPS (V2 phenomenon) is discussed. V-H gaps also explain the failure of some ventricular premature beats (VPBs) to show the effects of concealed conduction in the A-V node. The similarities and differences between V-A and V-H gaps during retrograde conduction are discussed.