C. Pratap Reddy

Use of isoproterenol as an aid to electric induction of chronic recurrent ventricular tachycardia

Abstract Initiation of ventricular tachycardia using isoproterenol administration and programmed stimulation of the heart was attempted in 11 patients with recurrent ventricular tachycardia in whom standard stimulation techniques alone failed to induce the tachycardia. Seven patients had nonsustained and four had sustained ventricular tachycardla. In four patients, ventricular tachycardia was induced by exercise; in the remaining seven, tachycardia was not exercise-induced. Before isoproterenol, single and double ventricular premature depolarizations and rapid ventricular pacing failed to induce the tachycardia in all patients. After intravenous administration of small amounts (6 to 16 μg) of isoproterenol, critically timed single and double ventricular premature depolarizations could reproducibly initiate and terminate the tachycardia in six of seven patients with nonsustained ventricular tachycardia and in three of four patients with sustained ventricular tachycardia. Propranolol (0.05 to 0.1 mg/kg body weight) was effective in blocking the arrhythmia-facilitating effect of isoproterenol in four patients and procainamide (10 mg/kg) was effective in three patients. In two patients, neither propranolol nor procainamide was effective. The precise mechanisms underlying the arrhythmogenic effects of isoproterenol in each patient are not obvious. Nonetheless, our results suggest that the administration of isoproterenol is a useful adjunct when attempting to initiate ventricular tachycardia by stimulation techniques. As such, it should be helpful in carrying out studies designed to establish appropriate therapeutic interventions in patients with recurrent ventricular tachycardia.

Treatment of ventricular tachycardia using an automatic scanning extrastimulus pacemaker

A patient with recurrent sustained ventricular tachycardia that was resistant to both conventional and experimental antiarrhythmic agents was treated with a programmable automatic scanning extrastimulus pacemaker. The antitachycardia pacemaker was implanted only after many episodes of spontaneous and laboratory-induced ventricular tachycardia were reliably and reproducibly terminated with programmed ventricular extrastimuli. In the 6 months since implantation of the automatic scanning pacemaker, all episodes of ventricular tachycardia have been terminated successfully by the pacemaker. Acceleration of rate of ventricular tachycardia or induction of ventricular fibrillation did not occur at any time during attempted termination of ventricular tachycardia by the pacemaker. The advantages of the automatic scanning extrastimulus pacemaker over other antitachycardia pacemakers are discussed.

Effect of lidocaine on escape rate in patients with complete atrioventricular block: B. Proximal his bundle block

Lidocaine was administered intravenously (a loading dose of 1.5 mg/kg body weight followed by a 3 mg/min infusion) to 10 patients with complete atrioventricular (A-V) block proximal to the His bundle and A-V junctional escape rhythm. A-V block was not due to an acute myocardial infarction in seven patients (group I) and was due to an acute inferior wall infarction in three patients (group II). Lidocaine had either no or only a slight depressant effect on the rate of the escape pacemaker in patients in group I but caused severe bradycardia or asystole in two of three patients in group II. Lidocaine had no consistent effect on the atrial rate and did not change the QRS duration and H-V intervals in any patient. These observations are consistent with the results of animal studies that showed that lidocaine selectively depressed conduction in ischemic or depolarized myocardium. The findings also suggest that the use of lidocaine without prior insertion of a pacemaker is unsafe in patients with acute myocardial infarction and complete A-V block proximal to the His bundle.

Effect of amiodarone on electric induction, morphology, and rate of ventricular tachycardia and its relation to clinical efficacy.

Using His bundle electrograms and programmed ventricular stimulation, the effects of chronic amiodarone treatment on induction, morphology, and the rate of ventricular tachycardia (VT) were studied in 17 consecutive patients treated with amiodarone for control of recurrent sustained VT or ventricular fibrilation. Studies were done before and after treatment with amiodarone for an average duration of 5.3 (range 2 to 18) months. During the control study, sustained VT could be induced in 16 patients. VT was initiated by single or double right ventricular (RV) extrastimuli in 14 patients, by double left ventricular (LV) extrastimuli in 1 patient, and by RV burst pacing in 1 patient. Only one pattern (morphology) of VT similar to that of spontaneous VT was induced in 12 patients and two patterns of VT in 4 patients. The average cycle length (CL) (mean ± SD) of induced VT was 325.8 ± 61.2 ms. After amiodarone, VT could be induced in 7 of 17 patients and was initiated by single RV extrastimuli in 5 patients, double RV extrastimuli in 1 patient, and RV burst pacing in 1 patient. In 3 of 5 patients in whom VT could be initiated by single RV extrastimuli, initiation of VT required double RV or double LV extrastimuli in the control study; in 1 of 5 patients VT could not be induced in the control study. Amiodarone induced nonclinical, polymorphic VT in 4 patients in whom only clinical VT could be induced during the control study. Compared to control, the CL of induced VT was significantly longer (322 ± 65.7 vs 416 ± 41.5 ms; P < 0.001). During a follow‐up period ranging from 4 to 53 (mean ± SD; 18.6 ± 11.4) months, VT did not recur in 8 patients with no inducible VT and in 6 patients with persistence of inducible VT. One patient without inducible VT died suddenly; VT recurred in 2 patients, one without inducible VT and one with inducible VT. The results show that programmed stimulation studies late in the course of treatment do not accurately reflect the clinical efficacy of amiodarone in VT.

Effect of verapamil on retrograde conduction in atrioventricular nodal reentrant tachycardia

Using His bundle electrograms, incremental ventricular pacing and the ventricular extrastimulus (V2) technique, the effects of intravenous verapamil, 0.2 mg/kg, on retrograde atrioventricular (AV) nodal conduction during ventricular pacing, premature ventricular stimulation (H2A2 interval) and paroxysmal supraventricular tachycardia (SVT) (H-Ae interval) were evaluated in 11 patients with AV nodal reentrant tachycardia. During the control study, SVT could be induced in all 11 patients. After verapamil administration, SVT or atrial echo beats could be induced in 5 patients. Verapamil produced ventriculoatrial (VA) block at a longer cycle length than that during the control study in 10 of 11 patients (295 +/- 27 vs 352 +/- 40 ms, p less than 0.01), but prolonged H2A2 interval in only 5 of 11 patients (37 +/- 6 vs 60 +/- 31 ms, p less than 0.05). In all 5 patients with persistence of inducible SVT or atrial echo beats after verapamil treatment, the H-Ae interval remained unchanged even though in 4 of these 5 patients VA conduction time or H2A2 interval was prolonged. Correlation between the paced cycle length which induced VA block, the shortest V1H2 interval achieved during premature ventricular stimulation and the cycle length of SVT revealed that in all instances in which verapamil induced VA block at a longer cycle length than in controls but did not prolong H2A2 or H-Ae interval, the shortest V1H2 interval and the cycle length of SVT (H-H interval) were significantly longer than the ventricular paced cycle length which produced VA block.(ABSTRACT TRUNCATED AT 250 WORDS)

Absence of slow channel-dependent conduction within the His-Purkinje (bundle branch) reentrant circuit: A clinical and experimental study of the effects of verapamil

Abstract The effects of intravenous verapamil on intraventricular conduction and reentry within the His-Purkinje system were studied in 10 patients and 8 dogs using His bundle electrograms and the ventricular extrastimulus method. In the clinical study, ventricular stimulation was performed by applying stimuli of two times diastolic threshold current strength and in the dog study by applying stimuli ranging in strength from two times diastolic threshold strength to 40 mA. In the clinical study, verapamil was given intravenously as a bolus injection (0.075 to 0.15 mg/kg body weight) and in the dog study as a rapid infusion (0.7 to 1 mg/kg) over 10 minutes followed by continuous infusion at a rate of 0.014 mg/kg per min. Plasma verapamil concentrations ranged from 91 to 173 ng/ml (mean ± standard deviation 138 ± 27) in the clinical study and from 103 to 638 ng/ml (mean 459 ± 174) in the dog study. In both studies, verapamil produced no change in latency and intramyocardial (duration of QRS complex) and His-Purkinje (V 2 -H 2 interval) conduction of even the earliest premature impulses delivered before the repolarization of the His-Purkinje system or ventricular muscle, or both, was completed; that is, some fibers might have been at the level of membrane potential at which conduction becomes wholly or in part dependent on the current flowing through the slow channel. Verapamil did not change significantly the determinants of reentry and did not abolish or modify the zone of reentry in any of the 10 patients. These results show that in patients with normal intraventricular conduction, slow channel-dependent conduction plays no role in the propagation of even the earliest premature impulses through the His-Purkinje reentrant circuit. In the absence of any evidence of slow channel-de-pendent conduction, one must assume that the slow propagation of very early premature impulses was mediated by incompletely reactivated rapid inward current system. These observations suggest that the system responsible for slow conduction cannot be recognized from the magnitude of conduction delay.

Re-entry near the site of the ventricular parasystolic focus: an ECG study of patients with artificial ventricular pacemakers.

Morphology of ventricular ectopic complexes was examined in 1,746 ECGs of 149 patients with permanent ventricular pacemakers. In 20 of 80 patients (25%) the morphology of ventricular ectopic complexes was similar to that of the paced complex. This resulted in a ventricular couplet where the spontaneous premature complex originated at the site of pacing, possibly due to local re-entry. Repeated re-entry (two ventricular ectopic complexes in a row) occurred only in one of these patients, and none had ventricular tachycardia. These observations 1) verify the existence of a mechanism which we have postulated in explaining the association between couplets and ventricular parasystole, and 2) confirm the rare occurrence of repeated reentry in such a setting. Other observations in this studyshow that premature stimulation during right ventricular pacing may alter morphology of the ventricular complex from a left to right bundle branch block pattern in some leads.

Intravenous disopyramide: safety and efficacy of a new dosage regimen.

The efficacy and safety of a new dosage regimen of intravenous disopyramide in ventricular arrhythmias were evaluated in 10 patients. Each had at least four premature ventricular contractions (PVCs)/min during a 30‐min period before dosing. By the classification of Lown et al.,18 grade III arrhythmia was present in four patients, grade IVA in three patients, and grade IVB in three patients. Disopyramide was injected intravenously as a bolus of 0.5 mg/kg over 5 min. Each patient received two to three additional boluses of same strength with 5‐min intervals between each dosing during the first hour. Continuous intravenous infusion was started with the first bolus and continued at a rate of 1 mg/kg/hr for 3 hr and at 0.4 mg/kg/hrfor 15 hr. All patients had continuous Hoher monitoring throughout the 18‐hr treatment period and for 30 to 60 min before treatment. In eight patients the grade of arrhythmia after drug decreased and the frequency of PVCs fell by 70% to 100% (>85% in six patients and <85% in two patients), and the response persisted during the continuous infusion. In two patients PVC frequency increased. For the group as a whole, PVC frequency decreased on the average by 68.4%. Therapeutic serum levels (>2 µg/ml) were reached after the first or second bolus and were maintained during the continuous infusion period. There were no side effects necessitating termination of disopyramide infusion. The dosage regimen of intravenous disopyramide evaluated was effective in 60% of patients with ventricular arrhythmia, induced no severe toxic effects, and rapidly achieved therapeutic serum levels that were maintained during continuous infusion.

Effects of verapamil on the arrhythmogenic action of acetylstrophanthidin.

Although coadministration of verapamil and digoxin results in significant increases in plasma glycoside concentrations, evidence of digitalis toxicity appears to be infrequent with this combination. To evaluate the effect of verapamil on electrophysiologic toxicity from digitalis, 5 anesthetized dogs were instrumented for physiologic recording and given acetylstrophanthidin by intravenous infusion until evidence of toxicity appeared. Each animal was then treated with verapamil intravenously, with mean steady-state plasma levels of 177 +/- 30 ng/ml, and acetylstrophanthidin infusion repeated; after return of sinus rhythm, the verapamil infusion was increased (producing mean levels of 379 +/- 50 ng/ml) and acetylstrophanthidin given a third time. Prior to verapamil dosing, ventricular ectopy was the manifestation of glycoside toxicity; following the first verapamil infusion, only 20% of the dogs developed ectopy, the remainder having second- or third-degree atrioventricular (AV) block, or AV junctional tachycardia. With the higher verapamil dose, AV block or junctional tachycardia occurred in all animals during acetylstrophanthidin infusion. In addition, the dose of glycoside required to produce electrophysiologic toxicity was significantly increased by verapamil. Therefore, verapamil appears to exert a protective effect against the development of digitalis-induced arrhythmia, possibly by suppressing delayed afterpotential generation, and significantly increases the dose of digitalis required to produce AV block.

Terminology of Tachycardias: Historical Background and Evolution

The purpose of this article is to review the evolution of the tern:is used to characterize tachycardias since the beginnings of modern cardiology. This evolution reflects the increasing understanding of the mechanisms and the clinical significance of cardiac arrhythmias, a process which introduces new terms while making some of the established terms inaccurate and ambiguous. However, the tradition yields slowly to tbe conceptual progress, and the changes in the nomenclature occur slower than the changes in meaning. Therefore, despite the periodic recommendations by varying authorities or organizations to modify and standardize the nomenclature of cardiac arrhythmias, the old terms frequently continue to influence tbe contemporary scientific language.