Kent J. Volosin

Spontaneous changes in ventricular tachycardia cycle length

Understanding spontaneous fluctuations in ventricular tachycardia cycle length is required to develop algorithms for ventricular tachycardia detection and termination. Variations in cycle length, time to stable cycle length and the range of RR intervals during ventricular tachycardia were analyzed in 74 episodes of sustained monomorphic ventricular tachycardia induced in patients not taking antiarrhythmic medication. Linear regression demonstrated cycle length variability to decrease over time (41 +/- 24 to 17 +/- 19 ms, p less than 0.001). Slower ventricular tachycardia had more cycle length variability than faster ventricular tachycardia (p less than 0.001). Ventricular tachycardia that was initially more variable tended to remain more variable (p less than 0.001). Fifty-four percent of episodes stabilized within the first 15 beats, 75% by 30 beats and 93% by 50 beats. The number of beats to stable cycle length was independent of ventricular tachycardia rate. The average range in cycle length per episode was 127 +/- 72 ms; 12% of ventricular tachycardia episodes varied by less than 50 ms and 45% by less than 150 ms. The maximal range in RR intervals from a single episode of ventricular tachycardia was 290 ms. Therefore, ventricular tachycardia demonstrates a wide range of cycle lengths and has time-dependent changes in variability and stability. These cycle length changes should be considered in the algorithms for ventricular tachycardia detection and termination by automatic antitachycardia devices.

Amiodarone therapy: Role of early and late electrophysiologic studies

Forty-two patients with a history of symptomatic ventricular tachycardia or cardiac arrest underwent electrophysiologic testing at control and early in the course of amiodarone therapy (mean 12 +/- 7 days). Late electrophysiologic studies (mean 17 +/- 4 weeks) were repeated in 23 patients on a maintenance dose of 400 mg/day. At control study, all patients had inducible ventricular tachyarrhythmias (sustained ventricular tachycardia in 35, nonsustained ventricular tachycardia in 4, ventricular fibrillation in 3), while after amiodarone loading (1,200 mg daily) 4 (10.5%) of the 42 patients developed noninducible ventricular arrhythmias. At late study, an additional 6 (26%) of the 23 patients with inducible arrhythmias at early study developed noninducible arrhythmias. The cycle length of induced ventricular tachycardia increased from 275 +/- 61 ms at control study to 340 +/- 58 ms at early study (p = 0.001). A further increase in ventricular tachycardia cycle length was noted in patients who underwent both early and late study (341 +/- 38 versus 375 +/- 63 ms, p less than 0.05). The percent of induced tachycardias that were clinically tolerated increased as patients were treated longer with amiodarone (control = 22%, early = 34%, late = 53%, p less than 0.001). Of the 23 patients who had both early and late electrophysiologic studies and were followed up for a mean of 21.7 months (range 4 to 47), there were no recurrences among the 6 patients with noninducible arrhythmias, but there were five recurrences among the 17 patients with persistently inducible arrhythmias. None of the four patients with noninducible arrhythmias at early study had a recurrence. On the basis of these findings, it is concluded that: 1) The timing of programmed electrical stimulation will affect the results of the study in patients treated with oral amiodarone.(ABSTRACT TRUNCATED AT 250 WORDS)

The effects of atrial pacing on the signal-averaged electrocardiogram in patients with coronary artery disease

The effects of atrial pacing on the signal-averaged electrocardiogram were studied in 14 patients with remote myocardial infarction and a history of cardiac arrest or sustained ventricular tachycardia (group I) and in 13 patients with coronary artery disease and no history of sustained ventricular tachyarrhythmia (group II). Recordings of the signal-averaged electrocardiogram were obtained at control and during atrial pacing at rates of 80, 100, and 120 beats/min. All patients had recordings analyzed from at least two paced rates. At control, the mean high frequency total duration of the QRS complex (HFTD) was significantly longer in group I versus group II patients (123 +/- 5.6 versus 111 +/- 3.5 msec, p less than 0.05). Although the duration of the QRS signal under 40 microV (D40) was higher in group I versus group II patients (42 +/- 4.7 versus 32.4 +/- 3.5 msec) and the root mean square amplitude of the terminal 40 msec QRS (RMSA) was lower in the group I patients (27 +/- 7.5 versus 38.1 +/- 8.8 microV), these differences did not achieve statistical significance. There was no effect of atrial pacing on the measured signal-averaged parameters of HFTD, D40, and RMSA. Although there was a difference between group I and group II at each paced rate analyzed, atrial pacing did not help to further stratify the groups. In patients with coronary artery disease, atrial pacing is not a useful method of stratifying high-risk patients. Changes in serial signal-averaged electrocardiograms from the same patient are not due to heart rate variability.

Swallowing-Induced Tachycardia: Electrophysiologic and Pharmacologic Observations

A 38‐year‐old man developed palpitations after swallowing. Intracardiac recordings and esophageal manometry were obtained during episodes of swallowing‐induced tachycardia. These studies demonstrated that the site of origin of the tachycardia was the high right atrium and that the onset of the tachycardia occurred prior to the arrival of the peristaltic wave in the esophagus. Evaluation of the tachycardia revealed that the likely mechanism for the tachycardia was triggered automaticity. Autonomic blockade and other pharmacologic interventions failed to prevent episodes of tachycardia. Swallowing‐induced tachycardia is a rare disorder triggered by an undefined neural reflex arc.

Use-dependent prolongation of ventricular tachycardia cycle length by type I antiarrhythmic drugs in humans.

BackgroundType I antiarrhythmic drugs block the cardiac sodium channel in a use-dependent fashion. This use-dependent behavior causes increased drug binding and consequently increased sodium channel blockade at faster stimulation rates. Importantly, the kinetics of drug association and dissociation from the sodium channel differ for each type I antiarrhythmic drug. Methods and ResultsThirty-five patients receiving type I antiarrhythmic drugs for the treatment of sustained monomorphic ventricular tachycardia (VT) were studied before and after drug therapy. A total of 41 drug studies were performed (lidocaine, n=10; procainamide, n=16; flecainide, n=15). Sustained monomorphic VT of an identical electrocardiographic morphology was induced during the control and follow-up drug studies. During the control study, there was no significant change in the VT cycle length over time. Compared with control, significant prolongation of the onset VT cycle length was observed after treatment with procainamide and flecainide (increase of 52±24 and 80±49 msec, respectively) but not after treatment with lidocaine (increase of 8±37 msec). Additional drug-induced prolongation of the VT cycle length occurred during a 40-second observation period. This secondary “use-dependent” cycle length prolongation contributed significantly to the steady-state VT cycle length during treatment with flecainide (increase of 82±34 msec;p <0.0001). Although a use-dependent increase in VT cycle length was observed with procainamide and lidocaine, the increase was not statistically significant (increase of 12±15 and 8±8 msec, respectively). The estimated time constants for the onset of use-dependent VT cycle length prolongation were distinctly different for the three drugs. Flecainides prolongation of the VT cycle length occurred slowly, with an estimated time constant of 12.5±5.0 seconds. In contrast, the time course of VT cycle length prolongation was rapid during treatment with lidocaine and intermediate during treatment with procainamide (time constants of 0.52±0.51 and 4.0±1.3 seconds, respectively). ConclusionsUse-dependent prolongation of VT cycle length during treatment with type I antiarrhythmic drugs was observed in humans. This effect was clinically significant during treatment with flecainide (i.e., the use-dependent slowing of the heart rate improved the hemodynamic tolerance of the arrhythmia). Finally, the estimated time constants for the use-dependent prolongation of VT cycle length by the three test drugs are similar to their reported in vitro time constants for use-dependent sodium channel blockade.

The Effects of Direct Current Countershock on Ventricular Late Potentials

Signal averaging is a noninvasive method of recording ventricular late potentials. These late potentials are present in many patients with sustained ventricular tachycardia. Analysis of ventricular late potential characteristics may develop as a useful marker of antiarrhythmic drug efficacy. Often antiarrhythmic drugs are tested acutely in the electrophysiology laboratory after direct current countershock (DC shock). The purpose of this study was to investigate the effects of DC shock delivered for cardioversion of sustained ventricular tachycardia or fibrillation on ventricular late potentials. Signal averaged electrocardiograms (SAEKGs) were recorded before and after 13 DC shocks. There was no significant change in QRS duration, duration of the high frequency filtered QRS, or duration of the high frequency signal under 40 microvolts. There was a small increase in the root mean square amplitudes of the terminal 40 milliseconds (41 μV to 49 μV). This degree of change is felt to be clinically insignificant. Except for one trial, no late potential appeared or disappeared after electrical cardioversion. We have shown that ventricular late potentials are only slightly altered by programmed ventricular stimulation, induced sustained ventricular tachycardia or ventricular fibrillation, and DC countershock. To analyze changes in ventricular late potentials after antiarrhythmic drug administration in the electrophysiology laboratory, in those patients requiring DC countershock, comparisons should be made to postshock SAEKGs rather than those obtained prestudy.

Use of External Muscle Stimulation in a Patient with a Unipolar DDD Pacemaker

Extraneous electrical activity has been shown to affect pacemaker function.̂ Application of therapeutic currents (i.e., electrical nerve or muscle stimulation, electrocautery or electrical cardioversion) to a patient with a permanent pacemaker can cause partial or complete inhibition of pacemaker output, or upper rate limit pacing. Therapeutic current may also result in either interference mode or back-up mode asynchronous pacing.̂ It has been suggested that transcutaneous nerve stimulation is contraindicated in patients with pacemakers capable of sensing,̂ but we were able to use safely external electrical muscle stimulation in a patient with a unipolar DDD pacemaker. The patient was a 70-year-old male with a congestive cardiomyopathy and recurrent ventricular tachycardia who developed sinus node dysfunction while on long-term amiodarone therapy. A Versatrax 7000A* permanent unipolar pacemaker was implanted. He suffered chronic dislocations of a prosthetic hip which was partly due to poor quadriceps muscle tone. Strengthening of these muscles by external electrical muscle stimulation was recommended. Prior to initiation of out-patient muscle stimulation, we evaluated potential interference of pacemaker function by an electrical muscle stimulator (NTRON-EMS-8000). During continuous ECG monitoring, electri-

Rate-modulated pacemakers.

Rate-modulated pacing is an advancement in pacing technology that has opened the way for the development of a wide variety of pacemaker generators and pacing modes. Rate-modulated pacemakers use a physiologic sensor other than the sinus node to adjust the pacing rate according to the physiologic needs of the patient. As rate-modulated pacemakers become more widely used, nurses caring for patients with these devices need to understand pacing physiology as well as rate-modulated pacing technology to provide optimal patient care.