Richard M. Greenberg

Incidence of unwarranted implantation of permanent cardiac pacemakers in a large medical population.

Because of allegations that the implantation of many permanent cardiac pacemakers has been unjustified, we reviewed the indications for all new pacemakers implanted at 30 hospitals in Philadelphia County between January 1 and June 30, 1983, and paid for by Medicare. Complete chart data were evaluated for 382 implants. We determined whether the indications for implantation were appropriate and adequately documented on the basis of standard clinical practice. Implants were classified as possibly indicated primarily because of inadequate diagnostic evaluation (63 percent) or inadequate documentation of an accepted indication (36 percent). Implants were classified as not indicated primarily because a rhythm abnormality was incorrectly identified as a justifiable indication (84 percent). We found that 168 implants (44 percent) were definitely indicated, 137 (36 percent) possibly indicated, and 77 (20 percent) not indicated. Unwarranted implantation was both prevalent (73 percent of hospitals had an incidence of 10 percent or more) and independent of the type of hospital (university teaching, university-affiliated, and community hospitals). The additional tests most often required to clarify the need for a pacemaker in inadequately evaluated cases included electrophysiologic studies (37 percent) and ambulatory monitoring (31 percent). We conclude that in a large medical population in 1983, the indications for a considerable number of permanent pacemakers were inadequate or incompletely documented.

Value of electrophysiologic testing in patients with previous myocardial infarction and nonsustained ventricular tachycardia

Previous studies of the value of electrophysiologic studies in patients with nonsustained ventricular tachycardia (VT) have been hampered by the inclusion of a small number of patients with various types of heart disease. This retrospective study was designed to assess the value of programmed stimulation in 205 asymptomatic patients who had had an acute myocardial infarction greater than 1 month before study. Inclusion was based on 24-hour Holter monitoring during which patients had to manifest greater than or equal to 3 consecutive ventricular beats at a rate greater than 135 beats/min. Forty-seven (23%) patients had normal, 70 (34%) mildly impaired and 88 (43%) severely impaired left ventricular function. Programmed stimulation, using up to 3 extrastimuli, was used in each. Seventy-five patients (36%) were noninducible, 59 (29%) had nonsustained VT (less than 30 seconds), 67 (33%) had sustained monomorphic VT and 4 (2%) had either polymorphic VT or ventricular fibrillation. Eighty-two patients were not treated with antiarrhythmic drugs, 57 others were placed on a program selected empirically and 66 had therapy guided by electrophysiologic testing. Satisfactory follow-up information was gathered in 187 of the 205 patients, with a mean follow-up of 18 months. One hundred forty-two patients are alive and well, 39 had sustained VT or sudden death and 6 others had a cardiac death. Only left ventricular function discriminated those who had a sustained arrhythmia or died from those who did not. Thus, programmed stimulation did not have independent predictive value in patients with nonsustained VT. However, definitive conclusions can be reached only with a large prospective study carried out in untreated patients.

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)

Tracking of Atrial Flutter During DDD Pacing: Another Form of Pacemaker‐Mediated Tachycardia

Two patients who had DDD pacemakers inserted for symptomatic sick, sinus syndrome developed sustained upper‐rate limit pacing. It was demonstrated in these two patients that pacemaker‐mediated tachycardia was due to tracking of atrial flutter. DDD pacemakers should be used with caution in patients with the sick sinus syndrome and associated atrial tachyarrhythmias. Medical treatment of recurrent atrial tachyarrhythmias may allow patients to remain in the DDD mode.

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.

Atrial Lead Dislodgement with a DDD Pacemaker

A 48‐year‐old man with previous aortic valve surgery and aortic root repair had a DDD pacemaker inserted (using transvenous leads) for the treatment of complete heart block. An atrial J active fixation electrode was used. Four weeks following implantation the patient returned with an unusual electrocardiographic rhythm demonstrating two separate QRS morphologies. Both PA and lateral chesf x‐ray failed to demonstrate a change in lead position. The MARKER CHANNELTM of the DDD pulse generator confirmed that the alternating QRS morphologies were due to atrial lead dislodgement. Although uncommon, displacement of atrial active fixation leads may occur and lead to unusual electrocardiographic rhythms. Use of a MARKER CHANNELTM may aid in the diagnosis.

Noninvasive Evaluation of Retrograde Conduction Times to Avoid Pacemaker-Mediated Tachycardia

Pacemaker-mediated tachycardia is a potential complication of atrioventricular (AV) universal DDD pacemakers when retrograde ventriculoatrial (VA) conduction is slower than the postventricular-atrial refractory period of the pulse generator. The propensity for pacemaker-mediated tachycardia was noninvasively assessed in 17 patients with a unipolar DDD pacemaker using chest wall stimulation. Low amplitude stimuli were delivered to chest wall electrodes through a programmed stimulator. Using this method, 13 of the 17 patients were found to have absent VA conduction or VA conduction time less than the postventricular-atrial refractory period. In the four patients with noninvasively measured VA conduction time greater than the postventricular-atrial refractory period, sustained pacemaker-mediated tachycardia was induced. Reprogramming of pacemaker parameters prevented repeat induction of pacemaker-mediated tachycardia in only one of four patients. The three remaining patients had clinical pacemaker-mediated tachycardia and underwent pacemaker programming to the DVI mode. A total of 13 patients continue to use DDD mode after a mean follow-up period of 9.5 +/- 5.4 months. Invasive measurement of VA conduction was performed in 13 of the 17 patients. The noninvasive method accurately predicted the invasive measurement in each case. Noninvasive evaluation of VA conduction accurately predicts the propensity for pacemaker-mediated tachycardia under a variety of clinical conditions. Serial testing can be performed after pacemaker reprogramming or drug intervention. Noninvasive evaluation of retrograde VA conduction should predict most clinical episodes of pacemaker-mediated tachycardia.

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-

The Role of Electrophysiologic Testing in the Therapy of Patients with Unexplained Syncope

The role of electrophysiologic testing in the diagnosis and therapy of patients with unexplained recurrent syncope was evaluated in twenty-six patients. Abnormalities were detected during the electrophysiology study in 17 of 26 patients (65%). Ventricular tachycardia (VT) was induced in 6 patients while conduction defects were detected in II patients. Therapeutic decisions based on the findings of the electrophysiology study were made in the patients with abnormal studies. Fifteen of the 17 patients with laboratory directed therapy were free of recurrent syncope when followed for a mean 12.2 ± 7.9 months. Syncope recurred in 4 of9 patients with a non-diagnostic study. One additional patient with a non-diagnostic study died suddenly. Eleven of the 26 patients had bundle branch block (BBB) or interventricular conduction defect (IVCD). In this subgroup of patients 4 patients had VT, 4 had conduction defects and 3 had nondiagnostic studies.