Rate Dependent Depression of Subsidiary Ventricular Impulse Formation—Cause of Stokes-Adams Attacks in a Patient with Rate Modulated Pacing

Following His bundle ablation and implantation of a rate adaptive pacemaker (Vitatron TX 911) a 52-year-old gentleman experienced several presyncopal attacks while driving a car. On examination pectoralis muscle contraction caused temporary pacemaker inhibition. Incremental overdrive stimulation demonstrated progressive depression idioventricular automaticity and was associated with similar symptoms following overdrive at high pacing rates. Following appropriate pacemaker programming the patient remained symptom free.     

The Effect of Overdrive Pacing Rate and Duration on Ventricular Escape Rhythms in Patients with Chronic Complete Atrioventricular Block

The effect of overdrive (OD) pacing rate and duration on subsidiary pacemakers was evaluated in 54 patients with third-degree AV block. They had a permanent pacemaker implanted 61 ± 56 months earlier because of complete AV block in 38 patients and, in 16 patients because of second-degree AV block, which in the interim advanced to complete AV block. The patients had a reliable infranodal escape rhythm, with a mean cycle length of 2,022 ± 603 msec, upon discontinuation of the ventricular OD pacing, at a rate of 40 beats/min. The escape interval and escape rhythm cycle length was evaluated after OD pacing at 40, 50, 60, 70, 80, 90, and 100 beats/ min for 30 seconds, at each rate. In 100% of the patients the subsidiary pacemaker recovered after OD pacing at 40 and 50 beats/min and the number decreased to 59% at a rate of 100 beats/min. The escape interval prolonged gradually between OD pacing at 40 and 100 beats/min, by 56%. The effect of OD pacing duration at 50 and 70 beats/min was evaluated. At an OD pacing rate of 70 beats/min there was a significant effect of the pacing duration on the escape interval. There were significant differences in the escape interval duration and escape rhythm cycle length between males and females, patients with or without coronary artery disease, and patients with narrow or wide QBS escape. However, the increase in the OD pacing rate had a similar effect on the escape interval in the above mentioned groups. There was no effect on the paced QRS duration and sinus cycle length at each OD pacing rate. In nine patients premature escape beats were present after OD pacing at 80 and 90 beats/min. In conclusion, OD pacing may suppress the infranodal subsidiary pacemakers originating at the proximal conduction system or from a ventricular site and this effect depends on the pacing rate and duration. An OD pacing at a rate of 50 beats/min or less has minimal or no effect on these inherent pacemakers. Overdrive stimulation in the form of premature escape beats is present in 17% of the patients.     

Termination of Ventricular Tachycardia by an Implantable Atrial Pacemaker and External Pacemaker Activator

An atrial pacemaker was implanted in a patient who had dilated cardiomyopathy, sinus node dysfunction, and drug-resistant ventricular tachycardia (VT). VT episodes were terminated by atrial overdrive pacing using an implanted pacemaker and a newly developed hand-held external programmer/transmitter. Although successful cases of termination of intractable VT by ventricular pacing have recently been reported, the ventricular method might increase the risk of accelerating VT. Atrial overdrive pacing is a safer method since it minimizes the possibility of tachycardia acceleration and, combined with antiarrhythmic drugs, it appeared to be a unique and useful approach for the treatment of drug-resistant VT.     

The Treatment of Ventricular Tachycardia Using an Automatic Tachycardia Terminating Pacemaker

Implanted cardiac pacemakers may be used in the management of selected patients with ventricular tachycardia unresponsive to other forms of medical and surgicaJ therapy. We would like to report the successful treatment of such a patient utilizing a new multiprogrammable automatically activating ventricular burst pacemaker. Thorough electrophysiologic study preceded implantation, and was instrumental in choosing an effective terminating technique, in identifying the need for adjunctive drug therapy, and in testing the safety and efficacy of the implanted system. (PACE, Vol. 4, September-October, 1981)     

Noninvasive Serial Electrophysiological Testing Using an Implanted Pacemaker for Management of Recurrent Ventricular Tachycardia

An implanted multiprogrammable pacemaker capable of performing both premature and burst stimulation can be teamed with a special external programmer for noninvasive electrophysiological testing. Such studies, combined with indications from provocative pharmacologic tests, allowed us to formulate effective antiarrhythmic therapies for three patients suffering from post-infarction, recurrent sustained ventricular tachycardia.     

Escape Rhythm in Complete A-V Block. The Recovery Phase after Overdrive Suppression from Artificial Ventricular Pacing

In 60 patients with third degree A-V block, recovery of escape rhythm from overdrive suppression after ventricular pacing has been studied. Implanted unipolar VVI pacemakers were inhibited by chest wall stimuli. A total of 165 rhythmograms were studied. In 37, the rate was irregular, in the other 128 the escape rate increased gradually, following an exponential curve until stabilization after 3 minutes. In 29 of these rhythmograms, a possible exit block of the first escape impulse was observed. In 99 rhythmograms without exit block, escape rhythm recovery time was an average 1.45 times basal escape RR intervals. Overdrive suppression was most marked in patients with a slow escape rhythm.     

Procainamide in the Induction and Perpetuation of Ventricular Tachycardia in Man

The effects of a single intravenous infusion of 750 mg of procainamide was studied in 12 patients with symptomatic chronic recurrent ventricular tachycardia in whom arrhythmias could reproducibly be initiated and terminated by programmed electrical stimulation of the heart. Sustained ventricular tachycardia was induced in 6 patients and non-sustained tachycardia was induced in the remaining 6 patients during control studies. Following procainamide (plasma level 10.3 +/- 3.7 mcg/ml), ventricular tachycardia could be induced in 10/12 patients, sustained in 4 patients and non-sustained in the remaining 6 patients. In 8/12 patients (66%), induction of ventricular tachycardia was facilitated as demonstrated by: (1) tachycardia zone was widened in 4 patients and was unchanged in another 3 patients; (2) non-sustained ventricular tachycardia was sustained ventricular tachycardia in one patient. the ventricular tachycardia had a faster rate and a different QRS morphology; (3) in 4 patients tachycardia was inducible with a lesser number of extrastimuli and/or by spontaneously occurring ventricular premature depolarization and; (4) increase of the number of induced ventricular responses of non-sustained ventricular tachycardia. In 4/12 patients (33%), procainamide abolished or modified the induction of ventricular tachycardia as demonstrated by: (1) inability to induce ventricular tachycardia in 2 patients; (2) narrowing of the tachycardia zone and conversion from sustained into non-sustained ventricular tachycardia (one patient) and; (3) decrease in the number of induced ventricular responses in one patient. The response to procainamide could not be predicted from rates of spontaneous ventricular tachycardia, induced ventricular tachycardia during control studies, degree of slowing of ventricular tachycardia or from prolongation of the coupling interval after procainamide. These results suggest that instead of abolishing the arrhythmia, procainamide in frequently employed doses in patients with chronic recurrent ventricular tachycardia can facilitate its initiation sometimes at even faster rates. Patients not responsive to the usual doses of procainamide should undergo acute drug trials to determine the optimal dose/drug levels.     

Effectiveness of Noninvasive Programmed Stimulation for Initiating Ventricular Tachyarrhythmias in Patients with Third-Generation Implantable Cardioverter Definrillators

Previous generations of implantable cardioverter defibrillators (ICDs) required invasive electrophysiological testing to assess defibrillator function. Newer third-generation ICDs include the capability for performing noninvasive programmed stimulation (NIPS) and may reduce the need for invasive studies to assess tachycardia recognition and antitachycardia therapy algorithms. The effectiveness of ICD-based NIPS for the induction of ventricular arrhythmias has not, however, been formally assessed. Third-generation ICDs were implanted in 79 patients, who underwent a total of 166 postoperative defibrillator tests. NIPS with rapid ventricular pacing was performed in all patients in an attempt to induce ventricular fibrillation. In patients with prior sustained uniform ventricular tachycardia, programmed stimulation with up to three extrastimuli was performed in order to attempt to initiate the clinical ventricular tachcardia. Ventricular fibrillation was induced with NIPS in 146 of 166 studies (88%). Ventricular tachycardia was initiated with NIPS in 104 of 123 studies (85%). The type of defibrillator and the use of endocardial or epicardial rate sensing/ pacing leads did not influence the efficacy of NIPS. NIPS with third-generation ICDs is generally effective at inducing ventricular fibrillation and clinically relevant ventricular tachycardias, and reduces the need to perform invasive electrophysiological testing following device implantation. In a minority of patients temporary transvenous pacing catheters must still be used to facilitate arrhythmia induction.     

Symptomatic Bradyarrhythmias in the Adult: Natural History Following Ventricular Pacemaker Implantation

The preimplantation arrhythmias, coexistent medical conditions, the causes of death, and survival course are described for 399 patients who received their initial ventricular pacemaker implantation for a bradyarrhythmia (AV block, sinus node disease, and hypersensitive carotid sinus syndrome) at the University of Michigan from 1961 to 1979. Factors which correlated with a poor survival are elucidated. Survival for those with sinus node disease was virtually identical to those with AV block, with only 63% surviving over five years. Advanced age and congestive heart failure prior to implantation, and underlying ischemic or hypertensive heart disease portended a poorer survival in both groups. Patients with hypersensitive carotid sinus syndrome had a distinctly better prognosis--no deaths occurred until the eight year after pacing. Patients with no underlying heart disease and those with valvular disease did remarkably better than those with an ischemic or myopathic etiology. Apparent progression or complications of the underlying heart disease was the major cause of mortality. Sudden death, congestive heart failure, myocardial infarction, and major arrhythmias were the causes of death in 48% of those who died. Implications of improved pacing modalities on late complications and death are discussed.     

Diagnosis of Ventricular Tachycardia Using a Pacemaker Holter Function

The diagnosis of ventricular tachycardia (VT) using the Holter function of an implanted pacemaker has not yet been reported. We present the case of a patient with episodes of slow VT. hemodynamically stable, but in whom long lasting attacks were not identified by the patient as VT recurrences, finally leading to progressive heart failure. Prospective analysis of the 24-hour ECG and comparison with the pacemaker Holter data allowed us to determine diagnostic criteria to recognize VT using the pacemaker Holter function. Using these criteria it was possible to retrospectively diagnose VT occurrence during the weeks when the patient was out-of-hospital.     

Ventricular Fibrillation Following Elective Cardioversion in a Patient with Permanent Pacemaker

Elective cardioversion was undertaken in a patient with a VVI pacemaker and atrial tachyarrhythmia after converting the pacemaker to a VOO mode of function. The cardioverter output energy was unwittingly synchronized to the pacemaker output pulses that were falling randomly in various portions of the cardiac cycle. This resulted in the cardioverter DC shock being discharged in the ST segment of (he native QRS with consequent ventricular fibrillation.     

Predictive Value of Various Types of Ventricular Response to Programmed Ventricular Stimulation: Relation to Holter Monitoring

The study was performed to determine the predictive value of programmed stimulation for identification of pts with ventricular arrhythmias: 75 patients were studied by means of 24-hour ambulatory ECG (24 ECG) and programmed right (in some patients also left) ventricle stimulation at sinus and two or three pacing rates using two (standard) and three extrastimuli or burst stimulation (extensive protocol). Lown classes 0.1–3 and 4a–4h were observed in 24 ECG in 35, 14, and 26 patients, respectively. In programmed stimulation 1–6 repetitive ventricular responses (RVR) were found in 56 pts, nonsustained ventricular tachycardia in 11 and sustained ventricular tachycardia in 21 pts. High incidence of induced VT was found in pts with complex ventricular arrhythmia in 24 ECG, 81% of this group, in all but six pts only standard protocol was used. The 1–6 RVR were observed in almost 40% of pts without any arrhythmia. Conclusion; Only VT induction is a useful index for high risk patients.     

Actual Pacemaker Longevity: The Benefit of Stimulation by Automatic Capture Verification

Background: We evaluated the impact of an algorithm for automatic right ventricular (RV) stimulation compared to fixed‐output pacing (FOP) stimulation on actual pacemaker longevity over a 9‐year follow‐up. Methods: Prospective observation of 300 patients implanted with VDDR/DDDR pacemakers in 1999–2000 up to October 31, 2008. Sixty‐one patients were paced by Autocapture? pacing (ACP), 239 were paced by FOP; they were seen twice yearly at the pacemaker clinic. Factors known to affect pacemaker longevity were collected: median heart rate, %A&V paced activity, pacing output, and impedance. Patients dead before pacemaker replacement, lost to follow‐up, or who developed permanent atrial fibrillation were excluded from analysis. Results: One hundred twenty‐six of three hundred patients completed the study. Adverse clinical events due to an increased RV threshold occurred in two FOP patients compared to none among ACP. Pacemaker replacement occurred in 1/34 ACP patients versus 60/92 FOP patients (P < 0.001). ACP was the single independent predictor of pacemaker longevity at multivariable analysis (hazard ratio = 0.03, P < 0.001) either in the overall population or in the specific patients subgroups (sick sinus syndrome, atrioventricular block, and neurally mediated syncope). Conclusions: Automatic verification of stimulation is reliable at long term, and warrants superior safety in the event of pacing threshold changes. It allows a significant longevity increase compared to FOP stimulation that may heavily impact the patients’ quality of life and the cost of pacing therapy. Moreover, it is a fundamental technology in a strategy of remote patient and device monitoring, and may enable automatic device follow‐up operated by trained, nonmedical personnel. (PACE 2010; 873–881)     

Antiarrhythmic Efficacy of Ethacizine Assessed by Programmed Electrical Stimulation in Patients with Ventricular Tachycardia

The efficacy of ethacizine, a Class Ic drug, was assessed by programmed electrical stimulation (PES), delivering single, double, and triple extrastimuli at paced drives of 100 and 140 beats/min from two right ventricular sites (apex and out flow tract) in 38 patients with recurrent sustained ventricular tachycardia (VT). Underlying disease was coronary artery disease (CAD) in 26 (group I) and other conditions in 12 patients (group II; hypertrophic cardiomyopathy in 7, mitral valve prolapse in 1, and no apparent heart disease in 4). In the baseline study VT was induced in all patients. After a single intravenous dose (0.6-0.7 mg/kg) of ethacizine, VT was still inducible in six patients in group I and seven patients in group II. Ethacizine was administered on a long-term basis to all patients in a dose of 200-400 mg per day. All but one CAD patient remained free of recurrences after a mean follow-up of 16.5 (range 3-22) months, while there were recurrences in six of 12 patients in group II. We conclude that: (1) ethacizine appears to be effective in the treatment of VT in CAD patients; (2) the study demonstrates the clinical utility of PES in the management of VT, although some patients in whom VT remains inducible on ethacizine may have good clinical outcome; and (3) the efficacy of ethacizine in other forms of heart disease remains to be studied.     

Role of Electrophysiologic Testing in the Therapy of Ventricular Arrhythmias

The past decade has witnessed important advances in the understanding of the mechanism underlying ventricular arrhythmias. It has become clear that sustained ventricular arrhythmias can generally be reproduced with programmed ventricular stimulation in the clinical elec-trophysiology laboratory. False positive results may, however, occur with very vigorous stimulation techniques, particularly in patients without documented arrhythmias. False negative results are not infrequent in victims of cardiac arrest. Ability or inability to initiate ventricular tachycardia duringacute and chronic drug testing has predicted clinical failure or success, at least for conventional antiar-rhythmics. Patients with sustained ventric ular tachycardia and cardiac arrest occurring outside the peri-infarction period are those most likely to benefit from study. Conventional antiarrhythmic agents are successful in about one-third of patients with a high degree of concordance among these drugs. Amio-darone is frequently effective in patients with drug-refractory ventricular arrhythmias. However, its efficacy cannot be predicted by programmed stimulation. This is in striking contrast to Type 1A anti-arrhythmic agents.     

Phenytoin in the Treatment of Inducible Ventricular Tachycardia: Results of Electrophysiologic Testing and Long-Term FoUow-Up

Phenytoin treatment of inducible ventricular tachyarrhythmias was assessed by serial electrophysiologic studies (EPS) in 64 patients with spontaneous ventricular tachycardia, cardiac arrest, or symptoms compatible with a ventricular tachyarrhythmia. Coronary artery disease was the primary cardiac disease in 75% of the patients. All subjects had either inducible ventricular tachycardia (greater than or equal to 10 repetitive beats) or ventricular fibrillation at electrophysiologic study. Phenytoin was administered intravenously in 38 studies and orally in 31 studies. The mean serum phenytoin level was 19.5 +/- 4.7 mcg/ml. Only seven patients (11%) had a negative electrophysiologic study (less than or equal to 10 repetitive beats) after the administration of phenytoin and were classified as phenytoin responders (group I). The remaining 54 patients (89%) were classified as nonresponders (group II). For the nonresponders, phenytoin increased the cycle length of identical monomorphic ventricular tachycardias from a mean of 31 ms to a mean of 327 ms (p less than 0.001). For the four patients tested receiving both intravenous and oral phenytoin, the intravenous response always predicted the oral response. For the seven patients in whom electrophysiologic study indicated phenytoin efficacy, two are alive and arrhythmia-event free, two had sudden death when the regimen was changed (one case, quinidine added; one case, subtherapeutic serum level), and three died from nonarrhythmic causes. For the 10 patients treated empirically with phenytoin, either alone (seven patients) or in combination with another antiarrhythmic agent (three patients), four died secondary to an arrhythmic event.(ABSTRACT TRUNCATED AT 250 WORDS)     

Bradycardia Dependent Ventricular Tachycardia Facilitated by Myopotential Inhibition of a VVI Pacemaker

Bradycardia-dependent ventricular tachycardia was facilitated by long asystolic pauses caused by myopotential inhibition of a VVI pacemaker. Increasing the pacemaker rate by reprogramming temporariiy eliminated the problem. This case demonstrates that myopotential inhibition can result in serious clinical ventricular tachyarrhythmias     

Clinical Testing of a New Pacemaker Function to Monitor Ventricular Capture

Automatic beat-by-beat capture functions are designed to minimize the pacing energy delivered, while maintaining the highest safety by delivering an immediate back-up stimulus in case of loss of capture. The objective of this study was to estimate the lowering of ventricular pacing amplitude allowed by such a function, compared to amplitudes usually set manually in routine practice. An automatic ventricular pacing threshold test is launched every 6 hours to measure the automatic capture threshold (AT). From AT the function calculates: (1) the "capture amplitude" (V_c) = AT + 0.5 V at a minimum output of 1 V and (2) the "safety amplitude " (V_s) = twice AT at a minimum output of 2.5 V. The function preferentially uses V_c and verifies capture after each paced beat. In case of loss of capture, a back-up spike is delivered and V_s is implemented until the next threshold measurement. We estimated the ventricular amplitude delivered by the pacemaker from data stored in the pacemaker memory. We compared these values with the pacing amplitude typically programmed manually (MPA) by physicians at twice AT and a minimum of 2.5 V. Data from 57 recipients of Talent 3 DR pacemakers were analyzed. Complete data sets were available in 25 patients at 1 day, 28 at 1 month, and 39 between 1 day and 1 month. No loss of capture or ventricular pause was observed on 53 ambulatory electrocardiograms (ECG); and pulse amplitude automatically delivered by the device was significantly lower than the MPA at each of the three time points analyzed. This new beat-by-beat capture function allows a significant lowering of the pacing amplitude compared to manual settings, while preserving a 100% safety.