Lawrence E. Waspe

Automatic implantable cardioverter-defibrillator: Patient survival, battery longevity and shock delivery analysis

The automatic implantable cardioverter-defibrillator (AICD) has been shown to reduce the mortality rate of patients with malignant ventricular tachyarrhythmias. This report describes experience with implantation of 36 automatic implantable cardioverter-defibrillators (AID-B and AID-BR models) in 22 persons over a 44 month patient follow-up period (mean 19.6 months). There were five deaths: two patients died suddenly 22 and 29 months, respectively, after their second implant, one died of congestive heart failure, one died of respiratory failure and one died of catheter sepsis. Although 11 (50%) of the 22 patients never received a countershock for a ventricular tachyarrhythmia and are still alive, the other 11 received one or more spontaneous countershocks. Nine patients (41%) experienced spurious shocks during the follow-up period. Assuming that the first shock for presumed ventricular tachyarrhythmia prevented death, the hypothetical cumulative survival of patients at 42 months would have been 34 +/- 14.1% in the absence of an automatic implantable cardioverter defibrillator rather than the actual survival rate of 59 +/- 16.8%. The cumulative device survival of the 36 AID-B units was 92 +/- 5.62% at 15 months but diminished to 37 +/- 14.4% by 20 months. No unit lasted longer than 22 months. There were 12 battery depletions. The number of shocks emitted did not influence unit longevity. The manufacturers elective replacement indicator is of uncertain validity. Six units remained active 7 to 17 months after surpassing their replacement indicator. The automatic implantable cardioverter-defibrillator prolongs the life of many patients with otherwise intractable arrhythmias.(ABSTRACT TRUNCATED AT 250 WORDS)

Attempted nonsurgical electrical ablation of accessory pathways via the coronary sinus in the Wolff-Parkinson-White syndrome.

Previous canine experiments suggested that transvenous catheters placed in the coronary sinus could be used to deliver limited energy shocks, resulting in fibrosis in the atrial wall and coronary sulcus with sparing of the coronary artery. From the distribution of the fibrosis, it appeared that this approach could be used for attempted ablation of accessory pathways in patients with the Wolff-Parkinson-White syndrome. Eight patients with symptomatic Wolff-Parkinson-White syndrome underwent electrophysiologic testing with attempted ablation of 10 accessory pathways. Shocks were limited to 40 to 80 J, except in one patient who received shocks of 100 and 150 J. From 2 to 26 shocks were given to each accessory pathway. All the accessory pathways were blocked completely immediately after the shocks. Subsequently, evidence of accessory pathway conduction recurred in each patient. Three had early promise of long-term improvement after the procedure, with prolongation of the refractory periods of the accessory pathways during the remainder of the initial hospitalization. Several weeks later, however, there was evidence of return toward original values in two of these. Another patient who appeared not to benefit during her initial hospitalization returned 7 weeks later with very depressed accessory pathway conduction, possibly due to developing fibrosis. The only significant complication occurred in the patient receiving shocks of 100 and 150 J; he had apparent rupture of the coronary sinus requiring pericardial drainage. In two patients in whom nonsurgical ablation was not successful, intraoperative mapping showed that the accessory pathway was located in an area of fibrosis at the site of the attempted ablation. In summary, nonsurgical electrical ablation of accessory pathways via the coronary sinus may be successful using limited energy levels in a few patients. The procedure remains experimental, and widespread application must await more effective means of delivering the shocks.

The value of electrophysiologic studies in syncope of undetermined origin: report of 150 cases

A prospective study examined the diagnostic yield and therapeutic efficacy of electrophysiologic studies in patients with SUO. We defined SUO as those syncopal or near-syncopal events remaining unexplained after a standardized, noninvasive evaluation that included a history, physical examination, routine laboratory screening, EEG, nuclear brain scan or CAT scan, 12-lead ECG, chest x-ray, orthostatic vital signs, bedside carotid sinus massage, and at least 24 hours of continuous ECG monitoring. The 150 SUO patients included 95 men and 55 women (mean age 62.0 years); 35 had recurrent SUO, 75 (50%) had organic heart disease, and 129 (86%) had abnormal ECGs. There were 162 abnormal electrophysiologic findings that could explain the SUO uncovered in 112 patients, a diagnostic yield of 75%: one finding in 71 patients, two findings in 32, and three findings in nine. These findings were: His-Purkinje disease in 49 patients (30%), inducible ventricular arrhythmias in 36 (22%), AV nodal disease in 20 (12%), sinus node disease in 19 (12%), inducible supraventricular arrhythmias in 18 (11%), carotid sinus hypersensitivity (not elicited by carotid sinus massage prior to electrophysiologic studies) in 15 (9%), and hypervagotonia in five (3%). When electrophysiologic study findings were classified as clearly abnormal or borderline, 54 patients had at least one clearly abnormal finding, a diagnostic yield of 36%. Subgroups of patients presenting with only a single SUO event, no evidence of organic heart disease, or normal baseline ECGs all had substantial diagnostic yields during electrophysiologic studies. Follow-up data in 137 patients (91%) (mean 31 months) showed recurrences in 16 of 34 patients (47%) without and 15 of 103 patients (15%) with electrophysiologic findings despite therapy directed by electrophysiologic testing (p less than 0.0005). This study and a review of the literature indicate that electrophysiologic testing is useful in elucidating the causes of SUO and directing therapy. A significant number of patients benefit from electrophysiologic studies, even when only clearly abnormal findings are considered diagnostic, when only a single syncopal event has occurred, or whether or not organic heart disease or an abnormal ECG is present.

Susceptibility to atrial fibrillation and ventricular tachyarrhythmia in the Wolff-Parkinson-White syndrome: Role of the accessory pathway

Clinical and electrophysiologic characteristics associated with spontaneous and inducible atrial fibrillation and ventricular tachyarrhythmia were assessed in 20 consecutive patients with Wolff-Parkinson-White (WPW) syndrome undergoing surgical division (n = 12) or transcatheter electrical ablation (n = 8) of accessory pathways. Patients with spontaneous atrial fibrillation were characterized by the trend (not significant) of a shorter antegrade accessory pathway effective refractory period (256 +/- 26 vs 303 +/- 109 msec). However, patients with and without spontaneous atrial fibrillation did not differ with respect to prevalence of structural heart disease (3 of 11 vs 2 of 9), intra-atrial conduction time (34 +/- 10 vs 32 +/- 10 msec), or interatrial conduction time (86 +/- 21 vs 88 +/- 17 msec). Thus, atrial and accessory pathway electrophysiologic properties (per se) were not clear determinants of susceptibility to atrial fibrillation. Among the 20 patients, 10 to 35 beats of nonsustained ventricular tachycardia (seven patients) or ventricular fibrillation (three patients) were induced at electrophysiologic study with one to three programmed extrastimuli. Clinically, a ventricular arrhythmia (ventricular fibrillation during atrial fibrillation) had occurred in only one of these patients. The discordance of these observations was significant (p less than 0.01). Patients with and without inducible ventricular arrhythmias were not distinguished by clinical factors or by electrophysiologic properties of the accessory pathway or ventricles. Accessory pathway conduction was completely or partially eliminated by ablation procedures in 14 of 20 patients. During a mean follow-up of 27 months, atrial fibrillation recurred in two patients with failed ablation procedures and in one patient with left atrial enlargement (despite accessory pathway division) (p = 0.019 vs pre-ablation). Ventricular arrhythmias remained inducible in two patients in whom accessory pathway ablation failed (p = 0.01 vs initial study). However, spontaneous ventricular tachyarrhythmias did not occur during follow-up. We conclude that susceptibility to spontaneous or inducible atrial fibrillation and ventricular tachyarrhythmia in patients with WPW syndrome and no organic heart disease depends primarily on the existence of a functional accessory pathway. These susceptibilities are eliminated by interruption of accessory pathway conduction. Ventricular tachyarrhythmias remain infrequent spontaneous events in the WPW syndrome. Their more frequent induction at electrophysiologic study is not predictive of clinical occurrence.

Unipolar pacer artifacts induced failure of an automatic implantable cardioverter/defibrillator to detect ventricular fibrillation

Abstract The automatic implantable cardioverter-defibrillator (AICD®)1–5 has been implanted in over 500 patients with life-threatening ventricular arrhythmias. For detection of ventricular tachycardia or fibrillation (VF), the sensing system of the standard AICD uses a combination of the rate of electric signals received by sensing leads, and a probability density function.1–3 Because of the nature of sensing system of the AICD, several kinds of interactions with temporary or permanent pacemakers have been described.4,6 We have observed another phenomenon: failure of an AICD to detect VF due to large electrical signals from a unipolar pacemaker.

Role of a catheter lead system for transvenous countershock and pacing during electrophysiologic tests: An assessment of the usefulness of catheter shocks for terminating ventricular tachyarrhythmias

The practicality and safety of using a single catheter system for transvenous countershock, programmed stimulation and ventricular pacing during electrophysiologic tests were evaluated in 13 patients with inducible sustained ventricular tachycardia (VT) or ventricular fibrillation (VF). The efficacy and patient toleration of transvenous countershock were compared with other methods of arrhythmia termination. The same lead was used for programmed stimulation at the right ventricular apex and for VT termination by pacing methods during serial testing (20 ± 15 days [mean ± standard deviation]). Synchronized countershock using energies that patients found tolerable (0.01 to 5 J) terminated 31 of 50 episodes (62%) of induced VT. Episodes of VT cardioverted with these low energies were distinguished from other episodes by a longer cycle length (352 ± 62 ms versus 297 ± 50 ms, p < 0.004). Among paired episodes of VT matched for patient, date of induction, morphologic characteristics, cycle length and drugs administered, pacing methods (single extrastimuli and bursts of rapid pacing) were just as effective as low-energy countershock for VT termination (25 of 25 versus 21 of 25, difference not significant). Transvenous countershock was uniformly effective for termination of ventricular flutter and VF when sufficient energy was used (range 5 to 30 J, mean 20.4 ± 7.7). This required interfacing leads to a defibrillation unit. VT acceleration occurred during 7 of 50 synchronized low-energy cardioversion attempts (14%). There was no evidence of myocardial injury as a result of shocks as high as 30 J, but patients required increasing sedation when energy exceeded 0.5 J. Thus, a single catheter system can be used for programmed stimulation, ventricular pacing and countershock during electrophysiologic tests. Low-energy countershock (0.01 to 5 J) is no more effective than pacing methods for VT termination and is tolerated less well. The most practical use of this catheter system, including any implantable unit, may be for slightly higher energy (5 to 30 J) countershock termination of repeated episodes of very rapid VT or VF, in which pacing techniques are ineffective. This method may be safer and less traumatic than conventional transthoracic countershock.

Is Programmed Stimulation of Value in Predicting the Long-Term Success of Antiarrhythmic Therapy for Ventricular Tachycardias?

We studied the value of programmed stimulation in assessing the efficacy of antiarrhythmic agents in 52 patients with sustained ventricular tachycardia. All patients in this nonrandomized study had ventricular tachycardia inducible by programmed stimulation and also had frequent ventricular premature complexes (greater than or equal to 30 per hour) on Holter-monitor recordings before therapy. The efficacy of antiarrhythmic agents was assessed by both programmed stimulation and Holter recordings during serial drug testing. A regimen was deemed effective according to the programmed-stimulation criteria in 25 patients (Group 1). Twenty-seven patients in whom tachycardia could still be induced during programmed stimulation despite extensive drug trials were discharged on a regimen that caused a marked reduction of ventricular premature complexes according to Holter monitoring (Group 2). In 23 patients no effective drug regimen was identified by either set of efficacy criteria, and these patients were excluded from the present analysis. Follow-up lasted 18.6 +/- 13.9 months. Rates of arrhythmia-free survival at 12 and 24 months were 88 percent and 72 percent, respectively, in Group 1 and 84 percent and 75 percent in Group 2 (P = 0.637). We conclude that demonstration of antiarrhythmic efficacy by programmed stimulation predicts a good clinical outcome, that inefficacy as shown by the programmed-stimulation protocol used in this study may not preclude a good outcome if there is a marked reduction of spontaneous ventricular premature complexes on Holter monitoring, and that randomized trials should be conducted to validate the results of this observational study.

Nonsurgical electrical ablation of tachycardias: importance of prior in vitro testing of catheter leads.

Nonsurgical electrical ablation of tachycardia pathways or foci has been attempted or carried out using a variety of temporary pacing catheter leads. To determine the ability of such leads to withstand the high energies used in such procedures, 34 leads were suspended in saline, and subjected to repeated electrical shocks. Small (4 French) temporary pacing leads made by a variety of manufacturers tolerated multiple shocks up to 100 joules; above this level, failures became increasingly common, although usually the failure mode was benign with respect to patient care implications. Testing of 6, 7, and 8 French leads revealed considerable inter‐and intra‐manufacturer differences in the ability to withstand higher energy shocks, reflecting differences in materials and fabrication techniques. It is concluded that careful in vitro lead testing is required prior to using identical models in humans for arrhythmia ablation procedures.

Activation mapping in patients with coronary artery disease with multiple ventricular tachycardia configurations: Occurrence and therapeutic implications of widely separate apparent sites of origin

Catheter or intraoperative activation mapping studies, or both, were performed in 17 patients with coronary artery disease with two to four distinct configurations of ventricular tachycardia, resistant to a mean of 12.1 +/- 6.0 antiarrhythmic drug trials per patient. Mapping studies were performed to guide anticipated surgical ablation of arrhythmias. Activation map data were adequate to determine sites of origin of 30 (64%) of 47 observed tachycardia configurations. These 30 ventricular tachycardias (26 observed clinically) were mapped to 22 separate endocardial sites of origin. Sites of origin of distinct tachycardias were identical or closely adjacent (within 3 cm) in six patients and widely separate (greater than or equal to 4 cm) in eight patients (47% of the group). Activation maps were not adequate to determine sites of origin of 17 (36%) of the 47 tachycardias, including all configurations in three patients. Fifteen patients underwent surgery for control of ventricular tachycardia: aggressive, map-guided endocardial resection (mean 26.5 +/- 14.2 cm2) in 12 patients with identified sites of tachycardia origin and extensive resection of visible endocardial scar (2 patients) or encircling endocardial ventriculotomy (1 patient) in those in whom the sites of origin of all clinical tachycardias remained undetermined. Two inoperable patients were treated with amiodarone. During postoperative electrophysiologic tests (11 of 13 surgical survivors), ventricular tachyarrhythmias were initially uninducible in only 4 of 11 patients. However, in two patients only nonclinical arrhythmias (ventricular flutter) were induced. Six (21%) of 29 clinical tachycardias whose sites of origin were either not determined or not resected (right septum or papillary muscle) remained inducible in five patients. Using previously ineffective antiarrhythmic drugs, initially inducible arrhythmias became uninducible (two patients), or harder to induce than preoperatively (five patients). As a result of surgical resections alone or in combination with previously ineffective drugs (and amiodarone in two inoperable patients), there were no recurrences of ventricular tachycardia in 14 (93%) of 15 patients discharged during 19.0 +/- 14.3 months of follow-up study. Thus, activation mapping may commonly reveal separate apparent sites of origin for clinically observed, morphologically distinct, highly drug-refractory ventricular tachycardias in patients with coronary artery disease with multiple tachycardia configurations. Extensive surgical resection of identified sites of origin may be required to ablate arrhythmias in these patients.(ABSTRACT TRUNCATED AT 400 WORDS)

Antiarrhythmic Effects of VVI Pacing at Physiologic Rates: A Crossover Controlled Evaluation

Ventricular pacing can prevent bradycardia‐dependent ventricular ectopic activity (VEA) and is helpful in some cases of drug‐refractory venfricuiar tachycardia (VT). This study is a prospective evaluation of VVI pacing for the control of VEA not related to underlying bradycardia, drug side‐effects, or prolonged QT interval syndromes. Twenty‐nine patients undergoing serial electrophysioiogic‐pharmacoiogic testing for VT control were studied. Eighteen of these patients (12 men; meon age = 60.1) both completed ihe protocol and had sufficient VEA for analysis. Coronary disease was present in 13 patients, cardiomyopathy in two patients, and one patient each had myocarditis, mitral valve prolapse, and no structural heart disease. Ambulatory (Holter) monitor recordings during VVI pacing were compared with control recordings made in the absence of pacing, VVI pacing rates were 10–15 bpm above the mean daily heart rate (mean = 92 bpm; range = 63–110). Hours from paced recordings were paired with hours from control (prior to analysis) according to time of day to reduce the effects of spontaneous variability in VEA frequency. Overall, VVI pacing reduced ventricular premature complexes (VPGs) 26% from 331 to 245/hour (p < 0.001). During pacing, couplets (pairs, successive VPGs) were reduced from 6.95 to 1.03/hour (p < 0.000001) and VT (≥3 successive VPCs) from 0.89 to 0.045 episodes/hour (p < 0.003). Of 13 patients with couplets, 11 had ≥50% reduction and five had ≥90% reduction. Baseline VT was eliminated in four out of nine patients during pacing. Pacing did not increase VEA significantly in any patient. In this group of patients, reduction of VEA by VVI pacing was significant and was comparable to pharmacologic interventions. Higher forms of VEA fcouplets and VT) appeared to respond better than single VPCs. Further studies may define patients with VEA who can benefit from pacing