Jeffrey A. Matos

Role of implantable pacemakers in control of recurrent ventricular tachycardia

Implanted pacemakers can provide a viable alternative to pharmacologic therapy or surgical management of patients with recurrent ventricular tachycardia. An increasing variety of pacemaker techniques are proving useful for preventing, controlling the effective rate of or terminating ventricular tachycardia. To assess the role of permanent pacing in the treatment of ventricular tachycardia, a consecutive series of 160 patients undergoing electrophysiologic testing for recurrent ventricular tachycardia were analyzed. Thirty-nine patients received implantable pacemakers, of which 13 were intended for bursts of rapid ventricular pacing. No adverse responses were attributed to these burst pacemakers, but concern for possible acceleration of tachycardia and appropriate identification of the arrhythmia were among factors limiting more widespread use of antitachycardia pacing. Some of these limitations may be resolved with further advances in electrophysiologic understanding of arrhythmias combined with strides in medical electronics, which will permit the development of new generations of highly sophisticated antitachycardia pacemakers.

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.

Prediction of sudden death and spontaneous ventricular tachycardia in survivors of complicated myocardial infarction: Value of the response to programmed stimulation using a maximum of three ventricular extrastimuli

The prognostic significance of ventricular arrhythmias induced by programmed electrical stimulation was evaluated in 50 survivors of acute myocardial infarction complicated by a major new conduction disturbance (38 patients), congestive heart failure (33 patients) or sustained ventricular tachyarrhythmias (22 patients), alone or in combination. Programmed stimulation was performed in patients in stable condition 7 to 36 days (mean 16) after infarction using one to three extrastimuli at four times diastolic threshold at a maximum of two right ventricular sites. Two groups were identified by the response to programmed stimulation: 17 patients with sustained (greater than 15 seconds) or nonsustained (greater than 7 beats but less than or equal to 15 seconds) ventricular tachycardia (group I), and 33 patients with 0 to 7 intraventricular reentrant complexes in response to maximal stimulation efforts (group II). Group I patients had a higher incidence of anterior infarction than that of patients in group II (71 versus 42%), had lower left ventricular ejection fraction (mean 0.35 versus 0.48) and were more often treated with antiarrhythmic drugs (47 versus 18%, p less than 0.05). There were no significant differences between groups in the occurrence of congestive failure, new conduction disorders or sustained ventricular arrhythmias with infarction, or in the proportions treated with a beta-receptor blocking agent, coronary bypass grafting or a permanent pacemaker. Total cardiac mortality was 24% during a mean follow-up period of 23 months and did not differ between groups; however, the response to programmed stimulation identified a group at high risk of late sudden death or spontaneous ventricular tachycardia: 7 (41%) of 17 group I patients compared with 0 of 33 group II patients (p less than 0.001). The induction of sustained or nonsustained ventricular tachycardia identified all patients who died suddenly or had spontaneous tachycardia (sensitivity 100%), but triple extrastimuli were required to induce prognostically significant arrhythmias in five of these seven patients; the specificity of this protocol was only 57%. When the clinical variables of the group were evaluated individually, the response to programmed stimulation had a stronger association with occurrence of late sudden death than did any other factor (Fishers exact test, p less than 0.001); however, a type II error could not be excluded.(ABSTRACT TRUNCATED AT 400 WORDS)

Comparative effectiveness of pacing techniques for termination of well-tolerated sustained ventricular tachycardia

Ventricular tachycardias can be terminated by a variety of pacemaker techniques, including rapid and slow stimulation. Fast tachycardias are typically poorly tolerated, and require prompt intervention, usually with rapid pacing. Termination of ventricular tachycardia by slow or single capture pacemaker stimulation techniques is attractive, because of its presumed safety and the possibility of using simple implantable pacers. To identify factors favoring termination, single capture stimulation was used in 390 episodes of ventricular tachycardia in 21 patients, 16 with coronary artery disease, able to tolerate ventricular tachycardia forseveral minutes. Single capture stimulation terminated 223 episodes (57%) in 18 patients, and two were accelerated. Of 157 episodes exposed to 2–3 programmed extrastimuli or rapid pacing 149 (94%) were terminated and 7 were accelerated. Direct current cardioversion was needed in 12 episodes. Without medications, only two patients tolerated VT. Only one patient had reliable termination with single capture stimulation over several days. Systolic blood pressure was similar in episodes terminated and not terminated by single capture stimulation, but the ventricular rate was significantly lower in episodes terminated, 116 ± 19 vs. 133 ±24 (p<0.001). Termination of ventricular tachycardia was not affected by QRS morphology. Single capture termination of ventricular tachycardia is largely unpredictable, with limited reproducibility over a period of time. Although comparatively safe, single capture techniques are not likely toprove useful in the long‐term treatment of many patients with recurrent ventricular tachycardia.

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.

Maximal Rate of Tachycardia Development: Sinus Tachycardia with Sudden Exercise vs. Spontaneous Ventricular Tachycardia

In addition to providing basic physiologic information, knowledge of the maximal rate of sinus tachycardia development may be helpful in developing algorithms permitting new generations of antitachycardia pacemakers to distinguish accurately between sinus and ventricular tachycardia. To determine the maximal rate of sinus tachycardia development, 50 normal subjects rushed up 100 stairs as rapidly as possible, with continuous electrocardiographic monitoring. During the first second of exercise, the mean cardiac cycle length shortened from 709 to 570 ms, equivalent to an increase in heart rate from 85 to 105 beats per minute, or 20 beats per minute per second. Thereafter, a more gradual decrease in cycle length occurred. Differences between men and women, smokers and non‐smokers, and sedentary compared to active subjects were all insignificant. Analysis of 50 spontaneous episodes of ventricular tachycardia also revealed a sequential but more abrupt decrease in the cycle length during the first second from 757 to 360 ms, equivalent to a rate increase from 79 to 167 beats per minute, or 88 beats per minute per second. After approximately 1 1/4 seconds, the ventricular tachycardia cycle length remained virtually constant. Baseline cycle lengths were similar in the sinus and ventricular tachycardia groups, but differed in all subsequent beats, although overlap for individual subjects did occur.

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.

Discordance between ambulatory monitoring and programmed stimulation in assessing efficacy of class IA antiarrhythmic agents in patients with ventricular tachycardia

Concordance between programmed stimulation and 24 hour ambulatory electrocardiographic (Holter) monitoring was studied in 54 patients with sustained ventricular tachycardia during 84 therapeutic trials with class IA antiarrhythmic agents. During baseline studies before treatment, all patients had frequent (greater than or equal to 30/h) ventricular premature complexes on Holter recordings and sustained ventricular tachycardia inducible by one to three extrastimuli. During treatment, programmed stimulation and Holter monitoring were repeated. Efficacy of treatment determined by programmed stimulation (ventricular tachycardia no longer inducible or nonsustained) was compared with three Holter criteria of efficacy: I = 83% or more reduction of ventricular premature complexes and abolition of ventricular tachycardia; II = 50% or more reduction of ventricular premature complexes and 90% or more reduction of couplets and abolition of ventricular tachycardia; III = abolition of ventricular tachycardia in patients with ventricular tachycardia during a baseline Holter recording. Treatments were judged effective by programmed stimulation criteria in only 25% of cases but in 51, 63 and 75% of cases by Holter criterion I, II and III, respectively. Results of programmed stimulation and Holter monitor were discordant (effective by one criterion but ineffective by the other) in 50% of cases using Holter criterion I, in 54% using Holter criterion II and in 61% using Holter criterion III. In the majority of discordant results, treatments appeared efficacious by Holter criteria but ineffective by programmed stimulation criteria, suggesting insensitivity of efficacy by Holter criteria or nonspecificity of induced ventricular tachycardia during treatment, or both.

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)