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 manufacturer's 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)
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)
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.
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