Biomedical subjects
Publications and source records attributed to C D Gottlieb.
A patient with an implantable cardioverter defibrillator (ICD) and a dual chamber pacemaker experienced inappropriate ICD therapies only during periods of rate-dependent right bundle branch block. Analysis of both stored and real-time ICD electrograms was critical to correctly diagnosing the problem and offering a solution.
Antiarrhythmic drugs and separate bradycardia pacing systems are prescribed commonly in patients with implantable cardioverter defibrillators (ICDs). Adverse effects of antiarrhythmic drugs on ICD function and adverse interactions between ICDs and pacemakers have been documented. The effect of antiarrhythmic drugs on the defibrillation threshold (DFT) in patients has not been well assessed. Most studies have been performed in animal models in which cardiac function was normal and drug doses were supraphysiologic. In addition, most studies have utilized monophasic defibrillation shock waveforms and epicardial lead systems. Despite the lack of clinical data applicable to current defibrillation systems, it appears that chronic amiodarone administration causes a significant DFT increase. In addition, antiarrhythmic drugs can influence antitachycardia pacing and tachycardia sensing. Defibrillation shocks can cause transient failure of pacemaker sensing and pacing, and cause spurious pacemaker reprogramming. Pacemaker function can result in ICD oversensing, leading to inappropriate therapy, or cause ICD undersensing, potentially resulting in failure to deliver therapy during ventricular fibrillation. The susceptibility of an ICD to undersensing appears related to the amplitude of the pacing stimulus artifact recorded by the ICD rate-sensing circuit and to the characteristics of the fibrillation electrogram. Preliminary data suggest that undersensing of ventricular fibrillation by current ICDs is an unlikely event.
OBJECTIVES: We sought to 1) correlate conduction block in the isthmus of the right atrium between the inferior vena cava and the tricuspid annulus with the efficacy of catheter ablation of type I atrial flutter, and 2) characterize the effects of ablative lesions on the properties of isthmus conduction. BACKGROUND: There are few data on the mechanism of persistent suppression of recurrence of atrial flutter by catheter ablation. METHODS: Thirty-five patients with type I atrial flutter underwent catheter mapping and ablation. Radiofrequency lesions were applied in the isthmus. Transisthmus conduction before and after the lesions was assessed during atrial pacing in sinus rhythm from the medial and lateral margins of the isthmus at cycle lengths of 600, 400 and 300 ms and the native flutter cycle length. Isthmus conduction block was defined using multipolar recording techniques. There were three treatment groups: group 1 = radiofrequency energy applied during flutter, until termination (n = 14); group 2 = radiofrequency energy applied during atrial pacing in sinus rhythm from the proximal coronary sinus at a cycle length of 600 ms, until isthmus conduction block was observed (n = 14); and group 3 = radiofrequency energy applied until an initial flutter termination, after which further energy was applied during atrial pacing in sinus rhythm until isthmus conduction block was observed (n = 7). RESULTS: In group 1, after the initial flutter termination, isthmus conduction block was observed in 9 of the 14 patients. In each of these nine patients, flutter could not be reinitiated. In each of the remaining five patients, after the initial flutter termination, isthmus conduction was intact and atrial flutter could be reinitiated. Ultimately, successful ablation in each of these patients was also associated with isthmus conduction block. In groups 2 and 3, isthmus conduction block was achieved during radiofrequency energy application, and flutter could not subsequently be reinitiated. Before achieving conduction block, marked conduction slowing or intermittent block, or both, was observed in some patients. In some patients, isthmus conduction block was pacing rate dependent. In addition, recovery from conduction block was common in the laboratory and had a variable time course. At a mean follow-up interval of 10 months (range 1 to 21), the actuarial incidence of freedom from type I flutter was 80% (recurrence in three patients at 7 to 15 months). CONCLUSIONS: Isthmus conduction block is associated with flutter ablation success. Conduction slowing or intermittent block, or both, in the isthmus can occur before achieving persistent block. Recovery of conduction after achieving block is common. Follow-up has revealed a low rate of flutter recurrence after achieving isthmus conduction block, whether the block was achieved in conjunction with termination of flutter.
OBJECTIVES: This study sought to investigate the influence of stimulation site on the properties of the circuit in ventricular tachycardia. BACKGROUND: A fully excitable gap can be demonstrated in most human ventricular tachycardias. This requires the presence of an arc of block so that the entire circuit can recover from refractoriness within the period of the cycle length. Resetting characterizes the conduction properties of the tissue within the ventricular tachycardia circuit. Previous studies have not investigated the possibility of site-dependent differences in the resetting response. METHODS: Resetting was performed from the right ventricular apex and outflow tract in 23 patients. Two characteristics of the resetting response were analyzed: 1) the total duration of the flat portion, and 2) the slope of the increasing portion. RESULTS: A flat portion of the resetting response was observed in 18 tachycardias; in 8 of the 18, there was a significant site-dependent difference (> or = 40 ms) in the duration of the flat portion. A significant site-dependent difference in the slope of the increasing portion of the resetting curve was seen in 6 of 22 tachycardias. In all, a stimulation site-dependent change in at least one characteristic of the resetting response was seen in 12 (52%) of the 23 tachycardias. CONCLUSIONS: A stimulation site-dependent change in the flat portion of the resetting response is compatible with an arc of block that is at least partially functional in nature. A change in the slope of the increasing portion is compatible with either partially functional circuit barriers or variation in properties of conduction and refractoriness at different locations within the circuit, or both. These observations suggest that a spectrum of circuit properties may exist in humans, with a variable contribution of anatomic and functional characteristics.
Two hundred forty-three consecutive patients underwent attempted implantation of nonthoracotomy defibrillation lead (NTL) systems. The importance of clinical and lead-related factors were analyzed regarding their relation with implantation failure caused by an unacceptably high defibrillation threshold (DFT). Overall, 33 (14%) of 243 patients failed NTL implantation. Patients undergoing attempted implantation of NTL systems with monophasic shock waveforms (monophasic group, n = 145) had an incidence of failed implantation of 22% (n = 32) versus an incidence of 1% (n = 1) among patients undergoing attempted implantation by using biphasic shock waveforms (biphasic group, n = 98; odds ratio, 26.9; p < 0.001). The incidence of success and simplicity of implantation of NTL systems was markedly improved in patients undergoing NTL implantation by using biphasic shock waveforms. Clinical factors could be used to stratify patients in the monophasic group for their risk of implantation failure. In the biphasic group, no clinical factor could be correlated with a low DFT with a fully endovascular system.
Pace mapping used to locate the site for ablation of idiopathic right ventricular outflow tract (RVOT) ventricular tachycardia remains difficult and time-consuming. A method to facilitate pace mapping and the most common site of ablation of this tachycardia are reported. In 18 consecutive patients with RVOT ventricular tachycardia, electrocardiographic criteria based on the QRS orientation in lead 1 and the R wave progression in the precordial leads were used to find pace maps matching the arrhythmia. Identical pace maps were obtained on the septum of the RVOT in 16 patients and resulted in successful ablations. These sites were concentrated in the anterior superior aspect of the RVOT determined by fluoroscopic imaging. In the remaining two cases identical pace maps could not be found in this area. The results of this study narrow the anatomic location for radiofrequency ablation of idiopathic RVOT ventricular tachycardia. This is the first description of an electrocardiography-guided approach to finding an identical pace map in the RVOT.
Explore the source record for details and available documents.
Two cases of successful radiofrequency catheter ablation of adult-onset atrial tachycardia originating from the left atrium adjacent to the mitral annulus are presented. Endocardial catheter activation mapping performed by retrograde or atrial transseptal approach revealed presystolic activation at the successful ablation site in both patients, and fractionation during sinus rhythm and tachycardia in one. The 12-lead electrocardiographic P wave appearance was suggestive of a left atrial tachycardia origin in both cases.
We describe a patient with bundle branch reentry ventricular tachycardia with 1:1 VA conduction in whom resetting was performed while obtaining simultaneous recordings from the right ventricular apex (V) and His-bundle electrogram. Both the tachycardia return cycle and the V-His interval demonstrated an increasing reset response, while the His-V interval demonstrated a flat reset response. These reset responses are consistent with a partially excitable gap localizing to the V-His portion of the bundle branch reentry circuit.
INTRODUCTION: The purpose of this investigation was to prospectively evaluate the voltage- and time-dependent characteristics of a biphasic defibrillator discharge on the amplitude of the rate sensing electrogram recorded from two "integrated" and one true bipolar nonthoracotomy lead system. Prolongation of redetection time has been noted after a failed first shock with nonthoracotomy lead systems. However, a prospective evaluation of the time- and voltage-dependent effects of biphasic shocks on electrogram amplitude with clinically utilized lead systems has not been systematically performed. METHODS AND RESULTS: Five- then 30-J R wave synchronous biphasic discharges were delivered during the supraventricular rhythm through three nonthoracotomy lead systems (Medtronic Transvene, Ventritex TVL, and CPI Endotak C 60 Series). The R wave amplitude was measured immediately postshock and for up to 1 minute. Amplitude changes were compared with preshock baseline value. A 5-J discharge had minimal effect on the R wave amplitude recorded from the three lead systems; however, 30 J resulted in significant diminution in R wave amplitude recorded from the integrated bipolar leads (in the Endotak lead to a greater extent than the TVL lead) with minimal effects on the Transvene lead. Following a 30-J discharge, the time constant for R wave recovery was 4.2, 14.9, and 15.3 seconds for Transvene, TVL, and Endotak 60 leads, respectively. CONCLUSION: There are voltage- and time-dependent reductions in postshock R wave amplitude. Integrated bipolar systems appear more affected than the "true" bipolar lead evaluated. This may be due, in part, to lead design, distance of distal defibrillating surface from rate sensing cathode, and the incorporation of the defibrillating surface as the rate sensing anode. The influence of post-shock R wave diminution on subsequent redetection remains speculative but may have implications for subsequent lead development.
INTRODUCTION: In patients with non-thoracotomy defibrillation lead (NTL) systems coupled with monophasic shock waveforms, the defibrillation threshold (DFT) rises early after implantation. There is little information regarding features predictive of the DFT rise, or DFT changes early after implantation of NTL systems coupled with biphasic shock waveforms. METHODS AND RESULTS: DFT measurements were performed serially at implantation, prior to hospital discharge (mean 4 +/- 3 days), and at follow-up (mean 49 +/- 22 days) in 146 patients with an NTL system. Factors were assessed for association with a "clinically important" early postimplantation DFT rise, defined as a rise of > or = 2 energy steps (2 to 4 J per step; > or = 5 J total). A clinically important early postimplantation DFT rise occurred in 48 patients (33%). Univariate predictors of the rise included the monophasic shock waveform, the Medtronic Transvene lead system, the presence of a subcutaneous defibrillation patch, and the number of shocks delivered during the implantation procedure. However, the only independent predictor of a clinically important DFT rise was the monophasic shock waveform (F = 18, P < 0.001). For the monophasic patient group (n = 79), the incidence of a DFT rise was 53% (n = 42). For the biphasic patient group (n = 67), the incidence of a DFT rise was 9% (n = 6). The clinical characteristics of the monophasic and biphasic groups were not significantly different, nor were their DFTs at implantation. Among a subgroup of 18 consecutive patients who underwent serial DFT testing utilizing both monophasic and biphasic waveforms, the incidence of a clinically important DFT rise with monophasic (n = 9,50%) was higher than with biphasic shocks (n = 3,17%; P = 0.05). CONCLUSION: NTL systems coupled with biphasic shock waveforms have an attenuated incidence of a clinically important DFT rise early after implantation, relative to patients with NTL systems coupled to monophasic waveforms.
INTRODUCTION: The stability of implantable cardiac defibrillation lead impedance subsequent to implantation has not been reported and may have important clinical implications. The objective was to characterize the incidence and degree of impedance changes occurring after implantation of defibrillation lead systems. METHODS AND RESULTS: The study cohort consisted of patients who received epicardial or nonthoracotomy lead systems. Defibrillation impedance was recorded at implantation, prior to hospital discharge (predischarge), and during follow-up. For each individual the magnitude of the impedance change relative to implantation was characterized. Among patients with an epicardial system, a significant decrease in impedance was observed at predischarge (mean 9.3 omega). The magnitude of the decrease was large in 39% and moderate in 31% of individuals. Subsequently, a gradual rise in mean impedance was apparent. At 18-21 months postimplantation, impedance was significantly increased relative to implantation (mean 6.8 omega). At this time, the magnitude of the increase was large in 46% and moderate in 23% of patients. Among patients with a nonthoracotomy lead system including a subcutaneous patch, a significant decrease in mean impedance was observed at predischarge (mean 3.5 omega). The magnitude of the decrease was large in 8% and moderate in 50% of individuals. Subsequently, a gradual rise in impedance was apparent. At 5-6 months, it was significantly increased relative to implantation (mean 2.3 omega). The magnitude of the increase was large in 10% and moderate in 33% of patients. Among the group of patients whose nonthoracotomy lead system did not include a subcutaneous patch, there was no significant change in mean impedance at predischarge relative to implantation. In subsequent intervals, a gradual rise was apparent. At 5-6 months, impedance was significantly increased relative to implantation (mean 4.3 omega). The magnitude of the increase was large in 16% and moderate in 47% of individuals. CONCLUSION: Significant changes in defibrillation lead impedance occur after implantation of epicardial and nonthoracotomy defibrillation lead systems. These data may serve as a standard for identifying the anticipated maximum change in lead impedance and thus may be useful as a tool for recognizing problems with defibrillation lead integrity.
The success of catheter ablation has greatly improved the care of patients with paroxysmal tachycardias and has caused a revolution in the practice of electrophysiology. Some investigators have expressed that concern over procedural success in an increasingly interventional specialty threatens to eclipse attempts to understand the physiology of arrhythmia syndromes. Alternatively, due to the precise and directed nature of the lesions created with radiofrequency energy, catheter ablation procedures have allowed investigation to continue at a more focused level. In this article, the insights provided by the catheter ablation experience into the physiology of arrhythmias mediated by accessory AV pathways will be reviewed. Although the learning process was sometimes delayed by the nearly immediate success of radiofrequency catheter ablation, difficult situations have continued to renew efforts for understanding at a deeper level. Conscious attempts at "learning while burning" will provide the opportunity to investigate aspects of bypass tract physiology that remain incompletely characterized, such as partial response to therapy and late recurrence.
Past studies using Holter monitoring and retrospective reviews of death certificates have documented peak occurrence of sudden death and nonsustained ventricular tachycardia (VT) in the morning hours. We used the Ventritex Cadence device (Ventritex, Sunnyvale, California) which documents the date and time of all stored arrhythmias leading to device therapy to evaluate the circadian pattern of sustained ventricular arrhythmia recurrence. Mean follow-up after defibrillator implantation was 628 +/- 285 days. All 390 patients had at least 1 episode (range 1 to 43) of sustained VT documented from analysis of the stored electrograms associated with an arrhythmia event. Stored electrograms were available for review and analysis in 3,041 device detections; 349 stored events were excluded because they did not fulfill the diagnostic criteria for VT or failed to document the onset of the ventricular arrhythmia at the beginning of the recorded event of the arrhythmia episode. Criteria for the diagnosis of VT or ventricular fibrillation were met in 2,692 arrhythmia episodes occurring in 390 patients. There was circadian variation for ventricular arrhythmia recurrence for the whole patient group with the data fit to the sinusoidal density function: f(t) = 126 - 51 x cos (-57 + 2 pi t/24) - 25 x sin (63 + 2 pi t/12) (p < 0.0001). Ventricular arrhythmia occurrence rate was lowest between 2:00 and 3:00 A.M., and highest between 10:00 and 11:00 A.M. In addition, the same circadian pattern was demonstrated regardless of patient age, gender, left ventricular ejection fraction (< 35% or > or = 35%), and VT cycle length (< 300 or > or = 300 ms).(ABSTRACT TRUNCATED AT 250 WORDS)
Explore the source record for details and available documents.
The purpose of this investigation was to develop an algorithm on the basis of the QRS morphology observed on the 12-lead ECG that would rapidly locate the site of origin of the monomorphic ventricular tachycardia arising from the septal portion of the RVOT. Radiofrequency catheter ablation guided by pace-mapping techniques has proven effective in eliminating the ventricular tachycardia originating from the RVOT in the absence of structural heart disease. A method that would rapidly identify the portion of the RVOT septum toward which more detailed pace-mapping should be directed before catheter ablation would be useful in decreasing procedure time and radiation exposure and potentially facilitating a successful ablation procedure. The RVOT septum was divided into nine sites. In 11 patients, bipolar pacing was performed at each of the nine designated sites to mimic ventricular tachycardia. A standard 12-lead surface ECG was recorded during pacing. The QRS morphology in the limb leads was characterized and the site of the R-wave transition was determined in the precordial leads. A QS in lead a VR and a monophasic R wave in leads II, III, aVF, and V6 were noted in each patient at all paced sites. In lead I, pacing at the three posterior septal sites always resulted in an R wave. Pacing at the three anterior sites produced a dominant Q wave (either QS or Qr) at 17 (52%) of 33 sites or a qR complex at 16 (48%) of 33 sites.(ABSTRACT TRUNCATED AT 250 WORDS)
OBJECTIVES: The purpose of this study was to prospectively evaluate postshock redetection of ventricular fibrillation by a system that coupled an implantable cardioverter-defibrillator with an automatic gain control sense amplifier and a transvenous lead system. BACKGROUND: Redetection of ventricular fibrillation after an unsuccessful first shock has not been systematically evaluated. Previous studies have suggested that sensing performance of some lead systems may be adversely affected by the delivery of subthreshold shocks. METHODS: The time required for both initial detection and redetection of ventricular fibrillation was compared in 22 patients. These times were estimated by subtracting the capacitor charge time from the total event time. RESULTS: A total of 113 successful and 57 unsuccessful initial shocks were delivered during induced ventricular fibrillation. The mean +/- SD initial time to detection of ventricular fibrillation was 5.5 +/- 1.7 s (range 2.4 to 10.8); the time to redetection ranged from 1.5 to 18.5 s (mean 4.5 +/- 2.8, p = NS vs. detection time). Abnormal redetection episodes, defined as a redetection time > 10.2 s (i.e., > 2 SD above the mean redetection time), were observed in 4 (18%) of 22 patients. CONCLUSIONS: Redetection of ventricular fibrillation after a subthreshold first shock may be delayed. Device testing with intentional delivery of subthreshold shocks to verify successful postshock redetection of ventricular fibrillation should be performed routinely in all patients.
OBJECTIVES: This study sought to document postoperative complications attributable to nonthoracotomy defibrillation lead systems in a large cohort. BACKGROUND: The incidence of postoperative complications specifically associated with nonthoracotomy defibrillation lead systems is unknown. METHODS: Postoperative lead-related complications were evaluated in 170 patients with a nonthoracotomy defibrillation lead system who were followed up for a mean (+/- SD) of 17 +/- 12 months. Each system incorporated one or more intravascular leads. In 117 patients (69%), the system incorporated a subcutaneous defibrillation patch. All implantations were performed in an operating room by cardiothoracic surgeons. Defibrillation thresholds were measured at implantation, before hospital discharge (mean 3 +/- 2 days) and at 4 to 18 weeks after implantation. Patients were evaluated every 2 to 3 months after implantation or as indicated by clinical exigency. RESULTS: Twenty-seven patients (15.9%) were diagnosed with a lead-related complication that either extended the initial hospital period or led to a second hospital admission. Complications included endocardial lead or subcutaneous defibrillation patch dislodgment in eight patients (4.7%), which was diagnosed between 2 and 345 days after implantation; endocardial or subcutaneous patch lead fracture in six (3.5%), which was diagnosed between 53 and 600 days after implantation; subcutaneous patch mesh fracture in one, which was diagnosed at 150 days after implantation; subclavian vein thrombosis in three (1.8%), which was diagnosed at 2 to 50 days after implantation; and unacceptably elevated defibrillation threshold (within 5 J of maximal device output) in nine (5.3%), which was documented at one of the two postimplantation evaluations in eight patients or at the time of failure to terminate a spontaneous ventricular tachycardia in one. Seventeen of the 27 patients required reoperation for correction of their complication. In addition, system infection requiring complete explantation occurred in seven other patients (4.1%) at an interval from implantation ranging from 14 to 120 days. CONCLUSIONS: Postoperative complications related to a nonthoracotomy defibrillation lead system were common and frequently required reoperation for correction. The rate of system explantation due to infection was also significant. Postoperative defibrillation testing and vigilant outpatient follow-up evaluation are necessary to ensure normal lead function.