Incidence and management of prolonged charge times in the Medtronic model 7219 implantable cardioverter defibrillator.

The Medtronic Jewel PCD model 7219, introduced in 1994, was the first downsized, pectoral implantable cardioverter defibrillator (ICD), and many of these units are approaching or have reached the elective replacement indicator (ERI). Unlike later Medtronic ICDs and most other ICDs, in which ERI is defined by battery voltage, the ERI in the model 7219 series is defined when either the capacitor charge time to full output is repeatedly> or =14.5 s or when battery voltage is< or =4.91 V. In this study we examined which of the two ERI criteria was met first in patients with this device model. We also assessed the effects of manual dumping and recharging and of increasing the automatic capacitor reformation frequency on prolonged charge times. In 16 patients with follow-up <2 years, 15 reached the charge time ERI before battery voltage ERI. Manual dumping and recharging led to spuriously low charge times due to residual charge at the start of recharging, and increasing the automatic capacitor reformation frequency to once a month did not decrease prolonged charge times. Because of persistently prolonged charge times, 15 patients had generator changes. None of these patients had reached battery voltage ERI (battery voltage at time of explantation 5.06+/-0.06 V). Thus in this early pectoral device, prolonged charge times occur commonly before battery voltage ERI is reached. Whether prolonged charge times will have an impact on device longevity in later model ICDs is unknown.

Spurious redetection of sinus rhythm by an implantable cardioverter defibrillator during spontaneous ventricular fibrillation.

Implantable cardioverter defibrillator undersensing leading to delayed or aborted therapy delivery has been reported with induced arrhythmias and following failed defibrillator shocks. We describe a case in which spurious redetection of sinus rhythm during a spontaneous episode of ventricular fibrillation resulted in aborted device therapy.

Significant differences in charge times among currently available implantable cardioverter defibrillators.

Capacitor charging accounts for most of the delay between arrhythmia detection and therapy delivery in ICDs. Long capacitor charge times may increase the risk of syncope in patients with poorly tolerated arrhythmias. To determine if there are clinically important differences in charge time among currently available devices, we analyzed charge times at various delivered energy levels in three manufacturers' devices: Medtronic, CPI, and Ventritex. Charge times were measured for shocks delivered for spontaneous or induced arrhythmias occurring from time of implant to 4 months after implant. A total of 343 shocks were assessed in 63 patients with ICDs: 16 Medtronic (MicroJewel II, model 7223Cx), 14 CPI (Mini II, model 1762), and 33 Ventritex (Cadet and Contour, models V-115 and V-145). The curves of the relationship between charge time and delivered energy for the three types of devices were significantly different, with Medtronic charge times shorter than CPI or Ventritex (P < 0.0001), and CPI charge times shorter than Ventritex (P = 0.002). The difference in mean charge times between the Ventritex and Medtronic devices ranged from 1.7 seconds at a delivered energy of 10 +/- 2.5 J to 8.0 seconds at a delivered energy of 30 +/- 2.5 J. Thus, clinically important differences in charge time exist among the three types of defibrillators studied. These results should be considered in selecting an ICD for patients with poorly tolerated arrhythmias.

Inappropriate shock therapy for nonsustained ventricular tachycardia in a dual chamber pacemaker defibrillator.

We report a patient who received a CPI Ventak AV II DR ICD for ventricular tachycardia and complete heart block without an escape rhythm. During induced nonsustained ventricular tachycardia, the device, although programmed to deliver noncommitted shocks, acted like a committed device. This phenomenon is due to undocumented behavior that is likely to occur in any patient who is pacemaker dependent and has nonsustained ventricular tachycardia.

Comparison of oversensing during bradycardia pacing in two types of implantable cardioverter-defibrillator systems.

BACKGROUND: During bradycardia pacing in Ventritex Cadence (Models V-100 and V-110) implantable cardioverter-defibrillators, amplifier gain is maximal and oversensing and false tachyarrhythmia detection have been reported. Newer Ventritex devices (Cadet, Model V-115 and Contour, Model V-145) have a modified automatic gain control that may minimize oversensing. METHODS AND RESULTS: We prospectively studied 50 patients (22 with Cadence, 28 with Cadet or Contour). Electrograms were evaluated for oversensing during bradycardia pacing. The bradycardia pacing refractory period required to prevent oversensing of T waves of paced beats and the time and number of beats required to achieve minimum gain after cessation of pacing were assessed. The bradycardia pacing refractory period could be left at its default setting of 350 ms in only 15 (30%) of 50 patients. The mean bradycardia pacing refractory period required to avoid oversensing of paced T waves was 386+/-32 ms. During pacing, oversensing of nonpaced T waves was seen in 12 (24%) devices, with similar incidence in Cadence devices (18%) and Cadet and Contour devices (29%, p = not significant). The time and number of beats to achieve minimum gain after pacing were longer in Cadence devices (19.0+/-4.5 vs 4.6+/-1.2 sec; 21.3+/-3.3 vs 5.0+/-0.4 beats, both p < 0.001). CONCLUSIONS: The incidence of oversensing at maximum gain is similar in both types of devices, but more rapid changes in autogain levels in the newer devices may reduce the likelihood of false tachyarrhythmia detection.

Ischemic colitis and acquired resistance to activated protein C in a woman using oral contraceptives.

We present the case history of a 22-yr-old woman diagnosed with ischemic colitis associated with the use of oral contraceptives (OC). At the time of her presenting symptoms activated protein C (APC) resistance, a risk factor for thrombosis, was demonstrated. There was no laboratory evidence of inherited thrombophilia; that is, antithrombin III, protein C and protein S levels were normal and the factor V Leiden mutation was not present. The OC were discontinued and the patient's symptoms improved. Subsequent evaluation revealed that the activated protein C resistance had resolved. This case illustrates APC resistance as a potential link between OC use and its known association with ischemic colitis.

Radiofrequency catheter ablation of idiopathic left ventricular tachycardia originating in the left anterior fascicle.

Radiofrequency catheter ablation has been used to treat idiopathic left ventricular tachycardia with high success rates. The majority of reported cases have exhibited the typical findings of right bundle branch block morphology with left axis deviation and originate from within or near the left posterior fascicle. We report a case of idiopathic left ventricular tachycardia originating from within or near the left anterior fascicle, which was successfully ablated using a local Purkinje potential as a guide.

Effect of reproducibility of baseline arrhythmia induction on drug efficacy predictions and outcome in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial.

Spontaneous variability over time in the ease of induction of ventricular arrhythmias may mimic a drug effect and affect the predictive value of drug therapy guided by programmed stimulation. We assessed the effect of baseline reproducibility of arrhythmia induction on the incidence and accuracy of drug efficacy predictions in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. Patients with sustained ventricular tachyarrhythmias induced twice during baseline electrophysiologic testing with the same stimulation technique, i.e., induced at the same pacing site with the same drive cycle length and number of extrastimuli, were identified from the ESVEM database. These patients with highly reproducible arrhythmia induction were compared to those with less reproducible arrhythmias. Of 473 randomized patients with reproducibility data, 313 (66%) had highly reproducible arrhythmias. In patients randomized to electrophysiologic testing, baseline arrhythmia reproducibility did not affect the incidence of drug efficacy predictions (70 of 157 [45%], drug efficacy predictions in patients with highly reproducible arrhythmias vs 34 of 79 [43%] with less reproducible arrhythmias, p = 0.890). Drug efficacy predictions obtained by electrophysiologic testing in patients with highly reproducible arrhythmias were not associated with decreases in arrhythmia recurrence (p = 0.202), all-cause mortality (p = 0.301), cardiac death (p = 0.358), or arrhythmic death (p = 0.307) compared to those with less reproducible arrhythmias. Analysis of patients with highly reproducible sustained monomorphic ventricular tachycardia led to similar results. In the ESVEM trial, most patients had highly reproducible arrhythmia induction during baseline electrophysiologic testing. Reproducibility of arrhythmia induction in the baseline state had no effect on the incidence or accuracy of drug efficacy predictions.

Reproducibility of drug efficacy predictions by Holter monitoring in the electrophysiologic study versus electrocardiographic monitoring (ESVEM) trial. ESVEM Investigators.

Selection of antiarrhythmic therapy may be based on suppression of spontaneous ventricular arrhythmias assessed by Holter monitoring, but the implications of discordant Holter results on repeat 24-hour monitoring has not been defined. This study examines the frequency and significance of reproducible Holter suppression on two 24-hour recordings in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. Repeat 24-hour Holter monitoring was obtained in patients randomized to the Holter monitor limb of the ESVEM trial, during the same hospitalization, after a drug efficacy prediction. These Holters were not used to define drug efficacy but were subsequently analyzed to determine the reproducibility of drug efficacy predictions by Holter monitoring. A repeat 24-hour Holter monitor, following the one that predicted drug efficacy, was available in 119 patients. Ninety-nine patients (83%) also had suppression that met efficacy criteria on the second Holter monitor. There were no significant differences in arrhythmia recurrence (p = 0.612) or mortality (p = 0.638) in patients with concordant Holter results (n = 99; 1-year arrhythmia recurrence = 45%; 1-year mortality = 10%) compared with those with discordant Holter results (n = 20; 1-year arrhythmia recurrence = 45%; 1-year mortality = 16%). We conclude that (1) there is discordance between the first effective Holter monitor and a repeat Holter monitor in 17% of patients, and (2) suppression of ventricular ectopic activity on 2 separate 24-hour Holter monitors does not identify a group with a better outcome, nor does failure of suppression on the second Holter monitor identify a group with a worse prognosis.

Sensing and tachyarrhythmia detection problems in implantable cardioverter defibrillators.

Sensing of cardiac activity and detection of tachyarrhythmias in implantable cardioverter defibrillators (ICDs) are complex functions and errors occur. Sources of sensing-detection errors include the variable nature of intracardiac electrograms, the occasional inability of automatically adjusting signal amplifiers to cope with this variability, problems with sensing leads, inappropriate programming, and limitations of tachyarrhythmia detection algorithms, which are optimized to avoid underdetection of ventricular tachyarrhythmias. Current ICDs vary considerably in details of sensing and detection function, programmability, and diagnostic data, so that a through knowledge of each device is necessary to diagnose and correct these problems. Stored intracardiac electrograms and/or marker channels available in most of these devices have contributed much to our understanding of sensing-detection errors. Undersensing of individual signals, most frequently due to signal variability and/or inability of the amplifier to adjust adequately, can lead to delay or failure of tachyarrhythmia detection. Delay or failure of tachyarrhythmia detection can also occur if algorithms to enhance specificity, such as sudden onset or rate stability, are utilized. Oversensing of T waves or noise can lead to false detection; however, the most common cause of false detection is the inability of current detection algorithms to distinguish supraventricular from ventricular tachyarrhythmias. New algorithms that incorporate atrial sensing, electrogram morphology analysis, or hemodynamic monitoring may result in improved detection accuracy of ICDs in the future.

Tachycardia-induced cardiomyopathy in a cardiac transplant recipient: treatment with radiofrequency catheter ablation.

INTRODUCTION: Two years after orthotopic cardiac transplantation, a 60-year-old man presented with unexplained congestive heart failure and an incessant atrial tachycardia. METHODS AND RESULTS: Electrophysiologic evaluation identified the underlying arrhythmia as automatic atrial tachycardia with site of origin at the high anterior lateral right atrial wall. Radiofrequency catheter ablation successfully eliminated the tachycardia, which resulted in prompt improvement of this patient's congestive heart failure. CONCLUSION: This is the first reported case of tachycardia-induced cardiomyopathy in a cardiac transplant patient. Radiofrequency catheter ablation can be used successfully in this patient population.

Significance and incidence of concordance of drug efficacy predictions by Holter monitoring and electrophysiological study in the ESVEM Trial. Electrophysiologic Study Versus Electrocardiographic Monitoring.

BACKGROUND: Selection of antiarrhythmic therapy may be based on either suppression of spontaneous ventricular arrhythmias assessed by Holter monitoring or by suppression of inducible ventricular arrhythmias during electrophysiological study. This study examines the frequency and significance of concordance of these two approaches in the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial. METHODS AND RESULTS: Twenty-four-hour Holter monitoring was performed in patients randomized to the electrophysiology limb of the ESVEM study at the time of the first drug trial and at the time of an effective drug trial. Holter monitors were available in 65% (146/226) of patients at the time of the first drug trial and in 93% (100/108) of patients at the time of an electrophysiology study predicting drug efficacy. There were no clinical differences between patients who had and those who did not have a Holter monitor. At the time of the first drug trial, concordance of Holter and electrophysiological predictions of drug efficacy was observed in 46% of patients (both techniques predicted efficacy in 23%; neither predicted efficacy in 23%). Discordant results were observed in 54% (Holter suppression without electrophysiological suppression in 44%; electrophysiological suppression without Holter suppression in 10%). At the time of an electrophysiology study predicting drug efficacy, 68 of the 100 patients without inducible ventricular tachyarrhythmias also had suppression of spontaneous ventricular arrhythmias on the Holter recorded at the time of the electrophysiological study. Neither arrhythmia recurrence nor mortality was significantly different in patients with suppression of both inducible and spontaneous ventricular arrhythmias compared with those with only suppression of inducible arrhythmias. Comparison of patients with suppression of both inducible and spontaneous ventricular arrhythmias with the 188 patients in the Holter limb, in whom efficacy was predicted by Holter monitoring only, revealed no difference in outcome. CONCLUSIONS: In this population, (1) there is frequent discordance in prediction of drug efficacy and inefficacy between electrophysiological study and Holter monitoring; (2) a requirement to fulfill both Holter and electrophysiological efficacy criteria reduces the number of patients with an efficacy prediction; and (3) suppression of both spontaneous ventricular ectopy and inducible ventricular tachyarrhythmias does not identify a group with better outcome.

Atrial fibrillation after implantable cardioverter defibrillator implantation.

Atrial fibrillation is a reported complication of automatic defibrillator implantation. Its incidence, risk factors, time-course, and complications have not been well-defined. Accordingly, data from 117 patients who underwent defibrillator implantation via a thoracotomy (n = 71) or nonthoracotomy (n = 46) approach were reviewed. To identify risk factors, 15 variables of potential predictive value were chosen and analyzed. Atrial fibrillation developed in 26/117 patients (22%) during the early postoperative period and all but one of these 26 patients had undergone thoracotomy (P < 0.001). Patients who developed atrial fibrillation tended to be older than those who did not (63 +/- 2 vs 58 +/- 2 years, P = 0.04) and more frequently had a prior history of paroxysmal atrial fibrillation (31% vs 10%, P = 0.02). They were also less likely to be taking Class I or III antiarrhythmic drugs (1/26 vs 24/91, P = 0.01). By multivariate analysis, operative approach (P < 0.001), the absence of antiarrhythmic drug therapy (P = 0.006), and a prior history of atrial fibrillation (P = 0.003) were significant independent variables. Digoxin neither prevented the occurrence of atrial fibrillation nor slowed the maximal ventricular response. The mortality and complication rates did not differ between the two groups. The major adverse effect of postimplant atrial fibrillation was automatic defibrillator discharge; six patients received between 1 and 11 discharges for atrial fibrillation with rapid ventricular rates.

Implantation of an automatic defibrillator using a new nonthoracotomy approach.

Most current nonthoracotomy systems for defibrillator implantation use monophasic devices. To determine the safety and efficacy of a new nonthoracotomy lead configuration when used in conjunction with a device that used biphasic waveforms, 38 consecutive patients were taken to the operating room for implantation of a Cadence tiered therapy defibrillator system. The lead system consisted of a transvenous coil electrode positioned at the right atrial-superior vena caval junction, a bipolar endocardial right ventricular lead, and a large patch placed subcutaneously near the cardiac apex. Of the 38 nonthoracotomy defibrillator implantations attempted, 36 (95%) were completed with adequate defibrillation thresholds. The mean defibrillation threshold in these 36 patients was < or = 563 +/- 10 V (< or = 20 +/- 1 J). There was no perioperative mortality. Complications included coil lead migration (5), sensing lead migration (1), infection (3), pneumothorax (2), arterial embolism (1), and folding of the subcutaneous patch with an increase in defibrillation threshold (1). No patient died during a median follow-up period of 22 weeks. Fourteen patients (39%) had spontaneous sustained ventricular tachyarrhythmias, which were all successfully terminated by the implanted device. Shocks for nonsustained arrhythmias were aborted in eight patients (22%). Spurious discharges for sinus tachycardia or atrial fibrillation occurred in six patients (17%) and were readily diagnosed by examination of the stored electrograms. Thus, implantation of a biphasic tiered therapy defibrillator system using this nonthoracotomy approach is feasible in the majority of patients. The major complication associated with this procedure is lead dislodgment.(ABSTRACT TRUNCATED AT 250 WORDS)

Undersensing during ventricular tachyarrhythmias in a third-generation implantable cardioverter defibrillator: diagnosis using stored electrograms and correction with programming.

Third-generation implantable cardioverter defibrillators with stored electrograms allow diagnosis of various sensing problems that may lead to an inappropriate device response. Undersensing of ventricular tachyarrhythmias is a potentially serious problem, as it may lead to failure to deliver therapy. To determine the incidence of this problem, we reviewed 98 patients with Ventritex Cadence defibrillator systems and found 2 patients in whom defibrillation therapy was delayed or aborted because of undersensing during induced ventricular tachyarrhythmias. In both cases, examination of stored electrograms revealed variation in electrogram amplitude, which presumably resulted in failure of the autogain feature to increase its sensitivity enough to count each complex. During charging, criteria for redetection of sinus rhythm were met because of this undercounting, leading to failure to deliver defibrillation therapy. This problem was detected in both patients 4-6 weeks following device implant during device testing, and both patients had been started on antiarrhythmic drug therapy prior to this testing. Programming the sinus redetection parameter from nominal to slow, increasing the number of beats necessary to confirm resumption of sinus rhythm, corrected the problem in both patients. Device testing in the electrophysiology laboratory, routinely postoperatively and following initiation of antiarrhythmic drug therapy, and the ability to retrieve stored electrograms are useful in detecting such sensing anomalies.

Oversensing during ventricular pacing in patients with a third-generation implantable cardioverter-defibrillator.

OBJECTIVES: The purpose of this study was to identify the causes of oversensing during ventricular pacing in patients with a third-generation implantable cardioverter-defibrillator. BACKGROUND: Third-generation implantable cardioverter-defibrillators have the capability for bradycardia pacing as well as antitachycardia pacing and defibrillation. With the Ventritex Cadence Tiered Therapy Defibrillator System, the pulse generator sensitivity is increased during bradycardia pacing to prevent undersensing of an arrhythmia with small amplitude signals. METHODS: Records from 85 consecutive patients who underwent implantation of a Cadence device for treatment of ventricular tachyarrhythmias were reviewed. RESULTS: Four patients required continuous pacing for bradyarrhythmias. In three of these patients, ventricular pacing was accomplished using the bradycardia pacing feature of the Cadence device. All three experienced spurious device discharges or had aborted shocks for oversensing. Analysis of real-time and stored electrograms revealed intermittent high frequency, large amplitude noise in two patients and oversensing of maximally gained R and T waves in the remaining patient. No evidence of lead fracture was found in any patient. The problem was solved by implantation of a separate permanent pacemaker in two patients and was partially solved by reprogramming of the device in the remaining patient. CONCLUSIONS: Although the Cadence implantable cardioverter-defibrillator has the capability for ventricular pacing in patients with bradyarrhythmias, certain features of its automatic gain control circuit limit its utility in this instance. Oversensing occurs commonly, leading to device discharges or aborted shocks. Implantation of a separate permanent pacemaker may be required in patients who have a Cadence device for tachyarrhythmia control and who also need pacing for bradycardia.

Predictors of successful radiofrequency ablation of extranodal slow pathways.

Catheter positioning for radiofrequency ablation of extranodal slow pathways is often guided by local electrogram recordings. To determine the predictors of successful ablation sites, we reviewed data from 32 successful and 104 unsuccessful sites. Univariate predictors of a successful site included the occurrence of junctional rhythm during ablation (P < 0.001), shorter time to onset of junctional rhythm (P = 0.05), the presence of a discrete slow pathway potential (P < 0.001), a smaller ratio of the amplitude of the atrial:ventricular electrogram (P = 0.04), later timing (P = 0.001) and longer duration (P < 0.001) of the atrial slow pathway electrogram, and the duration of (P < 0.001), and maximal voltage used during ablation (P < 0.001). By multivariate analysis junctional rhythm (P < 0.001), a discrete slow pathway potential (P = 0.003), a longer duration of the atrial slow pathway electrogram (P = 0.01) and the duration of ablation (P = 0.02) were predictors of success. Because ablations at unsuccessful sites were often aborted at 10-30 seconds, a separate analysis was performed using only the 41 unsuccessful sites where the duration of ablation was > or = 30 seconds. The results were nearly identical. Thus, the occurrence of junctional rhythm during ablation and the morphology and duration of the atrial slow pathway electrogram may serve as guides for slow pathway ablation site selection.

Low dose disopyramide often fails to prevent neurogenic syncope during head-up tilt testing.

Low dose disopyramide has been used to prevent neurally-mediated syncope during head-up tilt testing but a correlation between blood levels and efficacy has not been described. We measured disopyramide levels in 15 patients with recurrent syncope and positive 70 degrees head-up tilt tests who underwent one or more repeat tests on the drug. There were 9 males and 6 females, age range 15-78 years. Fourteen of the 15 patients had structurally normal hearts. The daily disopyramide dose was 645 +/- 165 mg (mean +/- SD). Patients developed syncope during 9 tests and had no syncope during 12 tests. The mean disopyramide level in patients with positive tests was significantly lower than the level in patients with negative tests (2.4 +/- 0.15 mu/mL vs 3.2 +/- 0.22 mu/mL, P = 0.018). Six patients were tested twice on different disopyramide doses. Five of these six patients had syncope during head-up tilt testing on the lower dose and negative tests on the higher dose (disopyramide levels 2.2 +/- 0.17 mu/mL vs 3.2 +/- 0.17 mu/mL, P = 0.004). Thus, disopyramide is effective in preventing neurogenic syncope during head-up tilt testing, but higher blood levels are often necessary for efficacy. In a given patient, failure to respond to low dose disopyramide does not preclude success on higher doses.