Factors affecting the frequency of subcutaneous lead usage in implantable defibrillators.

Subcutaneous leads (SQ) add complexity to the defibrillation system and the implant procedure. New low output devices might increase the requirement for SQ arrays, although this might be offset by the effects of active can and biphasic technology. This study sought to assess the impact of these technologies on SQ lead usage, and to determine if clinical variables could predict the need for an SQ lead. Patients receiving nonthoracotomy systems (n = 554) at our institution underwent step-down-to-failure DFT testing with implant criteria of a 10-J safety margin. SQ leads were used only after several endovascular configurations failed. Use of biphasic waveforms significantly lowered the frequency of use of SQ leads from 48% to 3.7% (P < 0.000001). SQ leads were required in 4.4% of patients with cold can devices and 2.6% of patients with active can devices (P = NS). There was no increase in SQ lead usage with low energy (< 30-J delivered energy) devices. Clinical variables (including EF, heart disease, arrhythmia, and prior bypass) did not predict the need for an SQ lead. The implant DFT using SQ arrays (14.5 +/- 6.5 J) was not significantly lower than that for SQ patches (16.6 + 6.0 J). We conclude that biphasic waveforms significantly reduce the need for SQ leads. Despite this reduction, 3.7% of implants still use an SQ lead to achieve adequate safety margins. The introduction of lower output devices has not increased the need for SQ leads, and when an SQ lead is required, there is not a significant difference in the implant DFT of patches versus arrays. Clinical variables cannot predict which patients require SQ leads.

Are routine arrhythmia inductions necessary in patients with pectoral implantable cardioverter defibrillators?

INTRODUCTION: The value of ventricular arrhythmia inductions as part of routine implantable cardioverter defibrillator (ICD) follow-up in new-generation pectoral ICDs is unknown. METHODS AND RESULTS: We performed a retrospective analysis of a prospectively collected database analyzing data from 153 patients with pectoral ICDs who had routine arrhythmia inductions at predismissal, and 3 months and 1 year after implantation. Routine predismissal ventricular fibrillation (VF) induction yielded important findings in 8.8% of patients, all in patients with implantation defibrillation threshold (DFT) > or = 15 J or with concomitant pacemaker systems. At 3 months and 1 year, routine VF induction yielded important findings in 5.9% and 3.8% of tested patients, respectively, all in patients who had high DFT on prior testing. Ventricular tachycardia (VT) induction at predismissal, and 3 months and 1 year after implantation resulted in programming change in 37.4%, 28.1%, and 13.8% of tested patients, almost all in patients with inducible VT on baseline electrophysiologic study and clinical episodes since implantation. CONCLUSION: Although helpful in identifying potentially important ICD malfunctions, routine arrhythmia inductions during the first year after ICD implantation may not be necessary in all cases. VF inductions have a low yield in patients with previously low DFTs who lack concomitant pacemakers. VT inductions have a low yield in patients without baseline inducible VT and in the absence of clinical events. Definite recommendations regarding patient selection must await larger prospective studies as well as consensus in the medical community about what comprises an acceptable risk justifying avoidance of the costs and inconveniences of routine arrhythmia inductions.

Determination of pacing capture in implantable defibrillators: benefit of evoked response detection using RV coil to can vector.

Automatic detection of capture in ICDs would be useful for ensuring normal pacing function and lead integrity and may increase device longevity. Evoked response detection can be difficult due to postpace polarization. Polarization on the RV coil to can vector, however, should be absent when pacing with a true bipolar lead (pace tip to ring). Polarization on the RV coil to can vector should be low in an integrated bipolar lead due to the large surface area of the coil. Ventricular-paced responses were prospectively recorded in 20 patients during ICD implantation or replacement. Capture and loss of capture responses were noted during threshold searches with electrograms recorded between the RV coil and can. A detector was designed to discriminate between capture and noncapture-paced responses using data from the first 11 patients and validated on the remaining 9. The detector had a sensitivity of 99.9% (detected capture on capture beats), and had a specificity of 100% (detected no capture on noncapture beats) for all lead configurations. There was no measurable polarization with true bipolar leads. In integrated bipolar leads, maximum polarization ranged from 0.0 to 16.7 mV. In conclusion, paced evoked responses can be detected in ICDs using the RV coil to can vector using standard pacing waveforms. Special polarization reducing pacing waveforms are not required. These observations could be used to design ICDs with automatic pacing threshold detection.

Defibrillation thresholds are increased by right-sided implantation of totally transvenous implantable cardioverter defibrillators.

Whether an ICD is placed via a left- or right-sided approach depends on venous access, the presence of a preexisting pacemaker, and other factors. Since the DFT is affected by lead position, which in turn is determined in part by the side of access, right-sided venous access could adversely affect DFTs. Furthermore, right-sided active can placement directs electric current toward the right hemithorax, which could further increase DFTs. This study sought to determine whether DFTs were increased by right-sided vascular access, and whether active can technology was beneficial or detrimental with right-sided ICD placement. Stepdown to failure DFTs were found in 290 patients receiving transvenous systems at the time of initial ICD implantation. Of these, 271 (93%) received left-sided systems and 19 (7%) received right-sided systems. The mean DFT in systems placed via left-sided vascular access was 11.3 +/- 5.3 J versus 17.0 +/- 4.9 J for right-sided implantation (P < 0.0001); right-sided DFTs were elevated for both active can and cold can systems. Right-sided active can devices had a lower DFT than right-sided cold can systems (15 +/- 4.1 J vs 19 +/- 4.8 J, P = 0.05). The right-sided implantation of implantable defibrillators results in significantly higher DFTs than the left-sided approach. This may be due to the less favorable distribution of the defibrillating field relative to the myocardium with the devices on the right. When right-sided implantation is clinically mandated, active can devices result in lower thresholds and should be used.

A stepwise testing protocol for modern implantable cardioverter-defibrillator systems to prevent pacemaker-implantable cardioverter-defibrillator interactions.

Current use of newer implantable cardioverter-defibrillators (ICDs) has changed the spectrum of pacemaker-ICD interactions and provided new tools for testing and understanding those interactions. Testing for pacemaker-ICD interactions was performed in 31 procedures involving 22 patients. The protocol included: (1) evaluation of pacemaker stimulus artifact amplitude and its ratio to that of the evoked ventricular electrogram, (2) testing for inhibition of ventricular fibrillation (VF) detection by the ICD during asynchronous pacing at maximum output, (3) evaluation by pacemaker event marker recordings of pacemaker sensing behavior while programmed to nonasynchronous mode during ventricular tachycardia (VT) or VF, and (4) evaluation of postshock interactions. Inhibition of detection of VT/VF was found in 6 of 22 patients (27.2%). Large stimulus artifact amplitude (>2 mV) or stimulus artifact:evoked QRS ratio > 1/3 had a positive predictive accuracy of 18% and 14.4%, respectively, and a negative predictive accuracy of 100% and 92.3%, respectively, for clinically significant interaction. Asynchronous pacing occurred in 16 of 31 procedures (51.6%), and was due to underdetection by the pacemaker in 4 of 16 (25%) and noise reversion in 12 of 16 (75%). Postshock phenomena occurred in 6 cases, 3 of which were clinically significant. Overall, 11 of 22 patients (50%) had clinically significant interactions discovered by this protocol, which led to system revisions in 6 and to pacemaker output reprogramming in 5. Thus, pacemaker-ICD interactions are frequently detected using a thorough and systematic protocol. Most cases can be managed by system revision or pacemaker reprogramming.

Expression of the antiapoptotic MCL1 gene product is regulated by a mitogen activated protein kinase-mediated pathway triggered through microtubule disruption and protein kinase C.

Members of both the mitogen activated protein (MAP) kinase and BCL2 gene families, acting in concert with other gene products, are involved in the regulation of cell viability. However, the relationship between these families, and the signal transduction networks that control viability-regulating genes, are only beginning to be elucidated. MCL1 is a viability-promoting member of the BCL2 family that exhibits a rapid increase in expression in response to specific differentiation- and apoptosis-inducing stimuli. The signal transduction pathway involved in eliciting this increase has now been investigated. In the ML-1 human myeloblastic leukemia cell line, a rapid and sustained increase in phosphorylation of the extracellular signal-regulated kinase (ERK) members of the MAP kinase family was found to precede the increase in MCL1 expression produced by 12-O-tetradecanoylphorbol 13-acetate (TPA) or the microtubule-disrupting agents colchicine and vinblastine. ERK activation was necessary for the increase in MCL1, as inhibition of the increase in ERK phosphorylation (with the inhibitor PD 98059) prevented the increase in MCL1 expression and caused rapid cell death by apoptosis. In addition, other agents that markedly increased ERK phosphorylation (lipopolysaccharide, okadaic acid) also increased MCL1 expression. In contrast, agents that did not have this marked effect did not increase MCL1. Upstream components in this ERK-mediated pathway were also identified, where the pathway was found to be stimulated by microtubule disruption acting through protein kinase C (PKC). These results indicate that expression of the MCL1 viability-enhancing gene is regulated through a cytoskeletal disruption-induced ERK-mediated signal transduction pathway. They therefore suggest a mechanism through which the cytoskeleton and MAP kinases can exert effects on cell viability.

Importance of pacemaker noise reversion as a potential mechanism of pacemaker-ICD interactions.

Numerous types of interactions between pacemakers and implantable cardioverter defibrillators (ICDs) have been described. Pacemaker outputs preventing appropriate detection of ventricular tachycardia or ventricular fibrillation by the ICD is one of the more serious. Asynchronous pacemaker activity during ventricular arrhythmias may be caused by either nonsensing of the arrhythmia or by noise reversion, which is an algorithm that causes the pacemaker to switch to asynchronous pacing when repetitive sensing at a high rate occurs. We analyzed the mechanisms underlying asynchronous pacemaker activity in ventricular arrhythmias using pacemaker telemetry during the arrhythmia. Thirty-nine induced arrhythmias from 26 different procedures in 19 patients with both pacemakers and ICDs were analyzed. Of the 39 arrhythmias, asynchronous pacemaker activity occurred in 16. The underlying mechanism was nonsensing in 4 episodes and noise reversion in 12 episodes. Clinically significant interference with detection arose on three occasions. Conditions favoring the occurrence of noise reversion include specific pacemaker models, arrhythmia cycle lengths in the range causing noise reversion of the individual pacemaker model, long noise sampling periods, and VVI pacing mode. Noise reversion can be diagnosed by telemetering the pacemaker marker channel during ventricular arrhythmias as a part of routine pacemaker-ICD interaction evaluation. It can be prevented or minimized by programming short ventricular refractory periods or using pacemakers with short retriggerable refractory periods.

High failure rate for an epicardial implantable cardioverter-defibrillator lead: implications for long-term follow-up of patients with an implantable cardioverter-defibrillator.

OBJECTIVES: The purpose of this study was to determine the risk of epicardial lead failure during long-term follow-up and its mode of presentation. BACKGROUND: Despite the high prevalence of epicardial lead-based implantable cardioverter-defibrillators, their long-term performance is unknown, and appropriate follow-up has not been established. METHODS: The study group comprised all patients in whom an epicardial lead system was implanted at the Mayo Clinic between October 31, 1984 and November 3, 1994. The number of lead fractures and leads with fluid within the insulation and the mode of presentation were determined retrospectively by review of patient visits, radiographs of lead systems and data derived from formal lead testing. RESULTS: At 4 years, the survival rate free of lead malfunction, using formal lead testing, for 160 Medtronic epicardial patches (models 6897 and 6921) was 72% compared with 92.5% for the 179 Cardiac Pacemaker, Inc. (CPI) patches (models 0040 and 0041) (p = 0.01). In addition, five Medtronic patches in three patients had fluid within the lead insulation but no obvious fracture. No CPI patches had fluid identified within the leads. Of 330 Medtronic epicardial pace/sense leads (model 6917), the 4-year survival rate free of lead malfunction as assessed by lead testing was 96%. In all, 19 presentations of lead malfunction were found in 17 patients (2 patients had more than one lead fracture at different times). In 11 (58%) of these presentations, the patients were asymptomatic despite the presence of obvious lead fracture. CONCLUSIONS: Epicardial lead malfunction is common on long-term follow-up, and some leads have a failure rate of 28% at 4 years. Many patients with fractured leads remain asymptomatic, despite involvement of multiple leads in some cases. Therefore, consideration should be given to regular periodic lead testing in addition to routine X-ray examination, as asymptomatic lead malfunction can present with normal chest X-ray findings.

Dual-chamber pacing for hypertrophic cardiomyopathy: a randomized, double-blind, crossover trial.

OBJECTIVES: In a double-blind, randomized, crossover trial we sought to evaluate the effect of dual-chamber pacing in patients with severe symptoms of hypertrophic obstructive cardiomyopathy. BACKGROUND: Recently, several cohort trials showed that implantation of a dual-chamber pacemaker in patients with severely symptomatic hypertrophic obstructive cardiomyopathy can relieve symptoms and decrease the severity of the left ventricular outflow tract gradient. However, the outcome of dual-chamber pacing has not been compared with that of standard therapy in a randomized, double-blind trial. METHODS: Twenty-one patients with severely symptomatic hypertrophic obstructive cardiomyopathy were entered into this trial after baseline studies consisting of Minnesota quality-of-life assessment, two-dimensional and Doppler echocardiography and cardiopulmonary exercise tests. Nineteen patients completed the protocol and underwent double-blind randomization to either DDD pacing for 3 months followed by backup AAI pacing for 3 months, or the same study arms in reverse order. RESULTS: Left ventricular outflow tract gradient decreased significantly to 55 +/- 38 mm Hg after DDD pacing compared with the baseline gradient of 76 +/- 61 mm Hg (p < 0.05) and the gradient of 83 +/- 59 mm Hg after AAI pacing (p < 0.05). Quality-of-life score and exercise duration were significantly improved from the baseline state after the DDD arm but were not significantly different between the DDD arm and the backup AAI arm. Peak oxygen consumption did not significantly differ among the three periods. Overall, 63% of patients had symptomatic improvement during the DDD arm, but 42% also had symptomatic improvement during the AAI backup arm. In addition, 31% had no change and 5% had deterioration of symptoms during the DDD pacing arm. CONCLUSIONS: Dual-chamber pacing may relieve symptoms and decrease gradient in patients with hypertrophic obstructive cardiomyopathy. In some patients, however, symptoms do not change or even become worse with dual-chamber pacing. Subjective symptomatic improvement can also occur from implantation of the pacemaker without its hemodynamic benefit, suggesting the role of a placebo effect. Long-term follow-up of a large number of patients in randomized trials is necessary before dual-chamber pacing can be recommended for all patients with severely symptomatic hypertrophic obstructive cardiomyopathy.

Dual-chamber pacing for cardiomyopathies: a 1996 clinical perspective.

Implantation of a permanent pacemaker is an accepted mode of therapy for symptomatic bradyarrhythmias. Application of pacemaker technology for the treatment of cardiomyopathies has generated considerable interest and enthusiastic support in recent years. In both hypertrophic cardiomyopathy and dilated cardiomyopathy, dual-chamber pacing has been shown to decrease symptoms and improve hemodynamics; however, not all patients will benefit from dual-chamber pacing. Technical considerations must be acknowledged in order to obtain optimal benefit with dual-chamber pacing. In addition, other more accepted therapies are available for patients with symptomatic cardiomyopathies. The purposes of this article are to review critically the current literature on the use of dual-chamber pacemakers in patients with either hypertrophic or dilated cardiomyopathy and to provide a clinical perspective based on current knowledge.

Transtelephonic monitoring and transmission of stored arrhythmia detection and therapy data from an implantable cardioverter defibrillator.

A new transtelephonic monitoring device designed for use with implantable cardioverter defibrillators (ICDs) was evaluated. It is capable of interrogating ICDs and transmitting the following data via telephone: programmed parameters (e.g., ventricular tachycardia [VT] and ventricular fibrillation [VF] detection, therapies), number of VT and VF episodes, identification of successful therapies, the 20 cycle lengths preceding the last episode detected, the 10 cycle lengths after the last delivered therapy, battery voltage, and real-time transmission of the patient's rhythm. Eighteen patients (mean age 64 +/- 17 years; 15 males) were implanted with an ICD and epicardial lead system. The patients who did not live near the primary hospital were provided with this transmitter and instructed to transmit monthly and whenever presyncope, syncope, or a shock were experienced. Five hundred ten episodes of spontaneous arrhythmia (495 VT, 15 VF) were detected in 14 of 18 patients in a 24-month period and the success of each therapy (antitachycardia pacing, cardioversion 0.4-34 J, defibrillation 34 J) was analyzed. The number of therapies delivered and their success (%) in terminating the arrhythmia were: 380 ramp/86%, 116 burst/84%, 119 cardioversion/57%, and 15 defibrillations/100%. Sixty-three (42%) of the 152 transmissions indicated an arrhythmia. Twenty-five (16%) of the 152 were transmitted because of symptoms. Sixteen (9.7%) of 165 VT episodes could not be terminated by the full set of programmed VT therapies. Analysis of the pre- and post-episode intervals along with the patient's transmitted rhythm indicated that sinus tachycardia or atrial fibrillation were likely responsible for these episodes.(ABSTRACT TRUNCATED AT 250 WORDS)

Consistent subcutaneous prepectoral implantation of a new implantable cardioverter defibrillator.

OBJECTIVE: To describe the use of a new implantable cardioverter defibrillator (ICD) that can be placed in the prepectoral region rather than implanted in the abdominal wall. DESIGN: We report the experience of placement of this new ICD in the prepectoral region in 13 patients from Sept. 28, 1993, through Jan. 10, 1994, at the Mayo Clinic. MATERIAL AND METHODS: Thirteen consecutive patients offered this new ICD underwent placement of transvenous defibrillation leads, and the pulse generator was placed in a pocket formed in the subcutaneous, prepectoral space. Testing ensured a defibrillation threshold of 24 J or less. RESULTS: In all 13 patients, the pulse generator could be placed in the subcutaneous, prepectoral space. In all except one patient, acceptable defibrillation thresholds were achieved by using lead systems placed totally transvenously. Only one patient required placement of a subcutaneous patch. All but two patients were dismissed from the hospital within 3 days after the ICD implantation. CONCLUSION: Consistent subcutaneous, prepectoral placement of this new ICD pulse generator is possible. Because the entire procedure can be performed in the pacemaker implantation room, the potential exists for decreasing the duration of the hospitalization and associated costs.

Influence of ventricular function and presence or absence of coronary artery disease on results of electrophysiologic testing for asymptomatic nonsustained ventricular tachycardia.

One hundred ten patients with asymptomatic nonsustained ventricular tachycardia (VT) were evaluated prospectively to assess the value of electrophysiologic testing. This testing consisted of up to 3 extrastimuli delivered during 3 drive cycle lengths from 2 right ventricular sites. A positive study was defined as monomorphic VT lasting 30 seconds or requiring cardioversion. Patients with a positive study were treated, and serial drug testing was done. An event during follow-up was sustained VT or cardiac arrest. The mean follow-up was 15 months. Of 57 patients with an ejection fraction greater than or equal to 40%, 6 had a positive electrophysiologic test with 1 event and 51 had a negative test with 1 event. Twenty-eight patients had an ejection fraction less than 40% and coronary artery disease: 14 had a positive test with 1 event, and 14 had a negative test with 3 events. Twenty-five patients had an ejection fraction less than 40% and no coronary artery disease: 1 had a positive test with no events, and 24 had a negative test with 8 events. Only ejection fraction and congestive heart failure class were found to be independent predictors of outcome. Patients with an ejection fraction greater than 40% had low inducibility (11%), had few events (3.5%) and did not require electrophysiologic testing. In patients with an ejection fraction less than 40% and coronary artery disease, inducibility was high (50%) and a negative study was of no value. Patients with an ejection fraction less than 40% and no coronary artery disease had low inducibility (4%), had frequent events (33%) and did not benefit from electrophysiologic testing.

A shorter hospital stay after cardiac pacemaker implantation.

In an effort to shorten the hospital stay after implantation of a permanent cardiac pacemaker, some physicians have begun performing pacemaker implantation on an ambulatory basis. To assess the potential safety of shortening the duration of hospitalization after pacemaker implantation, we reviewed the complications that occurred in 100 consecutive patients after pacemaker implantation and noted the time after the implantation when the complications occurred. In our study group, all complications that necessitated invasive intervention occurred within 24 hours after the pacemaker implantation. Complications that necessitated noninvasive programming occurred as long as 72 hours after implantation, and all could have been safely corrected at the time of follow-up had the patient been dismissed at the 24-hour period. Although we do not believe that ambulatory pacemaker implantation should be routinely implemented at this time, the practice of dismissing patients at 24 hours after pacemaker implantation and scheduling subsequent outpatient follow-up seems to be safe and effective.

Transient atrioventricular block after open-heart surgery for congenital heart disease.

The records of 22 patients with transient atrioventricular (AV) block after open-heart surgery for congenital heart disease from 1972 to 1978 were reviewed to determine the natural history of this entity. Preoperatively, no patient had AV block; 3 had right bundle branch block (BBB), 1 had left BBB and 5 had nonspecific intraventricular conduction delay. Complete AV block developed in 20 patients and Mobitz II AV block in 2. Transient AV block occurred intraoperatively in 14 patients and within 48 hours postoperatively in 8; AV block persisted for greater than or equal to 48 hours postoperatively in all patients, for a mean of 7.3 days (range 2 to 28). During a follow-up of 5.5 years (range 2.5 to 10), late AV block developed in 2 patients. None of the 18 patients whose escape QRS complex morphology during AV block was similar to the final QRS complex during normal sinus rhythm or atrial fibrillation with AV conduction had late AV block, whereas 2 of the 4 in whom it differed did (p less than 0.01). There was no difference in the escape rate between the 2 groups. Thus, late development of high-grade AV block is infrequent among patients with transient postoperative AV block. An escape QRS complex during postoperative AV block that differs from the QRS complex seen on recovery of normal sinus rhythm or atrial fibrillation with anterograde conduction may identify those at high risk of late AV block.

Infected epicardial pacemaker systems. Partial versus total removal.

Nine patients with infected epicardial pacemakers are described. All of the patients had infection localized to the generator pocket. Staphylococcus epidermidis, the most common organism isolated, was found in seven (77.8%). Conservative nonsurgical treatment was initially attempted in five patients. This failed in all and necessitated subsequent operation. At the time of the initial operation, lead transection and partial removal of the system was performed in seven patients. In four of them (57%), persistent infection necessitated further operation and complete extraction to eradicate the infection. In contrast, in all six patients (100%) in whom total removal was achieved (two at the time of initial operation and four at the time of subsequent operation), there was successful resolution of the infection. Therefore, complete extraction of the entire pacing system should be carried out, whenever possible, to achieve the greatest likelihood of eradicating the infection.

Permanent pacemaker infections: characterization and management.

From January 1974 to June 1980, a total of 46 patients were treated for infections involving permanent pacing systems. Demographic characteristics, types of infecting organisms, specific clinical features, significance of an infected foreign body and various medical and surgical treatment methods are described. Likely infecting organisms depend on the mode of presentation and the time course of the infection. Optimal treatment for the large majority of patients requires removal of the entire infected pacing system. In a subgroup of patients, a short course of antibiotic therapy followed by one stage surgery involving implantation of a new pacing system and concurrent explanation of the infected pacemaker was used safely with excellent results.

An evaluation of long-term stimulation thresholds by measurement of chronic strength duration curve.

Successful long-term cardiac pacemaker therapy requires both reliable generator output and stable, attainable chronic stimulation thresholds. Strength duration curves, which display cardiac stimulation thresholds as a function of impulse duration, provide needed data to evaluate more thoroughly acute and chronic lead thresholds. We measured chronic strength duration curves at the time of generator replacement in 47 patients with three different types of lead systems of variable geometry and surface area and compared these curves with acute strength duration curves measured at the time of initial implantation in 19 patients. We found that strength duration curves has a characteristic shape; however, chronic strength duration curves were shifted upward and to the right of acute strength duration curves, regardless of electrode tip surface area or geometric design. Our data suggest that variable pulse width exceeding 1 ms may not significantly reduce stimulation thresholds.