Biomedical subjects

M J Reiter

Publications and source records attributed to M J Reiter.

At least 37 records · Page 2Linked to original sources

PubMed1997

Sotalol for ventricular tachyarrhythmias: beta-blocking and class III contributions, and relative efficacy versus class I drugs after prior drug failure. ESVEM Investigators. Electrophysiologic Study Versus Electrocardiographic Monitoring.

In the Electrophysiologic Study Versus Electrocardiographic Monitoring (ESVEM) trial, d,l-sotalol was associated with a lower arrhythmia recurrence and mortality than class I antiarrhythmic drugs. To further evaluate the relative efficacy of d,I-sotalol compared with class I drugs, and to assess the relative importance of its class II (beta-blocking) and class III effects, 6-year arrhythmia recurrence and mortality in patients receiving sotalol were compared with those in patients receiving class I drugs, subdivided according to whether they also received coadministered beta blockers. Relative efficacy was also determined for sotalol and for class I drugs as stratified by the presence/absence of prior drug failure. Arrhythmia recurrence was lower for the 84 patients receiving sotalol than for patients given class I agents with (n = 28) (p = 0.008) or without (n = 184) (p = 0.001) alpha beta blocker. Mortality was lower for patients taking sotalol than for those given a class I drug without alpha beta blocker (p = 0.034), but similar (p = 0.835) if alpha beta blocker was also administered. In contrast to class I drugs, which had lower efficacy rates when prior drug trials had failed, sotalol maintained its efficacy despite prior drug failures preceding or during the ESVEM trial. Both class II and III actions in the ESVEM trial were important to the clinical superiority of sotalol in the treatment of ventricular tachyarrhythmias.

Adrenergic beta-Antagonists↗

PubMed1997

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.

Aged↗

PubMed1997

The ESVEM trial: impact on treatment of ventricular tachyarrhythmias. Electrophysiologic Study Versus Electrocardiographic Monitoring.

The ESVEM (Electrophysiologic Study Versus Electrocardiographic Monitoring) trial was a prospective, randomized study, initiated in 1983, to compare the outcome of patients in whom antiarrhythmic therapy was guided by serial electrophysiological study with the outcome of patients in whom therapy was guided by electrocardiographic monitoring. In a surprising finding, there was no difference in rates of arrhythmia recurrence or mortality between the two methods. Subsequent reanalyses using more stringent criteria for both methods or a combined assessment have not significantly improved the predictive accuracy of guided therapy. Because drug therapy in each limb was also randomized, a comparison of specific antiarrhythmic agents was also possible: sotalol therapy and the absence of previous antiarrhythmic drug therapy were associated with a reduction in arrhythmia recurrence. Survey data suggest that the results of this trial have influenced clinical practice.

Electrocardiography, Ambulatory↗

PubMed1997

Effect of ventricular dilatation on defibrillation threshold in the isolated perfused rabbit heart.

INTRODUCTION: Ventricular dilatation has important electrophysiologic effects, but its effect on ventricular defibrillation threshold (DFT) is unknown. METHODS AND RESULTS: A fluid-filled, latex balloon was placed in the left ventricular cavity of 19 isolated rabbit hearts. In each experiment, an undilated volume (equivalent to a left ventricular end-diastolic pressure of approximately 0 mmHg) was compared to a dilated volume achieved by adding 1.0 mL of saline (n = 10) or 5% dextrose (n = 9) to the intracavitary balloon. Left ventricular effective refractory period (ERP) and DFT were determined at each volume. Defibrillation was attempted with a monophasic shock delivered between a patch electrode positioned over the posterior left ventricle (cathode) and a metallic aortic cannula (anode). DFT was determined using a modified "down/up" protocol with 10 V steps. Ventricular dilatation increased the left ventricular end-diastolic pressure from 0 +/- 0.5 mmHg to 35 +/- 3 mmHg (P < 0.001), decreased the average left ventricular ERP 15% (from 116 +/- 3 msec to 99 +/- 3 msec; P < 0.001), and increased the average DFT 30% (from 96 +/- 4 V to 125 +/- 7 V; P < 0.001). In one third of experiments, the dilated DFT was > or = 150% of the DFT at zero volume. The mechanism of the observed increase in DFT is unknown but may be related to the decrease in refractoriness observed with ventricular dilatation. CONCLUSION: Acute ventricular dilatation in this model increased DFT an average of 30%, an effect not previously described. This observation may have implications for patients with implantable cardioverter defibrillators.

Animals↗

PubMed1996

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.

Defibrillators, Implantable↗

PubMed1996

Effects of mechano-electrical feedback: potential arrhythmogenic influence in patients with congestive heart failure.

Experimental studies have demonstrated that changes in mechanical loading conditions have important, and potentially arrhythmogenic, electrophysiologic effects. These studies have, for the most part, involved the effects of acute dilatation in the structurally normal heart. The ionic basis of these changes remains incompletely understood. Although there is abundant evidence that mechano-electrical feedback occurs in man, additional studies are required to clarify whether the mechanical and hemodynamic abnormalities present in patients with congestive heart failure are a significant contributor to the clinical arrhythmias in these patients. Ongoing studies should clarify this important issue.

Arrhythmias, Cardiac↗

PubMed1995

Comparison of monophasic and biphasic defibrillating pulse waveforms for transthoracic cardioversion. Biphasic Waveform Defibrillation Investigators.

All transthoracic defibrillators on the US market use nominally monophasic shock waveforms. However, biphasic waveforms have a lower defibrillation threshold than monophasic waveforms for transthoracic defibrillation of animals and for defibrillation of humans by implantable cardioverter defibrillators. The relative efficacies of Edmark monophasic and Gurvich biphasic transthoracic cardioversion waveforms (200 J into 50 omega) were compared for transthoracic cardioversion in 171 patients undergoing electrophysiologic study for evaluation of ventricular arrhythmias. Patients were randomized in a blinded fashion to receive either a monophasic or a biphasic waveform for the initial shock for conversion of induced ventricular arrhythmias (ventricular fibrillation [VF] = 53, monomorphic ventricular tachycardia [VT] = 80, polymorphic VT = 30, ventricular flutter = 8). Delivered energies for the Edmark and Gurvich waveforms were 215 +/- 11 and 171 +/- 11 J, respectively. There were no significant differences in patient characteristics, use of antiarrhythmic agents, arrhythmia cycle length, or duration of arrhythmia prior to shock for monophasic and biphasic waveform groups. The first shock for all arrhythmias was successful in 75 of 88 patients (85.2%) for the monophasic waveform compared with 81 of 83 patients (97.6%) for the biphasic waveform, p = 0.0054. The first shock for VF was successful in 22 of 28 patients (78.6%) for the monophasic waveform compared with 25 of 25 (100%) for the biphasic waveform, p = 0.0241. The Gurvich biphasic waveforms delivering a mean of 171 J were superior to Edmark monophasic waveforms delivering a mean of 215 J for transthoracic cardioversion of arrhythmias of short duration. This finding may have important implications for the development of future transthoracic defibrillators.

Adult↗

PubMed1995

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.

Aged↗

PubMed1995

Cytokine induction by the immunomodulators imiquimod and S-27609.

Imiquimod (R-837, S-26308) and the analogue S-27609 were evaluated for cytokine induction in human blood cells. Both compounds induced interferon-alpha (IFN), tumor necrosis factor-alpha (TNF), interleukin (IL)-1 beta, and IL-6 with S-27609 being 5 to 10 times more potent. Imiquimod and S-27609 also induced IL-1 alpha, IL-1 receptor antagonist, IL-10, granulocyte-macrophage colony-stimulating factor (GM-CSF), granulocyte CSF (G-CSF), and macrophage inflammatory protein-1 alpha. The profile of cytokines induced by imiquimod and S-27609 was different from those seen with lipopolysaccharide and polyinosinic-polycytidylic acid. Kinetic studies with both imiquimod and S-27609 revealed induction of cytokines as early as 1-4 h after stimulation. Although most of the cytokines produced by S-27609 were secreted, significant concentrations of IL-1 alpha and IL-1 beta remained intracellular. Monocytes were largely responsible for the cytokines produced. Finally, S-27609-induced mRNA expression for TNF, IFN, and IL-8, and this induction did not require protein synthesis. Taken together, these studies extend previous findings by showing induction of additional cytokines and providing insight into the mechanism of cytokine induction by these molecules.

Adjuvants, Immunologic↗

PubMed1995

Immunomodulating and antiviral activities of the imidazoquinoline S-28463.

Recently, a new class of immunomodulating agents, represented by the molecules imiquimod and R-842, has demonstrated potent antiviral and antitumor activities in animal models. In this study, another representative of this class, S-28463 (4-amino-2-ethoxymethyl-alpha,alpha-dimethyl-1H-imidazo[4,5-c]quinoline- 1- ethanol) was evaluated for its immunomodulating and antiviral activities. S-28463 induced IFN and other cytokines in vivo in mice, rats, monkeys and in vitro in human peripheral blood mononuclear cell cultures. S-28463 showed potent antiviral activity against herpes simplex virus-challenged guinea pigs when given subcutaneously, dermally, or intravaginally 24 h before infection. Antiviral activity in guinea pigs correlated with the induction of serum 2',5'-oligoadenylate synthetase activity. Thus, S-28463, like the other imidazoquinolines, demonstrates potent antiviral and immunomodulating effects in a number of models.

2',5'-Oligoadenylate Synthetase↗

PubMed1995

Cellular requirements for cytokine production in response to the immunomodulators imiquimod and S-27609.

Imiquimod (R-837) and its analog, S-27609, belong to a class of imidazoquinolinamines that have potent antitumor and antiviral effects in animals. Much of their biologic activity is a result of the induction of cytokines, including interferon-alpha (IFN-alpha), tumor necrosis factor alpha (TNF), and others. In this study, the cells responsible for S-27609- and imiquimod-induced cytokine production were characterized. E rosette+ T cells were not the major cell population responsible for IFN-alpha and TNF in response to S-27609 or imiquimod. In contrast, E rosette- cells and unseparated PBMC produced similar concentrations of IFN-alpha and TNF in response to S-27609 and imiquimod. Elimination of monocytes by treatment with the lysosomotropic agent L-leucine methyl ester (LME) or depletion using antibody to CD14 and immunomagnetic beads abrogated IFN-alpha and TNF production induced by S-27609, imiquimod, or LPS but not poly(I)/(C). LME treatment also abolished interleukin (IL)-1 alpha, IL-beta, IL-6, and IL-8 production stimulated by S-27609 and imiquimod. Removal of HLA-DR+ or CD36+ monocytes also caused a significant reduction in S-27609- and imiquimod-induced IFN-alpha and TNF. Elimination of B cells, NK cells, and dendritic cells did not significantly reduce cytokine induction in response to S-27609. Thus, the cell population responsible for the majority of cytokine release in human PBMC in response to S-27609 and imiquimod is a E rosette-, CD14+, CD36+, HLA-DR+ monocyte.

Adjuvants, Immunologic↗

PubMed1995

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.

Adolescent↗

PubMed1995

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.

Bundle of His↗

PubMed1994

Cytokine induction in mice by the immunomodulator imiquimod.

Imiquimod has been identified as a potent antiviral and antitumor agent in animal models. The biological activity associated with imiquimod has been attributed to its induction of interferon (IFN)-alpha. The present studies evaluated imiquimod administered orally for its ability to stimulate production of IFN and other cytokines in mice. The cytokine profile induced by imiquimod was compared with other known immunomodulators. Imiquimod was found to stimulate increased serum IFN in mice. Daily dosing of imiquimod for five consecutive days led to diminished production of IFN in mice as measured after the final dose. Elevated levels of serum tumor necrosis factor (TNF)-alpha and interleukin (IL)-6 but not IL-1 alpha were found in serum from mice treated with imiquimod. Imiquimod produced significantly higher levels of IFN but lower levels of TNF and IL-6 and IL-1 alpha than lipopolysaccharide. Polyinosinic acid:polycytidylic acid induced significantly higher amounts of IFN but lower levels of TNF and IL-6 than imiquimod. Imiquimod stimulated significantly higher levels of IFN when compared with 2-amino-5-bromo-6-phenyl-4(3H)-pyrimidinone (ABPP) and similar levels of IFN when compared with tilorone. Neither ABPP nor tilorone induced TNF or IL-6. Finally, imiquimod stimulated TNF, IFN, and IL-6 production in cultures of mouse spleen and bone marrow cells. These studies demonstrate that imiquimod induces not only IFN but other cytokines as well, all of which may contribute to its biological activity.

Aminoquinolines↗

PubMed1994

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.

Aged↗

PubMed1994

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.

Adolescent↗

PubMed1994

Predictors of device activation for ventricular arrhythmias and survival in patients with implantable pacemakers/defibrillators. CADENCE Investigators.

Predictors of survival and arrhythmia recurrence for patients with implanted defibrillators have been reported but patients with sustained, well-tolerated ventricular tachycardia were often excluded from these trials. Arrhythmia recurrence and survival in populations including these patients have been less well studied. The purpose of the present study was to examine predictors of spontaneous ventricular arrhythmias and mortality in patients who received a tiered therapy antitachycardia pacemaker/defibrillator for ventricular tachycardia, fibrillation, or both. Three hundred thirty-seven patients who received a Ventritex CADENCE tiered therapy antitachycardia device at one of 19 participating centers between July 11, 1989 and March 4, 1991 are included in this retrospective analysis. Diagnostic summary data and stored electrograms telemetered from the implanted device were assessed to determine characteristics of recurrent arrhythmias. Mean follow-up was 360 +/- 10 (SEM) days. Thirty-three patients died during follow-up. At least one recurrent ventricular arrhythmia was observed in 205 patients (61%). A total of 7,539 episodes were observed with a mean of 37 +/- 5 per patient. Patients with recurrent ventricular arrhythmias were slightly but significantly older (64 +/- 0.7 vs 59 +/- 1.2 years; P < 0.001) but were not distinguished by gender or underlying structural disease. Patients whose presenting arrhythmia was monomorphic ventricular tachycardia were more likely to experience recurrent ventricular arrhythmias (69% recurrence rate) than patients presenting with ventricular fibrillation or polymorphic ventricular tachycardia (46% recurrence rate; P < 0.001). Cycle length of spontaneous tachycardia was also a predictor of arrhythmia recurrence. Patients having slower ventricular arrhythmias were less likely to remain recurrence free. Mean left ventricular ejection fraction was similar for patients with and without recurrences. Younger age and absence of arrhythmia recurrence but not presenting arrhythmia were predictors of survival. We conclude that age and presentation with monomorphic ventricular tachycardia are important predictors of arrhythmia recurrence for this patient population. Exclusion of patients with monomorphic ventricular tachycardia underestimates the rate of recurrent ventricular arrhythmias and utilization of device therapy.

Adolescent↗

PubMed1994

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.

Aged↗