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Biomedical subjects

F E Marchlinski

Publications and source records attributed to F E Marchlinski.

At least 91 records · Page 5Linked to original sources

Insights into the electrophysiology of ventricular tachycardia gained by the catheter ablation experience: "learning while burning".

The success of catheter ablation has significantly improved the treatment of patients with cardiac arrhythmias and has established electrophysiology as an increasingly interventional subspecialty. Some members of the electrophysiology community have expressed concern that this success has been purchased at the cost of undermining what had been our primary concern: understanding the anatomic and physiologic basis of arrhythmia syndromes. In many laboratories, endpoints such as case load and primary success have eclipsed physiologic investigation. Despite these trends, however, catheter ablation is not inherently at odds with investigation and education. On the contrary, because the lesions delivered with current techniques are much more discrete than the effects of antiarrhythmic agents or surgical ablation, catheter ablation can be used as a research tool directed toward a more precise understanding of arrhythmia substrates. Conscious attempts at "learning while burning" have already provided important and unique information about arrhythmia pathogenesis.

Cardiomyopathy, Dilated↗

Effects of incremental doses of procainamide in patients with sustained uniform ventricular tachycardia.

INTRODUCTION: Although intravenously administered procainamide has been used extensively during electropharmacologic testing for more than 10 years, there is little information available on the effects of incremental dosing of procainamide in patients with inducible, monomorphic ventricular tachycardia (VT). METHODS AND RESULTS: Twenty-nine patients with coronary artery disease had sustained monomorphic VT reproducibly induced in the baseline, drug-free state. Programmed stimulation was repeated 5 minutes after loading infusion (50 mg/min) of 7.5 and 15 mg/kg (all patients) and 22.5 mg/kg of procainamide (15 patients), while maintaining continuous infusion of 0.055, 0.11, and 0.165 mg/kg per minute after each increment in dose, respectively. Corresponding procainamide plasma concentrations were 5.6 +/- 2, 10.5 +/- 3, and 14.5 +/- 3 mg/L before, and 4.7 +/- 2, 9.6 +/- 3, and 14.6 +/- 4 mg/L after electrophysiologic study at each increment in dose of procainamide, respectively. Each incremental dose of procainamide resulted in significant prolongation of tachycardia cycle length and QRS duration during sinus rhythm and right ventricular pacing. Five (17%), 7 (24%), and 1 (7%) patients, respectively, had no inducible sustained VT following the incremental dosing of procainamide. Three of five patients who had no inducible VT at 7.5 mg/kg had VT induced again at a higher dose of procainamide. Four of 24 patients whose VT remained inducible at 7.5 mg/kg of procainamide had no VT induced at 15 mg/kg of procainamide. Twelve (41%), 15 (52%), and 6 (40%) patients, respectively, no longer had VT with baseline morphology induced following the incremental dosing of procainamide. VT with new morphology compared to baseline was induced in more than 40% of patients at one or more of the three different procainamide dosing regimens. The mean cycle length of VTs with new morphology was significantly shorter than the cycle length of tachycardias with baseline morphology at each particular dose of procainamide. CONCLUSION: Similar serum procainamide concentrations before and after programmed stimulation can be achieved at the described dosing regimen. Although 7.5 and 15 mg/kg of procainamide are both effective in suppressing induction of all VT in 20% to 25% of patients, non-inducibility at a particular dose of procainamide does not predict noninducibility at a respectively higher or lower dose. New morphologies of VT that are frequently faster than VTs with baseline morphology at a particular dose of procainamide can be induced in approximately half of the patients, and the clinical significance of these arrhythmias remains to be determined.

Adult↗

Symptoms and electrocardiographically documented rhythm preceding spontaneous shocks in patients with implantable cardioverter-defibrillator.

During a follow-up of 24 +/- 20 months after treatment with an implantable cardioverter-defibrillator (ICD), 101 of 241 patients (42%) received > or = 1 spontaneous ICD shocks with documentation of the rhythm leading to shock by Holter or telemetry monitoring or stored electrograms by the device. Sustained ventricular tachycardia (VT) or ventricular fibrillation (VF) was documented in 67 of the 101 patients (66%) with electrocardiographically documented shocks, nonsustained VT in 4 patients (4%), supraventricular tachyarrhythmias in 41 patients (41%), and normal sinus or pacemaker rhythm in 10 patients (10%). No, mild (palpitations and/or mild dizziness) and severe symptoms (presyncope/syncope) preceded spontaneous ICD shocks in 20 (30%), 33 (49%) and 27 (42%) of the 67 patients, respectively, with electrocardiographically documented VT or VF, and in 23 (56%), 16 (39%) and 1 (2%) of the 41 patients, respectively, with electrocardiographically documented supraventricular tachyarrhythmias. Three of the 4 patients with nonsustained VT had mild symptoms, and 1 patient with nonsustained VT had presyncope. None of the 10 patients with spurious discharges during normal sinus or pacemaker rhythm had symptoms preceding the ICD shocks. It is concluded that (1) most patients with either electrocardiographically documented VT/VF or a non-VT/VF rhythm preceding spontaneous ICD shocks have no or mild symptoms preceding the shock, and (2) severe symptoms preceding ICD shocks suggest sustained VT or VF as the underlying rhythm, although severe symptoms rarely occur in patients with supraventricular tachyarrhythmias or nonsustained VT.

Adult↗

Importance of abortive shock capability with electrogram storage in cardioverter-defibrillator devices.

OBJECTIVES: This study evaluates the ability of a third-generation cardioverter-defibrillator to abort energy delivery and the importance of electrogram storage in analyzing the aborted events. BACKGROUND: In the Cadence Tiered Therapy Defibrillator, when a tachycardia satisfies detection criteria for cardioversion or defibrillation therapy, high voltage capacitors begin charging. The Cadence defibrillator continues monitoring the rhythm during charging and if the rate decreases to below the rate triggering therapy, charging is terminated. This event is registered as an aborted shock. The defibrillator also has the ability to store intracardiac electrogram recordings of the electrical events that precipitate device therapy or aborted shocks. METHODS: During a mean follow-up interval of 10 +/- 7 months, 55 aborted events were registered by the Cadence defibrillator in 18 of the 49 patients who received it. Thirty-two stored ventricular electrograms of events leading to aborted shocks were available for analysis in 15 patients. RESULTS: Intracardiac electrogram recordings demonstrated the probable electrical events leading to these aborted shocks included nonsustained ventricular tachycardia (n = 10), nonsustained rapid polymorphic ventricular tachycardia/ventricular fibrillation (n = 2), atrial fibrillation (n = 5), supraventricular tachycardia (n = 2) and electrical noise (n = 13). Eleven patients had a therapeutic intervention initiated as a consequence of the diagnostic information provided by analysis of intracardiac electrogram recordings. Four of the 15 patients had no changes made. During a follow-up period of 9 +/- 5 months after therapy was altered, no patient had subsequent aborted shocks. Five patients have had seven appropriate shocks for sustained ventricular tachycardias. CONCLUSIONS: The ability of Cadence defibrillator to continue tachycardia sensing during capacitor charging and to abort shock therapy for self-terminating events prevented unnecessary shocks in 18 (37%) of the 49 patients. Intracardiac electrogram recordings were critical for instituting appropriate therapy that may have prevented unnecessary device charging and inappropriate discharges.

Adult↗

Ventricular tachycardia in patients without structural heart disease.

The existence of ventricular tachycardia in subjects without detectable heart disease has been recognized for more than half a century. These rhythms occur in younger individuals and account for about 5% of referrals to the electrophysiology service. In contrast, ventricular tachycardia in the setting of chronic ischemic heart disease occurs in an older age group and accounts for more than 90% of all referrals. It is important to be able to distinguish between the different varieties of ventricular tachycardia, because in patients without structural heart disease sudden cardiac death is rare, compared with the very high mortality associated with postischemic recurrent ventricular tachycardia. The natural history of ventricular tachycardia occurring without structural heart disease tends to be benign even when the tachycardia is untreated. Thus these rhythms are more of an annoyance than a life-threatening event. This variety of ventricular tachycardia is frequently not inducible by atrial or ventricular programmed stimulation but is inducible by atrial or ventricular pacing, exercise testing, or isoproterenol infusion. The ventricular tachycardia in patients without structural heart disease is frequently responsive to drugs such as beta-blockers, verapamil, or adenosine that have little or no effect on ventricular tachycardia associated with previous infarction. These differences strongly suggest the possibility of a tachycardia mechanism other than reentry, although conclusive evidence is still lacking.

Adult↗

Effect of rate and coupling interval on endocardial R wave amplitude variability in permanent ventricular sensing lead systems.

OBJECTIVES: We have observed sensing errors in third generation implantable cardioverter-defibrillators that appear to be caused by variation in the R wave amplitude during sinus rhythm, particularly after premature beats. The purpose of this study was to quantify spontaneous R wave variability during sinus rhythm and to determine whether abrupt changes in cycle length further augment R wave amplitude variability. BACKGROUND: Pacemaker sensing algorithms presume a relatively constant R wave signal to establish a sensing threshold. The concept of a fixed sensing threshold is not as applicable in third-generation cardioverter-defibrillators, which depend on automatic gain amplifiers to rapidly detect ventricular fibrillation. These devices may be susceptible to undersensing during sinus rhythm if significant variability in R wave signal characteristics occurs. METHODS: Twelve patients with combination bradycardia pacing cardioverter-defibrillators were studied. The device used (Cadence, Ventritex) allowed recording of real time, telemetered electrograms from the sensing lead system. Measurements were made of the maximal range of the R wave amplitude during sinus rhythm and in response to abrupt changes in heart rate produced by premature atrial and ventricular stimuli. RESULTS: The maximal range in R wave amplitude during sinus rhythm was 1.7 +/- 1.3 mV, or 23.7 +/- 19.2% of the mean R wave amplitude. The R wave amplitude variability increased with abrupt changes in cycle length, with a range of 2.8 +/- 1.5 mV, or 38.8 +/- 18.3% of the mean R wave amplitude (p < 0.05 compared with sinus rhythm). In most patients, R wave amplitude and coupling interval demonstrated an inverse proportional relation. CONCLUSIONS: There is substantial variability in the R wave amplitude during sinus rhythm measured by permanent ventricular sensing lead systems, and this variability is further augmented by abrupt changes in cycle length. This phenomenon may explain the occurrence of undersensing of sinus rhythm in implantable cardioverter-defibrillators with automatic gain sense amplifiers.

Analysis of Variance↗

Unique sensing errors in third-generation implantable cardioverter-defibrillators.

OBJECTIVES: Third-generation cardioverter-defibrillators appear to be susceptible to unique sensing errors. This study was performed to determine the incidence and types of sensing errors in combination therapy implantable devices. BACKGROUND: One of the advantages offered by third-generation implantable cardioverter-defibrillators is the combination of bradycardia and antitachycardia pacing and cardioversion-defibrillation capabilities in a single device. The potential for unique sensing errors, those caused by the conflicts presented by combining bradycardia and tachycardia sensing and therapy algorithms in the same device, has not been previously addressed. METHODS: To determine the incidence of important sensing errors, 61 patients with a combination therapy device (Cadence [Ventritex] and PCD [Medtronic]) were studied for a 25-month period. In addition to surface electrocardiographic recordings during implantation and routine device testing, real-time and stored electrograms recorded from the rate-sensing leads (Cadence) and real-time marker channel recordings (PCD) were reviewed to diagnose sensing errors that resulted in symptoms, device inefficacy or delivery of inappropriate therapy. After recognition, specific reprogramming steps were performed in an attempt to avoid recurrent sensing errors. RESULTS: A total of 13 sensing errors were diagnosed in 12 patients (19.7%); the incidence was similar in both devices. Five distinct categories of sensing errors were identified. After device reprogramming, only one recurrent error occurred in 98 patient-months of follow-up. CONCLUSIONS: Important sensing errors occur in approximately 20% of patients with third-generation combination therapy cardioverter-defibrillators. Prompt diagnosis of sensing errors can lead to specific reprogramming steps to avoid recurrent errors.

Algorithms↗

Polymorphic ventricular tachycardia induced by programmed stimulation: response to procainamide.

OBJECTIVES: This study was designed to evaluate the effects of procainamide on polymorphic ventricular tachycardia induced by programmed stimulation and to correlate the responses with heart disease, left ventricular endocardial activation abnormalities and the signal-averaged electrocardiogram (ECG). BACKGROUND: Polymorphic ventricular tachycardia is induced frequently during electrophysiologic studies. In many patients this response is an artifact of programmed stimulation; in others, it appears to be clinically relevant. Previous observations have suggested that in some patients type IA antiarrhythmic agents can change the response to programmed stimulation from polymorphic to uniform ventricular tachycardia. METHODS: Programmed right ventricular stimulation was performed in the absence of antiarrhythmic drugs and after procainamide. Signal-averaged ECGs and left ventricular maps were performed during sinus rhythm in the absence of antiarrhythmic drugs. RESULTS: We evaluated 79 consecutive patients undergoing clinical electrophysiologic studies, in whom polymorphic ventricular tachycardia was the only arrhythmia induced in the absence of antiarrhythmic drugs. After procainamide administration, uniform monomorphic ventricular tachycardia was induced in 24 patients (Group 1), inducible polymorphic ventricular tachycardia persisted in 30 patients (Group 2) and no ventricular tachycardia could be induced in the remaining 25 patients (Group 3). Twenty-three (96%) of 24 patients developing uniform ventricular tachycardia after procainamide administration had coronary artery disease compared with 63% of Group 2 and 48% of Group 3 patients (p = 0.003). Left ventricular aneurysms were also found more frequently (46%) in the patients developing uniform ventricular tachycardia after procainamide than in either Group 2 or Group 3 (13% and 0%, respectively, p < 0.008). Abnormalities of the signal-averaged ECG typically seen in patients with spontaneous reentrant sustained ventricular tachycardia were significantly more frequent in patients who developed inducible uniform ventricular tachycardia after procainamide than in those who did not. Similarly, patients developing uniform ventricular tachycardia after procainamide had more extensive abnormalities of left ventricular endocardial activation revealed by catheter maps during sinus rhythm. CONCLUSIONS: The conversion of inducible polymorphic ventricular tachycardia to uniform ventricular tachycardia after procainamide administration occurs almost exclusively in patients with coronary disease, previous myocardial infarction and abnormal left ventricular function. This response may permit activation mapping of tachycardias, allowing the application of surgical or catheter ablation techniques that would otherwise not be possible in such patients.

Cardiac Pacing, Artificial↗

Complications of implantable cardioverter defibrillator therapy: follow-up of 241 patients.

In order to determine the incidence of complications of implantable cardioverter defibrillator (ICD) therapy, 241 patients with a total of 353 ICD implantations were followed for 24 +/- 20 months. Complications were defined as any untoward effects experienced by the patient related to the ICD implantation and function or death within 4 weeks of implant or before hospital discharge. During follow-up, 129 of 241 patients (53%) had a total of 166 complications. An operative procedure was required to correct the complication in 50 of the 241 patients (21%). No patient died intraoperatively, but eight patients died within 4 weeks postoperatively or before hospital discharge. ICD infection required removal of the device in 13 patients (5%). Twenty-six patients (11%) had postoperative respiratory complications. Postoperative bleeding and/or thrombosis occurred in 11 patients (4%). Endocardial lead migration was observed in nine patients (4%) and lead adapter or insulation break occurred in nine patients (4%). Fifty-four patients (22%) experienced ECG-documented discharges for non-VT rhythm. In conclusion, although perioperative mortality in ICD patients is low, the majority of patients have complications during follow-up. Recognition of these complications may allow for advances in ICD technology and management strategies to avoid their occurrence.

Bacterial Infections↗

ICD data storage: value in arrhythmia management.

Sophisticated diagnostic information is provided by the latest generation of implantable defibrillators. The success of therapy and the type of therapy successful in terminating ventricular arrhythmias is provided by interrogating the ICD device. In addition, R to R interval information can be retrieved. In selected devices, either local bipolar electrograms from the rate sensing leads or wide bipolar electrograms from the energy delivering leads provide visual confirmation of the presence of ventricular tachyarrthythmic events leading to therapy. The value and limitations of this sophisticated diagnostic information in providing insight into the electrical events triggering therapy and the events triggering ventricular arrhythmias are discussed.

Arrhythmias, Cardiac↗

Shock occurrence and survival in 241 patients with implantable cardioverter-defibrillator therapy.

BACKGROUND: The purpose of this study was to determine the influence of clinical characteristics on shock occurrence and survival in 241 patients with implantable cardioverter-defibrillator (ICD) therapy. METHODS AND RESULTS: Two hundred forty-one consecutive patients underwent ICD implantation between November 1982 and November 1991 and were subsequently followed for 26 +/- 22 months (intention-to-treat analysis). Actuarial incidence of "appropriate" shocks was 13%, 42%, and 63%, and the incidence of any spontaneous shocks was 15%, 51%, and 76% at 1, 3, and 5 years of follow-up, respectively. Poor left ventricular function (ejection fraction < or = 30%) was associated with an earlier occurrence of both appropriate and any spontaneous ICD shocks (p = 0.001). Appropriate and any spontaneous shocks occurred significantly later in patients who presented with cardiac arrest and in patients in whom only ventricular fibrillation but no uniform ventricular tachycardia was induced during preoperative programmed stimulation. In addition, amiodarone treatment at implant was associated with later occurrence of any spontaneous shocks. Cumulative survival from all-cause mortality including perioperative mortality was 84%, 62%, and 57%, and survival from arrhythmic death was 97%, 89%, and 83% at 1, 3, and 5 years, respectively. Ejection fraction < or = 30% was the best predictor of both total arrhythmic death (p = 0.019) and total mortality (p = 0.003). Antiarrhythmic therapy with class 1 agents at implant was also associated with a higher total mortality during follow-up (p = 0.023) but not with total arrhythmic death. Age, sex, underlying heart disease, clinical presentation, and preoperative response to programmed stimulation did not predict long-term survival. In addition, survival curves were similar for patients with and without spontaneous shocks. CONCLUSIONS: The majority of patients receive shocks during long-term follow-up. The occurrence of appropriate or any spontaneous shocks during follow-up is not associated with increased arrhythmic or total mortality consistent with effective prevention of sudden cardiac death with ICD therapy in this high-risk patient population. Although low ejection fraction is the strongest predictor of both shock occurrence and mortality during follow-up, no easy algorithm can be derived from the analyzed clinical characteristics to predict which patients will benefit most from ICD implantation.

Actuarial Analysis↗

Implantable cardioverter-defibrillator therapy in the absence of significant symptoms. Rhythm diagnosis and management aided by stored electrogram analysis.

BACKGROUND: This report describes the value of stored ventricular electrogram analysis in the diagnosis and management of patients experiencing minimal or no symptoms before implantable cardioverter-defibrillator (ICD) therapy. METHODS AND RESULTS: The study population included 48 patients who received the Cadence Tiered Therapy Defibrillator System, an investigational third-generation ICD with ventricular electrogram storage capabilities. Criteria for arrhythmia diagnosis were based on analysis of the electrogram rate, RR interval variability, and morphology. Twenty-nine of the 48 patients (60%) experienced at least one episode of antitachycardia pacing or shock (one shock or more in 25 of 29 patients) that was preceded by minimal or no symptoms during a mean follow-up of 15.1 +/- 7.8 months. There were 194 tachycardia episodes registered by the device, including 101 for which ventricular electrograms were stored and available for analysis. Of the 101 stored electrograms, 74 were classified as ventricular tachycardia (VT), 24 as non-VT rhythms (atrial fibrillation, 13; supraventricular tachycardia, six; rate-sensing lead disruption, four; T wave oversensing, one), and only three as indeterminate rhythms. Based on the electrogram analysis, changes in tachycardia detection criteria and/or antiarrhythmic drug regimens were implemented and were associated with a reduction in the number of device responses for non-VT rhythms from 24 during the initial study period to three during 11.0 +/- 7.2 months of additional follow-up. CONCLUSIONS: ICD responses in the absence of symptoms are relatively common in third-generation devices with antitachycardia pacing capabilities. Despite potential limitations such as the effect of bundle branch block on the electrogram morphology during supraventricular tachycardia, the availability of electrogram storage capabilities allowed a presumptive diagnosis of the events precipitating asymptomatic device responses. Device reprogramming based on analysis of stored electrograms was associated with a dramatic reduction in the incidence of ICD responses for non-VT rhythms.

Atrial Fibrillation↗

Effect of high-current stimulation in patients with sustained ventricular tachycardia rendered noninducible by antiarrhythmic drugs.

Successful antiarrhythmic drug therapy for sustained ventricular tachycardia (VT) is presumed to be related to effects on myocardium within the re-entrant circuit. To test the hypothesis that prevention of VT induction may be related to effects on myocardium other than that directly involved in the tachycardia circuit, high-current stimulation was used to achieve shorter coupling intervals in 22 patients with sustained uniform VT that was rendered noninducible by antiarrhythmic agents during stimulation at twice threshold. Sustained uniform VT was induced in 10 patients in response to high-current stimulation (group 1), including 4 tachycardias with the same morphology observed in the baseline study. There were no inducible arrhythmias in 12 patients (group 2). Patients were receiving several different antiarrhythmic regimens, but there was no particular drug associated with the induction of VT using high-current stimulation. There was no statistically significant difference between groups 1 and 2 in baseline VT cycle length (247 +/- 41 vs 253 +/- 44 ms), drug-induced increase in effective refractory period (20 +/- 15 vs 16 +/- 7%), QRS duration (25 +/- 10 vs 20 +/- 17%) or maximal current strength delivered (10.9 +/- 5.3 vs 9.3 +/- 4.0 mA). There was no significant difference in local activation with high-current stimulation between groups 1 and 2. In conclusion, sustained uniform VT was induced in 45% (10 of 22) of patients whose arrhythmias were rendered noninducible by antiarrhythmic agents during programmed stimulation at twice threshold.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

Redefining the role of digoxin in the treatment of atrial fibrillation.

Atrial fibrillation (AF) encompasses a variety of discrete clinical syndromes, including paroxysmal, chronic, acute, and postoperative. Digoxin, long considered the mainstay of therapy for rate control in all types of AF, appears to have only modest electrophysiologic effects, which are mediated primarily by the autonomic nervous system. Digoxin has less potency than the calcium antagonists or beta-blocking drugs with respect to atrioventricular nodal blockade. Although less potent than calcium antagonists or beta-blocking drugs on the atrioventricular node, digoxin provides positive inotropic support, whereas the other 2 agents can suppress left ventricular function. Thus, digoxin is the agent of choice in patients with AF in the setting of significant left ventricular dysfunction. However, in the absence of left ventricular dysfunction, digoxin should be considered second-line therapy for the treatment of all AF syndromes.

Acute Disease↗

Dissociation of termination and prevention of inducibility of sustained ventricular tachycardia with infusion of procainamide: evidence for distinct mechanisms.

To determine if termination of hemodynamically tolerated, sustained ventricular tachycardia during intravenous infusion of procainamide predicts the success of procainamide therapy in preventing induction of tachycardia, 15 patients with inducible, sustained ventricular tachycardia in the setting of chronic coronary artery disease were studied. Procainamide was infused at a rate of 50 mg/min during ventricular tachycardia until the arrhythmia terminated spontaneously or a total dose of 15 mg/kg was administered. An infusion (2 to 10 mg/min) was given after the loading dose to maintain constant serum drug concentrations after termination of the tachycardia. The infusion of procainamide was well tolerated and resulted in termination of ventricular tachycardia in 14 (93%) of 15 patients after administration of 100 to 1,080 mg (median dose 600 mg). In all patients, programmed ventricular stimulation was repeated immediately after termination of the arrhythmia until ventricular tachycardia was reinitiated or until the stimulation protocol was completed. Of the 14 patients whose ventricular tachycardia terminated during the infusion of procainamide, 1 patient had no inducible sustained tachycardia with repeated programmed stimulation. In the remaining 13 patients, programmed stimulation resulted in initiation of sustained ventricular tachycardia of the same configuration in 7 patients and of a different configuration in 6. In the former 7 patients, the serum procainamide concentration (7.7 +/- 4 vs. 7.4 +/- 3.3 mg/liter, p = NS) and the observed drug effects on the tachycardia cycle length (449 +/- 78 vs. 450 +/- 81 ms, p = NS) and QRS duration (184 +/- 38 vs. 185 +/- 38 ms, p = NS) were similar at the times of termination and reinitiation of ventricular tachycardia.(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Pacing, Artificial↗

Acute and chronic cycle length dependent increase in ventricular pacing threshold.

Several factors have been shown to influence ventricular pacing threshold in humans, including pacing lead location (endocardial vs epicardial), lead maturation, and antiarrhythmic agents. To determine whether ventricular pacing rate has a significant influence on acute and chronic pacing thresholds, we measured pacing thresholds in 16 patients receiving an implantable antitachycardia pacemaker cardioverter defibrillator (Cadence). Ventricular pacing thresholds were determined using the device programmer at cycle lengths of 600, 400 and 300 msec at the time of implantation; prior to hospital discharge at 3-14 days; and during follow-up outpatient visits at 6-8 weeks, 3 months, and 6 months to 1 year. Eleven patients had an epicardial lead system and five an endocardial lead system. Eleven patients were being treated with antiarrhythmic drug therapy. Device output ranged from 1-10 V and was adjustable in 1-V increments (pulse width was held constant at 1 msec). A cycle length dependent increase in pacing threshold (defined as a > or = 1-V increase in threshold at 400 or 300 msec relative to 600 msec) was observed in 10/16 patients during 12/72 pacing trials at 400 msec, and in 15/16 patients during 31/67 trials at 300 msec. In trials in which an increase in pacing threshold occurred, the magnitude of the increase at 400 msec relative to 600 msec was only 1 V in all 12 trials, but at 300 msec the increase ranged from 4-9 V in 7/31 (23%) trials.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗

Electrocardiographically documented unnecessary, spontaneous shocks in 241 patients with implantable cardioverter defibrillators.

The incidence and cause of electrocardiographically documented spontaneous implantable cardioverter defibrillator (ICD) discharges for a rhythm other than ventricular tachycardia (VT) or fibrillation (VF) (unnecessary shocks) were determined in 241 patients who underwent ICD implantation between March 1983 and November 1991. During follow-up of 24 +/- 20 months, 54 of 241 patients (22%) received a total of 132 unnecessary ICD shocks confirmed by Holter or telemetry monitoring or stored electrograms (Egs) from the ICD. The rhythm preceding these unnecessary ICD shocks was atrial fibrillation in 30 patients, sinus or supraventricular tachycardia (SVT) in 11 patients, antitachycardia pacing triggered by atrial fibrillation or SVT resulting in VT in 5 patients, nonsustained VT in 3 patients, and normal sinus or pacemaker rhythm in 10 patients. Unnecessary ICD discharges occurred most frequently during the first week after implantation or generator replacement (18 of 54 patients [33%]). Unnecessary ICD discharges could be documented more often by stored Egs in patients with devices with Eg storage capability (Ventritex Cadence, 19 of 54 patients [35%]) than by Holter or telemetry monitoring in patients with devices without Egs storage capabilities (34 of 193 patients [18%], P < 0.01), despite a shorter mean follow-up duration of 14 +/- 9 months versus 26 +/- 21 months, respectively. Only six of 54 patients (11%) in whom unnecessary ICD discharges occurred had recurrent unnecessary shocks during 22 +/- 20 months of follow-up after treatment directed at the cause of the first episode or device reprogramming to preclude non-VT rhythm detection.(ABSTRACT TRUNCATED AT 250 WORDS)

Atrial Fibrillation↗