Incidence of Atrial Fibrillation Following Ventricular Defibrillation with Transvenous Lead Systems in Man

Atrial Fibrillation After Ventricular Defibrillation. Introduction: The induction of atrial fibrillation (AF) following implantable defibrillator therapy of ventricular fibrillation carries multiple risks. The frequency of shock-induced AF may be more problematic in patients with transvenous defibrillators because current is often delivered through atrial tissue. Thus, the purpose of this study was to determine the incidence of AF following transvenous ventricular defibrillation. Methods and Results: Atrial electrograms were recorded before and after energy delivery in patients undergoing intraoperative testing of transvenous defibrillation lead systems. A total of 114 tracings were examined from 21 patients following ventricular defibrillation. Transvenous deflbrillation shock strength ranged between 200–800 volts (2–40 joules). Bipolar atrial electrograms were obtained from atrial electrodes with 1-cm interelectrode spacing located on one of the defibrillation catheters. The timing of the ventricular defibrillation shock was expressed as a percentage of the preceding sinus PP interval. Three of the 114 transvenous shocks (2.6%) generated AF. Each episode of AF occurred in a different patient. The shocks responsible for AF occurred at 21%, 43%, and 84% of the preceding sinus PP interval. No relation was found between AF induction and the timing of pulse delivery, pulse strength, or pulse number. Conclusion: We conclude that transvenous ventricular defibrillation infrequently causes AF and that timing shock delivery to the atrial cycle is likely to be of marginal or no benefit in the prevention of shock-induced AF. (J Cardiovasc Electrophysiol, Vol. 3, pp. 411–417, October 1992)     

Selection of Pacing Mode after Interruption of Atrioventricular Conduction for Atrial Fibrillation: Observations from the PA3 Clinical Trial

The optimal pacing mode for patients with paroxysmal atrial fibrillation (AF) following AV junction ablation remains the subject of some debate. Recent clinical trials have not demonstrated a superior advantage of maintenance of sinus rhythm over the rate control approach. However, clinical trials in pacemaker populations have demonstrated that physiologic pacing reduces the probability of paroxysmal and persistent AF compared to ventricular pacing. In the second phase of the PA(3) study, patients were randomized to DDDR versus VDD pacing in a cross over study design. Of the 67 patients randomized, 42% developed permanent AF within one year following ablation. AF frequency and burden increases early following AV junction ablation suggesting that ventricular pacing even in an atrial synchronous mode promotes AF. Given the high probability of permanent AF developing early following ablation, VVIR pacing appears to be the appropriate pacing mode for symptomatic patients undergoing total AV junction ablation.     

Chronic myocardial infarction is a substrate for bradycardia-induced spontaneous tachyarrhythmias and sudden death in conscious animals

INTRODUCTION: Patients with bradycardia can have severe tachyarrhythmias but it is unclear whether bradycardia alone can induce arrhythmias or whether an additional substrate is necessary. While several animal models of ventricular tachycardia (VT) exist, no model has been reported to mimic the clinical condition of spontaneous VT and sudden cardiac death (SCD) in the presence of bradycardia and chronic myocardial infarction (MI) in large animals without manipulation of the autonomic nervous system. We tested the hypothesis that MI and bradycardia cause more spontaneous sustained VT than does bradycardia alone. METHODS AND RESULTS: Sheep (42-56 kg) underwent atrioventricular (AV) node catheter ablation alone (n = 5) or AV node ablation and 150 minutes of angioplasty balloon occlusion of the left anterior descending coronary artery (n = 9). An implantable cardioverter defibrillator delivered rescue shocks and demand pacing at 90 beats per minute for the first week and at 40 beats per minute thereafter. Electrograms were continuously radiotelemetered and recorded for 6 weeks. Acute post-MI VT disappeared by day 4. The sudden bradycardia on day 8 triggered numerous premature ventricular contractions (PVCs) and episodes of sustained VT lasting >30 seconds during the next 5 weeks. There were 43 episodes of sustained VT and no spontaneous ventricular fibrillation (VF) with bradycardia alone. However, in the presence of both MI and bradycardia there were 970 episodes of VT/VF (P < 0.05) and three deaths at days 13, 15, and 34. The average 24-hour count of PVCs was similar at day 7 between the two groups but by days 11 and 40, the PVC counts were 35 times and 4 times greater, respectively, in the presence of bradycardia and chronic MI compared to bradycardia alone. No significant difference in the incidence of PVCs was detected because of large individual variation between the two groups (P = 0.21). A high PVC count did not appear to predict SCD. CONCLUSION: The combination of MI and bradycardia secondary to AV node ablation in sheep produces a higher incidence of VT than bradycardia alone, suggesting that this preparation can serve as a model for the study of VT and sudden cardiac death.     

Ventricular tachycardia in myocardial infarction: Relation to heart rate and premature ventricular contractions

Analysis of monitored electrocardiograms, recorded in 77 patientsduring the first 48 hours following the onset of myocardialinfarction, revealed 492 episodes of ventricular tachycardiawith rates of 90–220 min^–1. Characteristics of theventricular tachycardia episodes were correlated with heartrate and with the rate and complexity of ventricular arrhythmiasin the 10-min period preceding ventricular tachycardia. Ventriculartachycardia with rates of 140–180 min^–1 and witha QS configuration was the most frequent event. The first ectopiccomplex of VT was R-on-Tin only 17.2%. Sinus tachycardia wasassociated with significantly fewer episodes of VT with ratesof 110–140min^–1 than when the sinus rate was normal.However episodes of ventricular tachycardia with rates of 181to 220 beats min^–1 were more frequent during sinus tachycardia.Analysis of the frequency of premature ventricular contractionsin the 10-min period immediately preceding ventricular tachycardiarevealed no premature ventricular contractions in 24.4% of cases.Multiple premature ventricular contractions with a frequencyof >5 min^-1 were observed in 8.4% of cases, multifocal in30.3%, couplets in 24% and early PVCs in 12.2%. In the minutebefore ventricular tachycardia, only 40.2% of cases displayedpremature ventricular contractions. In that minute, complexpremature ventricular contractions were distributed as follows:multifocal in 10%, couplets in 8.7% and early PVCs in 2.6% ofcases. Out of the total of 492 runs of ventricular tachycardia,5 cases (1%) resulted in ventricular fibrillation. The frequencyand complexity of premature ventricular contractions as wellas the characteristics of ventricular tachycardia were foundto be of little predictive value for the immediate developmentof ventricular fibrillation in patients with acute myocardialinfarction.     

What Is the Mechanism of the Atrial Arrhythmia in a Patient After Orthotopic Heart Transplantation?

Atrial arrhythmias are quite common in patients after heart transplantation; they can occur via focal or reentrant mechanisms and are amenable to curative therapy with catheter ablation. Integration of the individual patient's surgical anatomy with the arrhythmia pattern on 12-lead electrocardiogram can help both to narrow the potential arrhythmia diagnoses and to facilitate therapeutic decision making. This case highlights the differential diagnosis and management of such a patient.     

Cardiac arrhythmias in arterial hypertension

Patients with arterial hypertension frequently manifest various cardiac rhythm disturbances, ranging from bradyarrhythmias to supraventricular premature beats, atrial fibrillation, or other supraventricular and ventricular tachyarrhythmias. These cardiac arrhythmias may either cause symptoms or be completely asymptomatic, depending on the underlying cardiac function. Degenerative electrical disease and left ventricular hypertrophy constitute the principal pathophysiological mechanisms. This review summarizes all important existing evidence on cardiac arrhythmia manifestation in the setting of arterial hypertension, and it highlights known underlying pathophysiological mechanisms and therapeutic considerations.     

Intracardiac echocardiography in electrophysiology: a review of current applications in practice

Intracardiac echocardiography (ICE) has emerged as a widespread useful tool in the everyday practice of interventional electrophysiology. Advances in catheter-based ultrasound transducers and imaging technology have made this modality integral to guiding evaluation of anatomy and ablation therapy. Evolution of ablative procedures of the left heart for tachyarrhythmia has highlighted the importance of direct visualization of anatomic landmarks to guide transseptal catheterization and immediately identify complications. The ability to position mapping and ablation catheters according to anatomic landmarks (Fig. 1) has greatly enhanced the safety and efficacy of catheter ablation procedures. ICE has supplanted fluoroscopy as the gold standard for precise imaging of endocardial structures during complex procedures.     

埋藏式心脏复律除颤器与单极导线起搏器的合并应用一例报告

国内首次合并应用埋藏式心脏复律除颤器（ＩＣＤ）与单极起搏器１例。术中仔细观察起搏器对ＩＣＤ的影响，未发现ＩＣＤ对起搏心律的双感知，亦未发现对心室颤动（室颤）的感知不足，ＩＣＤ对３次诱发的室颤均迅速感知并一次除颤成功。术后１８９天储存资料显示患者共自发２１次室性心动过速，均被一次抗心动过速起搏有效终止，未发生误放电，亦未漏诊快速心律失常，初步观察效果满意。     

Sudden Cardiac Death: Future Approaches Based on Identification and Control of Transient Risk Factors

Sudden Cardiac Death . Future progress in the ability to control the problem of sudden cardiac death will require new approaches in applied epidemiology, methods of accurately evaluating therapeutic outcome, and techniques to identify and control those transient risk factors that are responsible for the initiation of fatal arrhythmias. In regard to the latter, transient risk factors are distinguished from classical risk factors in two ways: (1) they are not present continuously over time, thus confounding sampling techniques among a population; and (2) their dynamic nature suggests a proximate role in the initiation of potentially fatal arrhythmias in contrast to the role of classical risk factors in the genesis of the underlying diseases. Transient risk factors derive from the structure/function model of sudden cardiac death, which places structural abnormalities in a conditioning role, establishing the sensitivity to a transient destabilizing influence. In contrast, functional abnormalities are those conditions immediately responsible for destabilizing the system, establishing vulnerability to potentially fatal arrhythmias. They include four categories of risk: (1) transient ischemia and reperfusion; (2) systemic abnormalities, such as hemodynamic dysfunction and fluid and electrolyte imbalance; (3) autonomic fluctuations, both central and cardiac; and (4) cardiac toxic states, including proarrhythmic effects of antiarrhythmic drugs and arrhythmogenic effects of other substances. Sudden cardiac death is a dynamic problem, and its pathogenesis contains dynamic features. The ability to identify transient risk factors and to control them before they exert their influence on a conditioned electrophysiologic system will provide new inroads into the problem of sudden cardiac death.     

Atrial fibrillation in patients with a dual defibrillator: characteristics of spontaneous and induced episodes and effect of ventricular tachyarrhythmia induction

BACKGROUND: The pattern of FF intervals during atrial fibrillation (AF) has been analyzed in induced and spontaneous AF episodes, after the induction of ventricular fibrillation (VF) and after atrial shock, in order to suggest practical considerations for AF management in patients implanted with antitachycardia devices. METHODS: In 13 patients implanted with a dual-chamber defibrillator, FF intervals were analyzed during two separate induced AF episodes, before and after VF induction over AF, as well as during spontaneous AF episodes and after unsuccessful atrial shocks. The following parameters were considered: mean atrial cycle length (CL), atrial CL stability, and standard deviation of the atrial cycle. RESULTS: The AF pattern had comparable characteristics considering two separate inductions of AF, as well as spontaneous AF episodes. Ventricular tachyarrhythmia induction resulted in a shortening of atrial CL (P < 0.02) and in a less organized AF pattern (P < 0.005). Changes in the FF interval after ineffective shock therapy showed a shortening of AF cycles after shocks with energies far below the defibrillation threshold. CONCLUSIONS: (a) The AF pattern is reproducible in separate inductions of sustained AF and in spontaneous episodes, (b) dynamic changes involving a shortening of the AF cycle and an evolution to a less homogeneous pattern occur after VF induction, revealing a complex interplay between AF and VF, and (c) FF interval analysis after ineffective shock delivery may allow the relationship between delivered shock energy and effective defibrillation energy to be estimated, thereby providing practical suggestions for step-up protocols in atrial cardioversion.     

Automatic External Defibrillators for Prevention of Out-of-Hospital Sudden Death:

Approaches to the prevention of sudden cardiac death (SCD) include strategies designed to attack the problem from the multiple perspectives of primary prevention of the underlying diseases, prophylactic treatment of high-risk individuals with identified diseases, and responses to cardiac arrest victims in the community. The latter strategy began with conventional fire department-based emergency rescue systems (emergency medical services [EMS]) that originated in the early 1970s. Although such systems were innovative and impressive at the time, they are limited by less-than-optimal response times that translate to low survival rates. Newer strategies, designed to respond faster, include a variety of methods, including ambulance- and police-based automatic external defibrillators (AEDs), deployment of AEDs in settings in which crowds accumulate and designated rescuers are available, and more general public access sites. The value of conventional EMS systems remains because of their ability to provide advanced life support as part of a dual-response system. These approaches, in conjunction with better primary and secondary prevention strategies, offer the hope of reducing the SCD burden. (J Cardiovasc Electrophysiol, Vol. 14, pp. S108-S116, September 2003, Suppl.)