George Neal Kay

Selective radiofrequency ablation of the slow pathway for the treatment of atrioventricular nodal reentrant tachycardia. Evidence for involvement of perinodal myocardium within the reentrant circuit.

BackgroundThe circuit of atrioventricular (AV) nodal reentrant tachycardia may include perinodal atrial myocardium. Furthermore, in patients with dual AV nodal pathways, the atrial insertion of the slow pathway is likely to be located near the ostium of the coronary sinus, caudal to the expected location of the AV node. The present study was designed to evaluate the safety and efficacy of selective catheter ablation of the slow pathway using radiofrequency energy applied along the tricuspid annulus near the coronary sinus ostium as definitive therapy for AV nodal reentrant tachycardia. Methods and ResultsAmong 34 consecutive patients who were prospectively enrolled in the study, the slow pathway was selectively ablated in 30, and the fast pathway was ablated in four. Antegrade conduction over the fast pathway remained intact in all 30 patients after successful selective slow pathway ablation. There was no statistically significant change in the atrio-His interval (68.5±21.8 msec before and 69.6±23.9 msec after ablation) or AV Wenckebach rate (167±27 beats per minute before and 178±50 beats per minute after ablation) after selective ablation of the slow pathway. However, the antegrade effective refractory period of the fast pathway decreased from 348±94 msec before ablation to 309±79 msec after selective slow pathway ablation (p = 0.005). Retrograde conduction remained intact in 26 of 30 patients after selective ablation of the slow pathway. The retrograde refractory period of the ventriculoatrial conduction system was 285±55 msec before and 280±52 msec after slow pathway ablation in patients with intact retrograde conduction (p = NS). There were three complications in two patients, including an episode of pulmonary edema and the development of spontaneous AV Wenckebach block during sleep in one patient after slow pathway ablation and the late development of complete AV block in another patient after fast pathway ablation. Over a mean follow-up period of 322±73 days, AV nodal reentrant tachycardia recurred in three patients, all of whom were successfully treated in a second ablation session. ConclusionsRadiofrequency ablation of the slow AV pathway is highly effective and is associated with low rate of complications.

Effect of Radiofrequency Catheter Ablation on Health-Related Quality of Life and Activities of Daily Living in Patients With Recurrent Arrhythmias

BACKGROUND Although radiofrequency catheter ablation can be used to effectively treat a variety of arrhythmias, the effects of this procedure on health-related quality of life have not been systematically studied. METHODS AND RESULTS The SF-36 (a measure of general health status), the Symptom Checklist-Frequency and Severity Scale (an instrument specific for cardiac arrhythmias), and an Activities of Daily Living questionnaire were used to assess quality of life in 161 patients before radiofrequency catheter ablation. These same instruments were used to measure quality of life 1 and 6 months after ablation with complete data in 159 of the original 161 patients. Before ablation, SF-36 scores of the study population were low compared with the US normative data base reflecting significant impairment in physical functioning and well-being. The lowest scores were reported by patients with atrial fibrillation and atrial flutter. Catheter ablation was associated with significant improvement in quality of life that was sustained over the 6 months after ablation. Improvements were measured in both the generic SF-36 health status questionnaire and the disease-specific Symptom Checklist-Frequency and Severity Scale. Catheter ablation was followed by improved performance of activities of daily living and a marked decrease in the number of visits to physicians and emergency rooms in the 6 months after ablation compared with the 6 months before ablation. CONCLUSIONS Radiofrequency catheter ablation improves the health-related quality of life for patients with a variety of cardiac arrhythmias.

Clinical characteristics and outcome of patients with high defibrillation thresholds. A multicenter study.

BackgroundSuccessful defibrillation by an implantable cardioverter-defibrillator (ICD) depends on its ability to deliver shocks that exceed the defibrillation threshold. This study was designed to identify clinical characteristics that may predict the finding of an elevated defibrillation threshold and to describe the outcome of patients with high defibrillation thresholds Methods and ResultsThe records of 1,946 patients from 12 centers were screened to identify 90 patients (4.6%) with a defibrillation threshold ≥25 J. Excluding three patients who received ICDs that delivered >30 J, there were 81 men and six women with a mean age of 59.5plusmn;10.1 years, a mean left ventricular ejection fraction of 0.32plusmn;0.14, and a 76% prevalence of coronary artery disease. Sixty-one patients (70%) were receiving antiarrhythmic drugs, and 45 (52%) were receiving amiodarone. Seventy-one patients (82%) received an ICD. Death occurred in 27 patients −19 of the 71 (27%) with an ICD (eight arrhythmic), and eight of the 16 (50%) without an ICD (four arrhythmic). Actuarial survival for all patients at 5 years was 67%. Actuarial survival rates at 2 years for patients with and without an ICD were 81% and 36%, respectively (p = 0.0024). Actuarial survival at 5 years for the ICD patients was 73%; no patient without an ICD has lived longer than 32 months. Actuarial survival free of arrhythmic death in the ICD patients at 5 years was 84%. Although the only variable to predict survival was ICD implantation (p = 0.003), it is entirely possible that in this retrospective analysis, clinical selection decisions to implant or to not implant an ICD differentiated patients destined to have better or worse outcomes, respectively. ConclusionsAntiarrhythmic drug use may be causally related to the finding of an elevated defibrillation threshold. When patients with high defibrillation thresholds receive an ICD, arrhythmic death remains an important risk (42% of deaths in these patients were arrhythmia related, with 16% actuarial incidence at 5 years). Vigorous testing to optimize patch location can potentially benefit patients by enhancing the margin of safety for effective defibrillation.

The risk of atrial fibrillation following radiofrequency catheter ablation of atrial flutter

BACKGROUND Although radiofrequency catheter ablation of atrial flutter is associated with a high rate of initial success, several clinical issues regarding this therapy remain to be defined. For example, the risks of recurrent atrial flutter and of developing atrial fibrillation after flutter ablation are unknown. In addition, it is not known whether elimination of atrial flutter will modify the natural history of atrial fibrillation in patients who experience both of these arrhythmias. The purpose of the present study was to determine the actuarial freedom from recurrent or new atrial arrhythmias in patients with atrial flutter undergoing catheter ablation. METHODS AND RESULTS The study population consisted of 59 consecutive patients (mean age, 61.9 +/- 12.6 years) with typical atrial flutter who underwent catheter ablation of the reentrant circuit. Catheter ablation was not advised for patients in whom paroxysmal atrial fibrillation had been a major clinical problem. The inducibility of atrial fibrillation and atrial flutter was assessed after successful atrial flutter ablation with programmed atrial stimulation and rapid atrial pacing to a cycle length of 180 ms or 2:1 atrial capture. Atrial flutter was successfully ablated and rendered noninducible in 53 of 59 patients (90%). Over a mean follow-up period of 13.2 +/- 6.6 months, atrial flutter recurred in 5 patients (9.4%). Atrial fibrillation occurred in 14 of 53 patients after successful ablation (26.4%). Four clinical variables were associated by univariate analysis with the late occurrence of atrial fibrillation: (1) the presence of structural heart disease, (2) a history of atrial fibrillation before ablation of atrial flutter, (3) inducible sustained atrial fibrillation after ablation, and (4) a greater number of failed antiarrhythmic drugs. By multivariate analysis, only the persistent inducibility of sustained atrial fibrillation predicted the later development of atrial fibrillation. CONCLUSIONS Although atrial flutter ablation is highly effective and associated with a low risk of recurrent atrial flutter, atrial fibrillation continues to be a long-term risk for individuals undergoing this procedure. The risk of later atrial fibrillation is especially high for patients in whom sustained atrial fibrillation remains inducible after ablation of atrial flutter.

Ventricular Tachycardia Originating From the Posterior Papillary Muscle in the Left Ventricle A Distinct Clinical Syndrome

Background—Several distinct forms of focal ventricular tachycardia (VT) from the left ventricle (LV) have been described. We report a new syndrome of VT arising from the base of the posterior papillary muscle in the LV. Methods and Results—Among 290 consecutive patients who underwent ablation for VT or symptomatic premature ventricular complexes (PVCs) based on a focal mechanism, 7 patients were found to have an ablation site at the base of the posterior papillary muscle in the LV. All patients had normal LV systolic function and a normal baseline electrocardiogram. The electrocardiogram during VT or PVCs demonstrated a right bundle-branch block and superior-axis QRS morphology in all patients. VT was not inducible by programmed atrial or ventricular stimulation. In 2 patients with sustained VT, overdrive pacing neither terminated VT nor demonstrated any criterion for transient entrainment. Activation mapping localized the earliest site of activation to the base of the posterior papillary muscle in all patients. When Purkinje potentials were recorded at the site of successful ablation, these potentials preceded local ventricular muscle potentials during sinus rhythm. During VT or PVCs, however, the ventricular muscle potential always preceded the Purkinje potentials. After recurrence of VT or PVCs with standard radiofrequency ablation, irrigated ablation was successful in eliminating the arrhythmia in all patients. Over a mean follow-up period of 9 months, all patients have been free of PVCs and VT. Conclusion—We present a distinct syndrome of VT arising from the base of the posterior papillary muscle in the LV by a nonreentrant mechanism. Ablation can be challenging, and irrigated ablation may be necessary for long-term success.

Resetting of ventricular tachycardia by single extrastimuli. Relation to slow conduction within the reentrant circuit.

Although both transient entrainment and resetting with single extrastimuli have been demonstrated during sustained ventricular tachycardia related to previous myocardial infarction, the relation between these phenomena has not been defined. Because transient entrainment is only demonstrated when the mechanism of a tachycardia is reentry with an excitable gap, the resetting response to timed premature extrastimuli was studied in patients with ventricular tachycardia and correlated with the ability to demonstrate transient entrainment. The importance of the location of pacing and recording electrodes relative to regions of slow conduction within the reentry circuit for demonstrating specific characteristics of the resetting response after single extrastimuli was examined in 16 patients with 21 distinct morphologies of ventricular tachycardia related to coronary artery disease. At electrophysiological study, intracardiac electrograms were recorded simultaneously from four sites in the right ventricle and four sites in the left ventricle during ventricular tachycardia. Both resetting and transient entrainment could be demonstrated for 18 of the 21 (86%) ventricular tachycardias. The resetting response at each intracardiac recording site was defined as orthodromic or antidromic, based on the conduction time from the pacing stimulus to the recording site and the morphology of the captured (advanced) electrogram. An orthodromic resetting response was associated with demonstration of transient entrainment at 76 of 82 (93%) recording sites, implying that the pacing site was proximal and the recording site was distal to a region of slow conduction. In contrast, an antidromic resetting response was associated with transient entrainment at only six of 154 (4%) recording sites, suggesting that the pacing site was not separated from the recording site by a region of slow conduction (p = 0.001). The return cycle at the site of pacing exceeded the tachycardia cycle length in all episodes of ventricular tachycardia. At orthodromically activated recording sites, however, resetting was associated with a return cycle less than the tachycardia cycle length. Thus, orthodromic resetting demonstrates that a pause is not an integral part of the resetting response but that premature extrastimuli preexcite the reentrant circuit by entering the excitable gap, conducting through a region of slow conduction, and emerging distally without a change in activation sequence. In all episodes of ventricular tachycardia, the slope of the return cycle at the pacing site was determined by the conduction properties to the orthodromically activated sites, with increasing patterns (n = 6) produced by progressive conduction delay in the reentrant circuit at shorter coupling intervals and flat patterns (n = 3) produced by a constant orthodromic conduction interval.(ABSTRACT TRUNCATED AT 400 WORDS)

Inducibility of sustained ventricular tachycardia in a closed-chest ovine model of myocardial infarction.

The two goals of this study were (1) to develop a closed‐chest animal model of monomorphic ventricular tachycardia; and (2) to investigate the effect of dual site pacing on inducibility of ventricular tachycardia. In the first part of the study, 10 of 14 sheep underwent successful induction of myocardial infarction by temporary balloon occlusion of the left anterior descending coronary artery. After a follow‐up period of 21–43 days, sustained monomorphic ventricular tachycardia could be induced during programmed electrical stimulation using a “clinical” stimulation protocol in 8 of the 10 sheep. The number of ventricular tachycardia episodes per animal varied between 5 and 70. Ventricular fibrillation was never induced during programmed electrical stimulation. Ventricular tachycardia episodes lasted from 30 seconds up to 15 minutes and were terminated by antitachycardia pacing or DC cardioversion. In the second part of the study, the effect of dual site stimulation on ventricular tachycardia inducibility was investigated. High current stimuli from an area within the infarcted zone were given with the S1 programmed stimulation protocol. This dual site stimulation showed no effect on ventricular tachycardia induction during programmed electrical stimulation. This animal model shows a high induction rate of sustained monomorphic ventricular tachycardia in the chronic phase of myocardial infarction. The high incidence of ventricular tachycardia inducibility provides a reliable tool to study new techniques for the prevention of ventricular tachyarrhythmias.

PR/RR interval ratio during rapid atrial pacing: a simple method for confirming the presence of slow AV nodal pathway conduction.

Method for Confirming Slow Pathway Conduction. Introduction: Although the AV conduction curve in patients with AV nodal reentrant tachycardia (AVNRT) is usually discontinuous, many patients with this arrhythmia do not demonstrate criteria for dual AV nodal pathways. During rapid atrial pacing, the PR interval often exceeds the pacing cycle length when there is anterograde conduction over the slow pathway and AVNRT is induced. The purpose of this prospective study was to determine the diagnostic value of the ratio of the PR interval to the RR interval during rapid atrial pacing as an indicator of anterograde slow pathway conduction in patients undergoing electrophysioiogic testing.

Successful catheter ablation of atrial fibrillation in a patient with dextrocardia

A 49-year-old woman with dextrocardia and situs inversus underwent catheter ablation of paroxysmal atrial fibrillation. A contrast injection into the left atrium revealed that the left atrial appendage (LAA) was adjacent to the right-sided (anatomic left) superior pulmonary vein (PV). After successful isolation of that PV, LAA potentials were recorded from several electrode pairs of a circular PV mapping catheter. LAA may cause similar difficulties during PVI of the right-sided superior PV in a dextrocardia patient, as during PVI of the left superior PV in a normal heart.

Focal ventricular arrhythmias originating from the left ventricle adjacent to the membranous septum.

AIMS We report the features of focal ventricular arrhythmias (VAs) arising from the left ventricle (LV) adjacent to the membranous septum. METHODS AND RESULTS We studied eight patients (five men, 65 ± 10 years) with (n = 2) or without structural heart disease (n = 6) who had ventricular tachycardia (n = 4) or premature ventricular contractions (n = 4) originating from the LV septum underneath the aorta. Ventricular arrhythmias exhibited a focal activation pattern, left (n = 4) or right bundle branch block (n = 4), respectively, left superior (n = 4) or inferior axis QRS morphology (n = 4), negative QRS polarity in lead III and early or no precordial transition in all. During all of these VAs, far-field electrograms in the His bundle (HB) region preceded the QRS onset. In all patients, ventricular pre-potentials were recorded during VAs while late potentials were recorded in sinus rhythm at the border of a localized low-voltage area underneath the aorta. Radiofrequency catheter ablation at the presumed sites of origin successfully eliminated VAs in five patients and was abandoned in the remaining three because the HB electrogram was recorded at that site. CONCLUSION Focal VAs may arise from the LV adjacent to the membranous septum as a part of the LV ostium, and broadens the spectrum of LV ostium VAs.