Anwer Dhala

Selective transcatheter ablation of the fast and slow pathways using radiofrequency energy in patients with atrioventricular nodal reentrant tachycardia.

Background The safety and efficacy of selective fast versus slow pathway ablation using radiofrequency energy and a transcatheter technique in patients with atrioventricular nodal reentrant tachycardia (AVNRT) were evaluated. Methods and Results Forty-nine consecutive patients with symptomatic AVNRT were included. There were 37 women and 12 men (mean age, 43±20 years). The first 16 patients underwent a fast pathway ablation with radiofrequency current applied in the anterior/superior aspect of the tricuspid annulus. The remaining 33 patients initially had their slow pathway targeted at the posterior/inferior aspect of the right interatrial septum. The fast pathway was successfully ablated in the initial 16 patients and in three additional patients after an unsuccessful slow pathway ablation. A mean of 10±8 radiofrequency pulses were delivered; the last (successful) pulse was at a power of24±7W for a duration of22±15 seconds. Four of these 19 patients developed complete atrioventricular (AV) block. In the remaining 15 patients, the post-ablation atrio-His intervals prolonged from 89±30 to 138±43 msec (p < 0.001), whereas the shortest 1:1 AV conduction and effective refractory period of the AV node remained unchanged. Ten patients lost their ventriculoatrial (VA) conduction, and the other five had a significant prolongation of the shortest cycle length of 1:1 VA conduction (280±35 versus 468±30 msec, p < 0.0001). Slow pathway ablation was attempted initially in 33 patients and in another two who developed uncommon AVNRT after successful fast pathway ablation. Of these 35 patients, 32 had no AVNRT inducible after 6 4 radiofrequency pulses with the last (successful) pulse given at a power of 36±12 W for a duration of 35±15 seconds. After successful slow pathway ablation, the shortest cycle length of 1:1 AV conduction prolonged from 295±44 to 332±66 msec (p < 0.0005), the AV nodal effective refractory penrod increased from 232±36 to 281±61 msec (p < 0.0001), and the atrio-His interval as well as the shortest cycle length of 1:1 VA conduction remained unchanged. No patients developed AV block. Among the last 33 patients who underwent a slow pathway ablation as the initial attempt and a fast pathway ablation only when the former failed, 32 (97%) had successful AVNRT abolition with intact AV conduction. During a mean follow-up of 6.5±3.0 months, none of the 49 patients had recurrent tachycardia. Forty patients had repeat electrophysiological studies 4–8 weeks after their successful ablation, and AVNRT could not be induced in 39 patients Conclusions These data suggest that both fast and slow pathways can be selectively ablated for control of AVNRT. Slow pathway ablation, however, by obviating the risk of AV block, appears to be safer and should be considered as the first approach.

Comparison of cardiac pacing with drug therapy in the treatment of neurocardiogenic (vasovagal) syncope with bradycardia or asystole

BACKGROUND The efficacy of permanent cardiac pacing in patients with neurocardiogenic (or vasovagal) syncope associated with bradycardia or asystole is not clear. We compared the efficacy of cardiac pacing with that of oral drug therapy in the prevention of hypotension and syncope during head-up tilt testing. METHODS Among 70 patients with a history of syncope in whom hypotension and syncope could be provoked during head-up tilt testing, 22 had bradycardia (a heart rate < 60 beats per minute, with a decline in the rate by at least 20 beats per minute) or asystole along with hypotension during testing. There were 9 men and 13 women, with a mean (+/- SD) age of 41 +/- 17 years. Head-up tilt testing was repeated during atrioventricular sequential pacing (in 20 patients with sinus rhythm) or ventricular pacing (in 2 patients with atrial fibrillation). Regardless of the results obtained during artificial pacing, all the patients subsequently had upright-tilt testing repeated during therapy with oral metoprolol, theophylline, or disopyramide. RESULTS During the initial tilt test, 6 patients had asystole and 16 had bradycardia along with hypotension. Despite artificial pacing, the mean arterial pressure during head-up tilt testing still fell significantly, from 97 +/- 19 to 57 +/- 19 mm Hg (P < 0.001); 5 patients had syncope, and 15 had presyncope. By contrast, 19 patients who later received only medical therapy (metoprolol in 10, theophylline in 3, and disopyramide in 6), 2 patients who received both metoprolol and atrioventricular sequential pacing, and 1 patient who received only atrioventricular sequential pacing had negative head-up tilt tests. After a median follow-up of 16 months, 18 of the 19 patients who were treated with drugs alone (94 percent) remained free of recurrent syncope or presyncope, whereas the patient treated only with permanent dual-chamber pacemaker had recurrent syncope. CONCLUSIONS In patients with neurocardiogenic syncope associated with bradycardia or asystole, drug therapy is often effective in preventing syncope, whereas artificial pacing is not.

Bundle branch reentrant ventricular tachycardia: cumulative experience in 48 patients.

Sustained Bundle Branch Reentrant Tachycardia. introduction: The clinical, electrophysiologic features and follow‐up of 48 patients with inducible bundle branch reentrant (BBR) tachycardia are presented.

Atrioventricular nodal reentry. Clinical, electrophysiological, and therapeutic considerations.

BackgroundAtrioventricular (AV) nodal reentry is a relatively common cause of regular, narrow QRS tachycardia. The underlying basis for this arrhythmia is functional (and anatomic) duality of pathways in the region of the AV node, although the exact boundaries of the reentrant circuit have not been convincingly defined. During the more common type of AV nodal reentry (seen in approximately 90% of cases), a slow conducting pathway is used in the anterograde direction, and a fast pathway is operative in the retrograde direction. In the uncommon form, the direction of impulse propagation within the reentrant circuit is reversed. In this article, the clinical, ECG, and electrophysiological features of AV nodal reentry as well as approaches to therapy are discussed. Methods and ResultsClinical diagnosis may be made from the surface ECG. In the common type ofAV nodal reentry, the P wave is obscured by the QRS or may be present in its terminal portion. The P wave in the uncommon form occurs late (i.e., in or after the T wave), producing a pattern of long RP and short PR. Both forms of AV nodal reentry are controllable with various therapeutic modalities. For acute termination, adenosine is probably the ideal agent. Prevention of recurrences can be achieved with several pharmacological agents, including 1-blockers, calcium channel blockers, and class Ia, Ic, and III antiarrhythmic agents. Curative therapy is now available with a variety of nonpharmacological methods. However, the most promising therapy at the present time is catheter modification of the AV node by ablation of either the fast or slow pathway, using radiofrequency energy. Ablation of the fast pathway carries a higher risk of second- or third-degree AV block. Slow pathway ablation, by providing a high rate of success and minimal risk of AV block, seems to be a more acceptable initial approach. ConclusionsAV nodal reentry is a common cause of paroxysmal supraventricular tachycardia, and a precise diagnosis can be made with intracardiac electrophysiological evaluation. Although the arrhythmia responds to a variety of antiarrhythmic agents, curative therapy can now be offered with catheter modification of the AV node using radiofrequency energy. At the time of this writing, it seems that catheter modification of the AV node is rapidly becoming the therapy of initial choice in patients with symptomatic AV nodal reentrant tachycardia requiring treatment.

Provocation of Hypotension During Head-Up Tilt Testing in Subjects With No History of Syncope or Presyncope

BACKGROUND Head-up tilt test is increasingly being used to evaluate patients with syncope. This study was designed to evaluate the specificity of head-up tilt testing using different tilt angles and isoproterenol infusion doses in normal volunteers with no prior history of syncope or presyncope. METHODS AND RESULTS One hundred fifty volunteers were randomized to two groups of 75 each. In group 1, subjects were further randomized to have head-up tilt testing at a 60, 70, or 80 degree angle at baseline followed by repeat tilt testing during a low-dose isoproterenol infusion that increased the heart rate by an average of 20%. In group 2, after having a baseline head-up tilt test at a 70 degree angle for a maximum of 20 minutes, subjects were randomized to have a repeat tilt table testing at a 70 degree angle during a low-dose, 3 micrograms/min, or 5 micrograms/min isoproterenol infusion. In group 1, syncope or presyncope along with hypotension developed in 2 subjects during the baseline test at 60 and 70 degrees of tilt and in 5 subjects during tilting at 80 degrees. The addition of low-dose isoproterenol reduced the specificity minimally from 92% to 88% at both 60 and 70 degrees of tilt but substantially to 60% at an 80 degrees angle. However, 6 of the 10 subjects with a positive test at an 80 degree angle had an abnormal response after 10 minutes of tilt testing. In group 2, using various isoproterenol doses with tilt table testing at a 70 degree angle, low-dose (mean infusion dose, 1.5 +/- 0.45 microgram/min), 3 micrograms/min, and 5 micrograms/min isoproterenol infusions elicited an abnormal response in 1 (4%), 5 (20%), and 14 (56%) of the subjects, respectively. Using multiple logistic regression analysis, head-up tilt testing at an 80 degree angle (P = .01) or during 3 micrograms/min (P = .02) and 5 micrograms/min isoproterenol infusion rates (P < .001) was the most significant predictor of an abnormal response. CONCLUSIONS Head-up tilt testing at a 60 or 70 degree angle with or without low-dose isoproterenol infusion provides an adequate specificity. Caution is needed, however, in interpreting the results if the head-up tilt test at 80 degrees is extended beyond 10 minutes or if high doses of isoproterenol are used.

Circulatory and catecholamine changes during head-up tilt testing in neurocardiogenic (vasovagal) syncope.

Changes in heart rate, arterial pressure, norepinephrine and epinephrine levels were compared in 19 consecutive patients (10 men and 9 women, mean age 46 +/- 16 years) with neurocardiogenic syncope and 11 age- and sex-matched control subjects (5 men and 6 women, mean age 49 +/- 15 years) during head-up tilt testing. Norepinephrine and epinephrine levels were measured at the baseline supine position, in the initial upright position, every 90 seconds during the 70 degrees upright tilt, at the time of termination due to hypotension and syncope (or at 15 minutes in control subjects), and at 40 seconds and 1 minute and 40 seconds in the supine position after terminating the head-up tilt test. Baseline norepinephrine, epinephrine and heart rate were slightly higher in patients. Despite a significant decrease in mean arterial pressure during head-up tilt testing in patients (51 +/- 20 mm Hg; p < 0.001), norepinephrine levels in patients and control subjects at the time of terminating the head-up tilt test were comparable (459 +/- 204 vs 473 +/- 172 pg/ml). A fivefold increase in epinephrine levels (73 +/- 53 to 345 +/- 260 pg/ml; p < 0.01) were seen in patients, whereas control subjects had insignificant change (38 +/- 16 to 65 +/- 44 pg/ml). It is concluded that diminished neuronal sympathetic activity and enhanced adrenomedullary activity is demonstrated during head-up tilt testing in patients with neurocardiogenic syncope.

Computed Tomography‐Fluoroscopy Image Integration‐Guided Catheter Ablation of Atrial Fibrillation

Introduction: This study examines the feasibility of atrial fibrillation (AF) ablation using registered three‐dimensional computed tomography (CT) images of the left atrium with fluoroscopy.

Physics and engineering of transcatheter cardiac tissue ablation

Ablation of arrhythmogenic cardiac tissues has emerged as one of the most important advances in cardiac electrophysiology. With the introduction of transcatheter ablation, the treatment of ventricular tachycardia, Wolff-Parkinson-White syndrome and other cardiac arrhythmias has progressed from an expensive and painful surgical therapy accompanied by a long recovery period to the less expensive, less traumatic transcatheter approach. The feasibility of cardiac ablation, along with the increasing number of physicians using the technique, requires understanding of the anatomic and electrophysiologic bases of transcatheter ablation as well as the different technologies, their limitations and complications. This report provides an overview of the physical, scientific and technical aspects of cardiac ablation performed with the methods currently available and a summary of the limitations of each method and expected future technologic developments in this growing field. Emphasis is placed on radiofrequency and direct current energies, the primary methods now used. Methods such as cryoablation and laser, and microwave and chemical ablation are discussed with less detail because the method of delivering energy for these ablative procedures has not been fully developed.

Bundle branch reentry : a mechanism of ventricular tachycardia in the absence of myocardial or valvular dysfunction

OBJECTIVES The aim of this study was to present bundle branch reentry as the mechanism of sustained ventricular tachycardia in the absence of myocardial or valvular dysfunction. BACKGROUND Previous reports have documented the relation between structural heart disease and bundle branch reentrant ventricular tachycardia. Myocardial or valvular dysfunction has thus far been recognized as the only anatomic substrate for the development of this tachycardia. METHODS Three patients with a wide QRS complex tachycardia underwent noninvasive and invasive cardiac evaluation and electrophysiologic studies to identify the substrate and mechanism of tachycardia. Catheter ablation of the right bundle branch using radiofrequency current was performed in each patient. RESULTS The patients were all men (aged 54, 34 and 72 years) who presented with presyncope, palpitation and cardiac arrest, respectively. Electrocardiography during sinus rhythm revealed nonspecific intraventricular conduction delay in all three patients. Cardiac evaluation revealed no evidence of myocardial or valvular dysfunction in any patient. The baseline HV interval was prolonged in each patient (90, 100 and 75 ms, respectively). Programmed right ventricular stimulation initiated bundle branch reentrant tachycardia with typical left (three patients) and right (one patient) bundle branch block pattern. Catheter ablation of the right bundle branch using radiofrequency current abolished bundle branch reentry in all three patients. After 26-, 13- and 8-month follow-up periods, complete right bundle branch block persisted, and all three patients remained asymptomatic without antiarrhythmic drugs. CONCLUSIONS Sustained bundle branch reentry can be a clinical arrhythmia in patients with no identifiable myocardial or valvular dysfunction except for isolated conduction abnormalities in the His-Purkinje system. This mechanism of tachycardia should be recognized during electrophysiologic evaluation, given the seriousness of this arrhythmia and the availability of the effective treatment.

Ventricular Tachycardia in Valvular Heart Disease Facilitation of Sustained Bundle-Branch Reentry by Valve Surgery

BACKGROUND The clinical characteristics of sustained monomorphic ventricular tachycardia (SMVT), when it develops after valve surgery, have not been described. METHODS AND RESULTS Between 1985 and 1996, 31 patients (30 men and 1 woman) who had undergone valve surgery were found to have inducible SMVT. Nine patients (29%) had sustained VT due to bundle-branch reentry (BBR) (group 1). Four of these patients had normal left ventricular function, and VT with a right bundle-branch morphology was inducible in 4 patients. Group 2 included 20 patients with inducible myocardial (ie, non-BBR) VT. Coronary artery disease was present in 15 group 2 patients (75%) due to atherosclerotic (n=12) and nonatherosclerotic (n=3) causes. Two patients had both inducible sustained BBR and myocardial VT (group 3). Sustained BBR VT occurred significantly earlier after valve surgery (median, 10 days) than the onset of postoperative myocardial VT (median, 72 months; P<.005). CONCLUSIONS Myocardial VT was the most common type of inducible SMVT in patients with valvular heart disease. The majority of these patients had underlying coronary artery disease and significant left ventricular dysfunction. However, in almost one third of the patients, sustained BBR VT was the only type of inducible SMVT. This type of VT was facilitated by the valve procedure occurring within 4 weeks after surgery in most patients. In these patients, left ventricular function was relatively well preserved, and the right bundle-branch block type of BBR was frequently induced. Because a curative therapy can be offered to these patients (ie, bundle-branch ablation), BBR should be seriously considered as the mechanism of VT in patients with valvular heart disease, particularly if the arrhythmia occurs soon after valve surgery.