Aharon Glick

Efficacy of Quinidine in High-Risk Patients With Brugada Syndrome

Background—Automatic implantable cardioverter-defibrillator therapy is considered the only effective treatment for high-risk patients with Brugada syndrome. Quinidine depresses Ito current, which may play an important role in the arrhythmogenesis of this disease. Methods and Results—The effects of quinidine bisulfate (mean dose, 1483±240 mg) on the prevention of inducible and spontaneous ventricular fibrillation (VF) were prospectively evaluated in 25 patients (24 men, 1 woman; age, 19 to 80 years) with Brugada syndrome. There were 15 symptomatic patients (including 7 cardiac arrest survivors and 7 patients with unexplained syncope) and 10 asymptomatic patients. All 25 patients had inducible VF at baseline electrophysiological study. Quinidine prevented VF induction in 22 of the 25 patients (88%). After a follow-up period of 6 months to 22.2 years, all patients are alive. Nineteen patients were treated with quinidine for 6 to 219 months (mean±SD, 56±67 months). None had an arrhythmic event, although 2 had non–arrhythmia-related syncope. Administration of quinidine was associated with a 36% incidence of side effects that resolved after drug discontinuation. Conclusions—Quinidine effectively prevents VF induction in patients with Brugada syndrome. Our data suggest that quinidine also suppresses spontaneous arrhythmias and could prove to be a safe alternative to automatic implantable cardioverter-defibrillator therapy for a substantial proportion of patients with Brugada syndrome. Randomized studies comparing these two therapies seem warranted.

Excellent Long‐Term Reproducibility of the Electrophysiologic Efficacy of Quinidine in Patients with Idiopathic Ventricular Fibrillation and Brugada Syndrome

Background: Quinidine is very effective in preventing the reinduction of sustained ventricular fibrillation (VF) during electrophysiologic study (EPS) in patients with idiopathic VF and Brugada syndrome. However, there are no data on the long‐term reproducibility of this EP efficacy.

Management of Brugada Syndrome: Thirty-Three-Year Experience Using Electrophysiologically Guided Therapy With Class 1A Antiarrhythmic Drugs.

Background—Information on long-term clinical outcome of patients with Brugada syndrome treated with electrophysiologically guided class 1A antiarrhythmic drugs (AAD) is limited. Methods and Results—An aggressive protocol of programmed ventricular stimulation was performed in 96 patients with Brugada syndrome (88% males; mean age, 39.8±15.9 years). Ten patients were cardiac arrest survivors, 27 had presented with syncope, and 59 were asymptomatic. Ventricular fibrillation was induced in 66 patients, including 100%, 74%, and 61% of patients with cardiac arrest, syncope, and no symptoms, respectively. All but 6 of the 66 patients with inducible ventricular fibrillation underwent electrophysiological testing on quinidine (n=54), disopyramide (n=2), or both (n=4). Fifty-four (90%) patients were electrophysiological responders to >1 AAD with similar efficacy rates (≈90%) in all patients groups. Patients with no inducible ventricular fibrillation at baseline were left on no therapy. After a mean follow-up of 113.3±71.5 months, 92 patients were alive, whereas 4 died from noncardiac causes. No arrhythmic event occurred during class 1A AAD therapy in any of electrophysiological drug responders and in patients with no baseline inducible ventricular fibrillation. Arrhythmic events occurred in only 2 cardiac arrest survivors treated with implantable cardioverter–defibrillator alone but did not recur on quinidine. All cases of recurrent syncope (n=12) were attributed to a vasovagal (n=10) or nonarrhythmic mechanism (n=2). Class 1A AAD therapy resulted in 38% incidence of side effects that resolved after drug discontinuation. Conclusions—Our data suggest that electrophysiologically guided class 1A AAD treatment has a place in our therapeutic armamentarium for all types of patients with Brugada syndrome.

Radiofrequency ablation of paroxysmal atrial fibrillation with the new irrigated multipolar nMARQ ablation catheter: verification of intracardiac signals with a second circular mapping catheter.

BACKGROUNDnDuring radiofrequency (RF) ablation of paroxysmal atrial fibrillation, a circular multielectrode recording lasso catheter is generally positioned within each pulmonary vein (PV) to determine when pulmonary vein potentials (PVPs) are present and when they have been ablated. The new irrigated multipolar nMARQ circular ablation catheter is positioned within the left atrium to create contiguous circular ablation lines around each PV ostium.nnnOBJECTIVEnTo determine whether the recordings obtained from the nMARQ catheter position around the PV ostium accurately reproduce the recordings obtained from a lasso catheter positioned within that vein.nnnMETHODSnIn 10 patients undergoing RF ablation of paroxysmal atrial fibrillation, we placed an nMARQ and a lasso catheter around and within each PV, respectively. Recordings obtained from both catheters at baseline and after RF ablation were compared.nnnRESULTSnAt baseline, recordings of PVPs in both catheters were concordant in 92% of all PVs. However, after RF delivery, the concordance between the nMARQ and lasso recordings was poor. The discordant result most commonly observed was disappearance of PVPs from the nMARQ catheter with persistence of PVPs in the lasso catheter (12 of 39 [30%]). Conversely, the delivery of RF frequently resulted in fragmented electrograms (pseudo-PVPs) on the nMARQ catheter despite evidence of PV isolation by lasso catheter recordings.nnnCONCLUSIONSnThe use of an nMARQ catheter alone, as currently recommended, may lead to underestimation and overestimation of the number of RF applications required to achieve PV isolation.

The adenosine triphosphate test: a bedside diagnostic tool for identifying the mechanism of supraventricular tachycardia in patients with palpitations☆

OBJECTIVESnThis study assesses the value of the ATP test (injection of adenosine triphosphate [ATP] during sinus rhythm) for identifying patients with palpitations of unclear etiology who actually have atrioventricular (AV) nodal re-entry tachycardia (AVNRT) or AV re-entry tachycardia (AVRT).nnnBACKGROUNDnBecause AVNRT and AVRT can be cured with radiofrequency ablation, documentation of spontaneous AVNRT or AVRT usually prompts referral for electrophysiologic (EP) evaluation. However, these paroxysmal arrhythmias may elude clinical diagnosis. We recently showed that administration of ATP during sinus rhythm often reveals dual AV node physiology or a concealed accessory pathway (AP) in patients with documented AVNRT or AVRT. Thus, we postulated that the ATP test could identify patients with palpitations who actually have AVNRT or AVRT and would therefore benefit from EP evaluation.nnnMETHODSnOne hundred forty-six patients (54 with palpitations without documented arrhythmias and 92 with documentation of arrhythmias of unclear mechanism) underwent a noninvasive ATP test. ATP was injected during sinus rhythm using 10 mg increments. The ATP test was considered positive when prospectively defined signs of dual AV node physiology or concealed AP were disclosed in the electrocardiogram. These findings were correlated with the results of EP evaluation.nnnRESULTSnA positive ATP test predicted induction of AVNRT or AVRT with a positive predictive value of 93% (sensitivity 71%) but a negative predictive value of 37% (specificity 76%).nnnCONCLUSIONSnA bedside ATP test identifies patients with palpitations who are likely to have AVNRT or AVRT (and who are therefore likely to benefit from EP evaluation) with a high positive predictive value.

Frequency of Spontaneous and Inducible Atrioventricular Nodal Reentry Tachycardia in Patients with Idiopathic Outflow Tract Ventricular Arrhythmias

Objectives: We sought to assess the frequency of spontaneous or inducible atrioventricular nodal reentry tachycardia (AVNRT) in patients referred for radiofrequency ablation (RFA) of idiopathic outflow tract ventricular arrhythmias.

Atrioventricular block during radiofrequency catheter ablation of atrial flutter: incidence, mechanism, and clinical implications

AIMSnTo evaluate the incidence, mechanism, and clinical implications of atrioventricular (AV) block during catheter radiofrequency (RF) ablation of the cavotricuspid isthmus (CTI). Although RF ablation of atrial flutter is the most frequently performed ablation procedure, data on the incidence and significance of an AV block occurring during the procedure are scarce.nnnMETHODS AND RESULTSnConsecutive patients (n=845, 73.5% male) undergoing CTI ablation (913 procedures) between 1998 and 2010 were studied. Data on the occurrence of complete AV block (lasting≥3 s) during the procedure were prospectively collected. Sixteen (1.9%) patients experienced AV block, 12 during delivery of RF pulses (Group 1) and 4 (Group 2) during manipulation of catheters in the cardiac chambers. The AV block was short lived (<1 min), located in the AV node, and associated with septal isthmus RF lines in 11 Group 1 patients. It was long-lasting and led to pacemaker implantation in one Group 1 patient. Atrioventricular blocks had an infranodal location in four Group 2 patients, all of whom had a pre-existing complete left bundle branch block (LBBB). One Group 2 patient had an AV block during his two ablation procedures. Permanent pacemakers were implanted in five (0.6%) patients (one from Group 1 and four from Group 2).nnnCONCLUSIONSnAtrioventricular blocks requiring pacemaker implantation following administration of RF pulses at the CTI are rare (0.12%). The occurrence rate of AV block related to the procedure and requiring pacemaker implantation is, however, not negligible (0.6%) and mostly affects patients with a pre-existing complete LBBB.

Reentry in a Pulmonary Vein as a Possible Mechanism of Focal Atrial Fibrillation

The case of an 18‐year‐old woman with recurrent idiopathic catecholamine‐sensitive paroxysmal atrial fibrillation is reported. Recordings of multiple initiations of atrial fibrillation at the proximal part of the right superior pulmonary vein suggested local reentry in the vein as the mechanism of atrial fibrillation. A single radiofrequency pulse delivered at this site resulted in definite cure of the arrhythmia. (J Cardiovasc Electrophysiol, Vol. 15, pp. 824‐828, July 2004)

Ventricular Flutter Induced During Electrophysiologic Studies in Patients with Old Myocardial Infarction: Clinical and Electrophysiologic Predictors, and Prognostic Significance

Introduction: Induction of ventricular flutter during electrophysiologic (EP) studies (similar to that of ventricular fibrillation [VF]) often is viewed as a nonspecific response with limited prognostic significance. However, data supporting this dogma originate from patients without previously documented ventricular tachyarrhythmias. We examined the significance of ventricular flutter in patients with and without spontaneous ventricular arrhythmias.

QRS Complexes with a Left Bundle Branch Block Morphology During Adenosine Triphosphate Test: What is the Diagnosis?

An 11-year-old boy was referred for evaluation of recurrent short-lasting episodes of rapid palpitations, suggesting a paroxysmal tachycardia. He had no clinical or echocardiographic evidence of heart disease. The 12-lead ECG showed a short PR interval of 0.11 seconds with normal QRS complexes and no delta waves. Adenosine triphosphate (ATP) test (20 mg injected intravenously as a rapid bolus) was performed in an attempt to noninvasively diagnose the mechanism of palpitations.1 After a transient sinus bradycardia (not shown), sinus rate progressively increased and was associated 12 seconds after ATP injection with PR prolongation and QRS complexes with a left bundle branch block (LBBB) morphology (Fig. 1). Normal PR interval and QRS complexes resumed 8 seconds later, associated with sinus rates faster than those associated with the wide QRS complexes. What is the mechanism of the QRS complexes with an LBBB morphology?