[Alternative treatment strategies for atrial fibrillation : Benefits from yoga?] / Alternative Behandlungsverfahren bei Vorhofflimmern : Was bringt Yoga?

Atrial fibrillation, the most common sustained cardiac arrhythmia, is associated with significant morbidity, mortality, and healthcare utilization. Since the procedures used to treat atrial fibrillation have a number of limitations and risks, there is a growing interest in alternative treatment strategies for patients with atrial fibrillation. One such option is yoga. To date, only a few studies are available on its effect on atrial fibrillation. However, these suggest that yoga may indeed be able to reduce the frequency of the arrhythmia and its progression. The risk factors for atrial fibrillation and quality of life in affected patients are also positively affected. As adverse effects and complications are extremely rare with competent guidance, yoga may already be recommended now. However, further clinical studies are needed to provide recommendations that meet evidence-based criteria.

Does the extent of left atrial arrhythmogenic substrate depend on the electroanatomical mapping technique: impact of pulmonary vein mapping catheter vs. ablation catheter.

AIMS: In persistent atrial fibrillation (AF), left atrial low-voltage areas and complex fractionated atrial electrograms (CFAEs) have been thoroughly discussed as critical substrate points for AF perpetuation. Thus, in patients undergoing pulmonary vein isolation, these sites are often considered additional ablation targets. Currently, mapping techniques for these substrate indicators are still under discussion. The aim of this study was to evaluate the impact of different mapping catheters on the detection of low-voltage areas and CFAE. METHODS AND RESULTS: Two bipolar voltage maps and two CFAE left atrial maps were obtained each in 30 patients undergoing catheter ablation of AF using the following two different catheters: A four-pole ablation catheter (MAP, mapping and ablation catheter) (electrode size: tip: 4 mm, band: 1 mm; inter-electrode spacing: 0.5-5-2 mm) and a 10-pole circular pulmonary vein mapping catheter (CMC) (electrode size: 1 mm; inter-electrode spacing: 7-7-7 mm). Successively, low-voltage and CFAE area sizes were then compared between the two catheters. Areas with a bipolar voltage of <0.5 mV were significantly smaller when obtained with the CMC compared with the MAP (8.9 ± 8.9 vs. 17.4 ± 11.7 cm², P < 0.001). This was also significantly different for a bipolar voltage of <0.2 mV (2.3 ± 4.6 vs. 6.2 ± 9.6 cm², P < 0.001). Complex fractionated atrial electrogram area sizes were significantly larger when obtained with the CMC compared with the MAP group (14.6 ± 10.9 vs. 19.4 ± 9.4 cm², P = 0.011). CONCLUSION: Low-voltage and CFAE area size varies significantly between different mapping catheters. Mapping electrode settings have to be taken into consideration for the assessment of electroanatomical substrate of AF.

Impact of acute atrial fibrillation termination and prolongation of atrial fibrillation cycle length on the outcome of ablation of persistent atrial fibrillation: A substudy of the STAR AF II trial.

BACKGROUND: Controversy exists about the impact of acute atrial fibrillation (AF) termination and prolongation of atrial fibrillation cycle length (AFCL) during ablation on long-term procedural outcome. OBJECTIVE: The purpose of this study was to analyze the influence of AF termination and AFCL prolongation on freedom from AF in patients from the STAR AF II (Substrate and Trigger Ablation for Reduction of Atrial Fibrillation Trial-Part II) trial. METHODS: Acute changes in AFCL and AF termination were collected during the index procedure of the STAR AF II trial and compared to recurrence of AF at 18 months. Recurrence was assessed by ECG, Holter (3, 6, 9, 12, 18 months), and weekly transtelephonic ECG monitoring for 18 months. RESULTS: AF terminated in 8% of the pulmonary vein isolation (PVI) arm, 45% in the PVI+complex electrogram arm, and 22% of the PVI+linear ablation arm (P <.001), but freedom from AF did not differ among the 3 groups (P = .15). Freedom from AF was significantly higher in patients who presented to the laboratory in sinus rhythm (SR) compared to those without AF termination (63% vs 44%, P = .007). Patients with AF termination had an intermediate outcome (53%) that was not significantly different from those in SR (P = .84) or those who did not terminate (P = .08). AF termination was a univariable predictor of success (P = .007), but by multivariable analysis, presence of early SR was the strongest predictor of success (hazard ratio 0.67, P = .004). Prolongation of AFCL was not predictive of 18-month freedom from AF. CONCLUSION: Acute AF termination and prolongation in AFCL did not consistently predict 18-month freedom from AF. Presence of SR before or early during the ablation was the strongest predictor of better outcome.

The Lewis Lead for Detection of Ventriculoatrial Conduction Type.

BACKGROUND: Identification of a possible ventriculoatrial (VA) dissociation in wide QRS complex tachycardias is one of the most reliable criteria for differentiation of tachycardia origin. The Lewis lead has been proposed for detection of atrial activity during ventricular tachycardias. HYPOTHESIS: A modified Lewis-lead-ECG will be superior to the standard-lead ECG for detection of ventriculoatrial conduction during ventricular tachycardia. METHODS: Forty-seven patients underwent electrophysiological study, stimulated with a fixed cycle length of 400 ms in the ventricle. During stimulation, a standard-lead ECG and a modified Lewis-lead ECG were recorded. Simultaneously, VA conduction was documented by intracardiac electrograms. Surface ECGs were presented to 6 blinded examiners for VA conduction assessment. RESULTS: Type of VA conduction was correctly diagnosed in significantly more ECGs in the Lewis-lead ECG group (mean, 35.0 [75%]) than in the standard-lead ECG group (mean, 29.2 [62%]; P = 0.045). Ventriculoatrial dissociation also was significantly more often correctly diagnosed in the Lewis-lead ECG group (mean, 17.7 [71%]) than in the standard-lead ECG group (mean, 12.7 [49%]; P = 0.014). Interobserver agreement was moderate in both groups (κ = 0.45 and κ = 0.49, respectively). CONCLUSIONS: Compared with standard-lead ECG, modified Lewis-lead ECG is associated with significantly improved detection of VA conduction type during fast ventricular pacing and thus may help improve ECG diagnosis.

Left Atrial Appendage Conduction Jump for Real-Time Evaluation of Conduction Block Over the Anterior Mitral Annulus Line.

INTRODUCTION: Evaluation of conduction over a linear ablation lesion at the anterior mitral annulus can be time-consuming and difficult during ongoing radiofrequency application. The purpose of this study was to validate conduction time from the beginning of the p wave and from the coronary sinus ostium to the left atrial appendage (LAA) as a new method of conduction block surveillance. METHODS: Conduction across the anterior mitral annulus line was evaluated using a total of 55 patients. We verified completeness of conduction block by standard techniques including differential pacing, double potential mapping and activation mapping. Those methods were compared to the new method of observing an abrupt prolongation of conduction time into the LAA as well as a conduction sequence change on a circular multipolar mapping catheter placed inside the LAA during sinus rhythm. RESULTS: Bidirectional conduction block across the ablated line was achieved in 51 (92.7%) of the patients. Prior to ablation, mean conduction time across the line was 59 ± 21 milliseconds. This value increased to 163 ± 43 milliseconds after a successful ablation. An abrupt prolongation of conduction time into the LAA of at least 50 milliseconds was observed in all patients at the moment when a complete conduction block was achieved. Additionally, a change of conduction sequence recorded with the multi-electrode catheter placed in the LAA was observed in all of these patients. CONCLUSIONS: A sudden jump of p wave and coronary sinus ostium to LAA conduction time together with a change of conduction sequence recorded with a multi-electrode catheter placed inside the LAA during sinus rhythm is a simple and reliable approach for beat-to-beat surveillance of conduction block across the anterior mitral annulus during radiofrequency ablation.

Mapping of the left-sided phrenic nerve course in patients undergoing left atrial catheter ablations.

BACKGROUND: Catheter ablation of atrial fibrillation has been associated with left-sided phrenic nerve palsy. Knowledge of the individual left phrenic nerve course therefore is essential to prevent nerve injury. The aim of this study was to test the feasibility of an intraprocedural pace mapping and reconstruction of the left phrenic nerve course and to characterize which anatomical areas are affected. METHODS: In patients undergoing left atrial catheter ablation, a three-dimensional map of the left atrial anatomical structures was created. The left-sided phrenic nerve course was determined by high-output pace mapping and reconstructed in the map. RESULTS: In this study, 40 patients with atrial fibrillation or atrial tachycardias were included. Left phrenic nerve capture was observed in 23 (57.5%) patients. Phrenic nerve was captured in 22 (55%) patients inside the left atrial appendage, in 22 (55%) in distal parts, in 21 (53%) in medial parts, and in two (5%) in ostial parts of the appendage. In three (7.5%) patients, capture was found in the distal coronary sinus and in one (2.5%) patient in the left atrium near the left atrial appendage ostium. Ablation target was changed due to direct spatial relationship to the phrenic nerve in three (7.5%) patients. No phrenic nerve palsy was observed. CONCLUSIONS: Left-sided phrenic nerve capture was found inside and around the left atrial appendage in the majority of patients and additionally in the distal coronary sinus. Phrenic nerve mapping and reconstruction can easily be performed and should be considered prior catheter ablations in potential affected areas.

Effects of deep sedation on cardiac electrophysiology in patients undergoing radiofrequency ablation of supraventricular tachycardia: impact of propofol and ketamine.

AIMS: Propofol is commonly used as an anaesthetic during catheter ablation. Bradycardia and termination of supraventricular tachycardia (SVT) under propofol are reported. Ketamine is used for cardiac catheterization procedures and increases heart rate and blood pressure. Our study aimed to determine the effects of propopfol and ketamine on atrial electrophysiology. METHODS AND RESULTS: Thirty-one patients undergoing electrophysiological study prior to SVT ablation were enrolled. Patients received a combination of propofol/midazolam (n = 10), ketamine/midazolam (n = 9), or midazolam alone (n = 12). Electrophysiological study was performed before and after administration of the anaesthetic agents. Blood pressure, corrected sinus node recovery time, Wenckebach cycle length, and atrial conduction time were measured. We found a significant increase in heart rate, systolic, and diastolic blood pressure and a significant shortening of atrial conduction time after administration of ketamine compared with propofol and the control. Results for ketamine, propofol and the control, respectively: mean (SD) change in heart rate was 12.4 (8.3), -1.4 (8), and 1 (7.5) b.p.m. (P = 0.002); mean (SD) change in systolic blood pressure was 19.2 (8.1), -22 (9), and 0.1 (5.7) mmHg (P < 0.001); mean (SD) change in diastolic blood pressure was 6.6 (9.7), -7.8 (2.9), and 2.3 (4.5) mmHg (P = 0.001); and mean (SD) change in atrial conduction time was -13.7 (16.4), 4.5 (11.1), and -0.3 (3.8) ms (P = 0.008). No significant affection of sinus node or antrioventricular node function was seen. CONCLUSION: Our results show stimulatory effects of ketamine on heart rate, atrial conduction, and blood pressure. Ketamine, therefore, may be beneficial in patients with pre-existing hypotension and bradycardia.

"Largest amplitude ablation" is the optimal approach for typical atrial flutter ablation: a subanalysis from the AURUM 8 study.

INTRODUCTION: The recently proposed "maximum voltage-guided" (MVG) technique for radiofrequency catheter ablation of atrial flutter targets high-voltage electrograms along cavotricuspid isthmus (CTI) to ablate the functionally important anatomic muscle bundles alone, without drawing a complete anatomic line across the CTI. This innovative approach may shorten ablation time and procedure duration. METHODS AND RESULTS: Within the multicenter AURUM 8 study, which compared 8-mm gold- and Pt-Ir-tip catheters in atrial flutter ablation, we made a post hoc comparison of procedural data from 72 patients treated with MVG technique with data from 281 patients undergoing anatomic CTI ablation (unmatched) and with data from 72 patients selected from among those 281 patients such that they were matched with the MVG group with respect to selected baseline parameters and catheter type (matched). The MVG technique markedly reduced (P < 0.001) ablation time (mean 6.9 minutes vs 10.9/9.7 minutes [unmatched/matched]), number of lesions (8.3 vs 13.7/12.9), fluoroscopy time (9.5 minutes vs 20.6/17.9 minutes), procedure duration (59 minutes vs 93/86 minutes), and energy delivered (19 kJ vs 34/30 kJ) compared with anatomic CTI ablation. The incidence of charring was higher for MVG than for anatomic ablation technique (31.9% vs 18.5/15.3%, P < 0.05), where Pt-Ir tip catheters were 6-fold more susceptible to charring than gold-tip catheters (P < 0.001), likely because of a lower thermal conductivity of the Pt-Ir material. The acute success rate was slightly better for MVG than for anatomic ablation technique (97.2% vs 92.2/91.7%, P = n.s.). CONCLUSION: Major procedural parameters are remarkably improved with MVG technique. Gold-tip catheters are substantially less susceptible to charring and may therefore be preferred over Pt-Ir-tip catheters for MVG ablation technique.

Proarrhythmia as a class effect of quinolones: increased dispersion of repolarization and triangulation of action potential predict torsades de pointes.

BACKGROUND: Numerous noncardiovascular drugs prolong repolarization and thereby increase the risk for patients to develop life-threatening tachyarrhythmias of the torsade de pointes (TdP) type. The development of TdP is an individual, patient-specific response to a repolarization-prolonging drug, depending on the repolarization reserve. The aim of the present study was to analyze the underlying mechanisms that discriminate hearts that will develop TdP from hearts that will not develop TdP. We therefore investigated the group of quinolone antibiotics that reduce repolarization reserve via I(Kr) blockade in an intact heart model of proarrhythmia. METHODS AND RESULTS: In 47 Langendorff-perfused, AV-blocked rabbit hearts, ciprofloxacin (n = 10), ofloxacin (n = 14), levofloxacin (n = 10), and moxifloxacin (n = 13) in concentrations from 100 microM to 1,000 microM were infused. Eight monophasic action potentials (MAPs) and an ECG were recorded simultaneously. After incremental pacing at cycle lengths from 900 ms to 300 ms to compare the action potential duration, potassium concentration was lowered to provoke TdP. All antibiotics led to a significant increase in QT interval and MAP duration, and exhibited reverse-use dependence. Eight simultaneously recorded MAPs demonstrated an increase in dispersion of repolarization in the presence of all antibiotics. MAP triangulation (ratio: MAP(90/50)) and fluctuation of consecutive action potentials were increased for all tested drugs at high concentrations. In the presence of low potassium concentration, all quinolones led to TdP: ciprofloxacin, 4 out of 10 (40%); ofloxacin, 3 out of 14 (21%); moxifloxacin, 9 out of 13 (69%); and levofloxacin, 2 out of 10 (20%). Hearts that developed TdP demonstrated a significant greater influence on dispersion of repolarization and on triangulation as compared with hearts without TdP. CONCLUSION: Quinolone antibiotics may be proarrhythmic due to a significant effect on myocardial repolarization. The individual response of a heart to develop TdP in this experimental model is characterized by a greater effect on dispersion of repolarization and on triangulation of action potential as compared with hearts that do not develop TdP.

Phytanic acid accumulation is associated with conduction delay and sudden cardiac death in sterol carrier protein-2/sterol carrier protein-x deficient mice.

INTRODUCTION: The sterol carrier protein-2 gene encodes two functionally distinct proteins: sterol carrier protein-2 (SCP2, a peroxisomal lipid carrier) and sterol carrier protein-x (SCPx, a peroxisomal thiolase known as peroxisomal thiolase-2), which is involved in peroxisomal metabolism of bile acids and branched-chain fatty acids. We show in this study that mice deficient in SCP2 and SCPx (SCP2null) develop a cardiac phenotype leading to a high sudden cardiac death rate if mice are maintained on diets enriched for phytol (a metabolic precursor of branched-chain fatty acids). METHODS AND RESULTS: In 210 surface and 305 telemetric ECGs recorded in wild-type (C57BL/6; wt; n = 40) and SCP2 null mice (n = 40), no difference was observed at baseline. However, on diet, cycle lengths were prolonged in SCP2 null mice (262.9 +/- 190 vs 146.3 +/- 43 msec), AV conduction was prolonged (58.3 +/- 17 vs 42.6 +/- 4 ms), and QRS complexes were wider (19.1 +/- 5 vs 14.0 +/- 4 ms). In 11 gene-targeted Langendorff-perfused hearts isolated from SCP2 null mice after dietary challenge, complete AV blocks (n = 5/11) or impaired AV conduction (Wenckebach point 132 +/- 27 vs 92 +/- 10 msec; P < 0.05) could be confirmed. Monophasic action potentials were not different between the two genotypes. Left ventricular function studied by echocardiography was similar in both strains. Phytanic acid but not pristanic acid accumulated in the phospholipid fraction of myocardial membranes isolated from SCP2 null mice. CONCLUSION: Accumulation of phytanic acid in myocardial phospholipid membranes is associated with bradycardia and impaired AV nodal and intraventricular impulse conduction, which could provide an explanation for sudden cardiac death in this model.

Comparison of the in vitro electrophysiologic and proarrhythmic effects of amiodarone and sotalol in a rabbit model of acute atrioventricular block.

The mechanisms for the different proarrhythmic potential of antiarrhythmic drugs in the presence of comparable QT prolongation are not completely understood. The reasons for the lower proarrhythmic potential of amiodarone as compared with other class-III antiarrhythmic drugs such as sotalol, a fact that has been well established for years, is insufficiently known. Therefore, the aim of our study was to assess the different electrophysiologic effects of amiodarone and sotalol in a previously developed experimental model of proarrhythmia. In eight male rabbits, amiodarone (280-340 mg/d) was fed over a period of six weeks. Hearts were excised and retrogradely perfused. Up to eight simultaneous epi- and endocardial monophasic action potentials (MAP) were recorded. Results were compared with sotalol-treated (10-50-100 microM) hearts (n = 13). Amiodarone and sotalol (50 microM and 100 microM) led to a significant increase in QT interval (mean increase: amiodarone: 31 +/- 6 ms; sotalol: 41 +/- 4 ms and 61 +/- 9 ms) and MAP-duration (mean increase-MAP90: amiodarone: 20 +/- 5 ms; sotalol: 17 +/- 5 ms and 25 +/- 8 ms) (P < 0.01). In bradycardic (AV-blocked) hearts, MAP-recordings demonstrated reverse-use dependence and a significant increase in dispersion of repolarization (MAP90) in the presence of sotalol (P < 0.01), but not in amiodarone-treated hearts (10%; p = ns). Sotalol led to early afterdepolarizations (EAD) and torsade de pointes (TdP) after lowering of potassium concentration (6 of 13 hearts). In amiodarone-treated, hypokalemic hearts, no EAD or TdP occurred. Sotalol changed the MAP configuration to a triangular pattern (ratio-MAP90/50: 1.52 as compared with 1.36 at baseline) whereas amiodarone caused a rectangular pattern of MAP prolongation (ratio-MAP90/50: 1.36). In conclusion, these results show no direct correlation between the occurrence of TdP and the degree of QT prolongation. Several factors including reverse-use dependence, dispersion of repolarization, and the propensity to induce early afterdepolarizations but also differences in the action potential configuration may help to understand proarrhythmic side effects of drugs.

Endocardial mapping of right ventricular outflow tract tachycardia using noncontact activation mapping.

INTRODUCTION: Activation mapping and pace mapping identify successful ablation sites for catheter ablation of right ventricular outflow tract (RVOT) tachycardia. These methods are limited in patients with nonsustained tachycardia or isolated ventricular ectopic beats. We investigated the feasibility of using noncontact mapping to guide the ablation of RVOT arrhythmias. METHODS AND RESULTS: Nine patients with RVOT tachycardia and three patients with ectopic beats were studied using noncontact mapping. A multielectrode array catheter was introduced into the RVOT and tachycardia was analyzed using a virtual geometry. The earliest endocardial activation estimated by virtual electrograms was displayed on an isopotential color map and measured 33 +/- 13 msec before onset of QRS. Virtual unipolar electrograms at this site demonstrated QS morphology. Guided by a locator signal, ablation was performed with a mean of 6.9 +/- 2.2 radiofrequency deliveries. Acute success was achieved in all patients. During follow-up, one patient had a recurrence of RVOT tachycardia. Compared with patients (n = 21) who underwent catheter ablation using a conventional approach, a higher success rate was achieved by noncontact mapping. Procedure time was significantly longer in the noncontact mapping group. Fluoroscopy time was not significantly different in the two groups. CONCLUSION: Noncontact mapping can be used as a reliable tool to identify the site of earliest endocardial activation and to guide the ablation procedure in patients with RVOT tachycardia and in patients with ectopic beats originating from the RVOT.

Prolonged action potential durations, increased dispersion of repolarization, and polymorphic ventricular tachycardia in a mouse model of proarrhythmia.

INTRODUCTION: In the congenital long QT syndrome, inhomogeneously prolonged action potentials, bradycardia, and hypokalemia can cause afterdepolarizations and torsade de pointes. Other genetic factors may contribute to similar forms of ventricular tachycardias in hypertrophied or failing hearts, especially if the outward current I(Kr) is blocked pharmacologically. We sought to develop a mouse heart model for such arrhythmias in order to identify the proarrhythmic potential in transgenic animals. METHODS AND RESULTS: Hearts of adult wild-type (CD1) mice were isolated and the aorta was retrogradely perfused. Three monophasic action potentials and a volume-conducted ECG were simultaneously recorded. Sotalol (10(-5)M and 2 x 10(-5)M) prolonged action potential duration (APD) in a concentration-dependent and reverse frequency-dependent fashion (from 34 +/- 1 to 48 +/- 2 ms at 100 ms basic cycle length (BCL), from 38 +/- 2 to 54 +/- 3 ms at 180 ms BCL for APD90, p < 0.05). Sotalol did not alter the relation between refractoriness and APD (ERP/APD ratio = 0.76 - 0.93). AV nodal block caused ventricular bradycardia and doubled dispersion of APD (APD70max-min: 11 +/- 1 vs. 4 +/- 1 ms, APD90max-min: 12 +/- 1 vs. 5 +/- 1 ms, p < 0.05). If combined with hypokalemia, afterdepolarizations induced polymorphic ventricular tachycardias in 1 of 8 hearts at K(+) =3.0 mM and in 10 of 12 hearts at K(+) = 2.0 mM. Prior to polymorphic ventricular tachycardia, dispersion of APD further increased (APD70max-min: 17 +/- 3 ms; APD90max-min: 25 +/- 3 ms; p < 0.05). CONCLUSIONS: This isolated beating mouse heart model can be used to study drug-induced action potential prolongation and repolarization-related ventricular arrhythmias provoked by bradycardia and hypokalemia. It may be suitable to identify a genetic predisposition to ventricular arrhythmias that may only become apparent under such proarrhythmic conditions.

Body surface area of ST elevation and the presence of late potentials correlate to the inducibility of ventricular tachyarrhythmias in Brugada syndrome.

INTRODUCTION: The value of noninvasive markers reflecting repolarization and/or conduction abnormalities in identifying patients with abnormal ECG showing a pattern of atypical right bundle branch block and ST elevation syndrome (Brugada syndrome) at risk for life-threatening arrhythmias is controversial. Because right precordial ST elevation reflects inhomogeneous repolarization, we hypothesized that a correlation between the area of ST elevation, that is, the area of inhomogeneous repolarization, and the inducibility of ventricular tachyarrhythmias (VT) exists. Therefore, the body surface area of ST elevation and the presence of late potentials were compared to the inducibility of VT in patients with the characteristic ECG of Brugada syndrome. METHODS AND RESULTS: A 120-channel body surface potential map was recorded at rest and after administration of a Class I agent (ajmaline, 1 mg/kg) to measure the body surface area of ST elevation (> or = 0.2 mV) in 23 individuals (16 patients had been resuscitated from near sudden cardiac death or had suffered syncope) with an ECG compatible with the diagnosis of Brugada syndrome as well as in 15 healthy controls and in 15 patients with arrhythmogenic right ventricular cardiomyopathy. Late potentials were assessed in 20 of the Brugada patients using signal-averaged ECG. Programmed ventricular stimulation was performed at two ventricular sites with up to three extrastimuli. Mean body surface area of ST elevation (> or = 0.2 mV) of all Brugada syndrome patients was 154 +/- 139 cm2 (control 9 +/- 9 cm2; P < 0.001). In the group of patients with arrhythmogenic right ventricular cardiomyopathy, only one patient was found to have an area of ST elevation (165 cm2). In the presence of ajmaline, area size increased to 330 +/- 223 cm2 in Brugada syndrome patients (P < 0.05). In patients with inducible sustained (n = 15) and nonsustained VT (n = 3), a mean area of 183 +/- 139 cm2 was found, whereas the area was only 52 +/- 58 cm2 in those with no VT induction (P < 0.05). For an area > or = 50 cm2, there were positive and negative predictive values of 92% and 60%, respectively. Positive late potentials were found in 60% of patients and correlated to the inducibility during programmed ventricular stimulation (positive predictive value 100%, negative predictive value 75%; P < 0.001). CONCLUSION: In patients with Brugada syndrome, the body surface area of ST elevation and the presence of late potentials correlate to the inducibility of VT during programmed ventricular stimulation and may be of value as a new noninvasive marker for risk stratification in these patients.