Characteristics of induced ventricular fibrillation cycle length in symptomatic Brugada syndrome patients.

BACKGROUND: Limited information is available on the ventricular fibrillation (VF) spectrum in Brugada syndrome (BS) patients. We clarified differences in the VF cycle length (CL) using fast-Fourier transformation (FFT) analysis in symptomatic and asymptomatic BS patients. METHODS AND RESULTS: VF was induced by pacing from the right ventricular (RV) apex and/or RV outflow tract (RVOT) for >8s. A 4096-point FFT analysis of results from 28 male BS patients (51.1 ± 13.7 years old) was performed. Dominant frequency (DF) from phases 1 (4s) to 6 was obtained at 2-s intervals. The average DF from surface and intracardiac electrograms (ECG: DF(ECG); ICE: DF(ICE,), respectively) was compared between symptomatic and asymptomatic patients. Symptomatic patients had a significantly shorter effective refractory period at a CL of 600 ms at the RVOT than asymptomatic patients. DF(ECG) significantly increased with phase (5.64 ± 0.32 Hz in phase 1 to 6.16 ± 0.52 Hz in phase 6) and was significantly higher in symptomatic patients than in asymptomatic patients. DF(ICE) had the same characteristics as DF(ECG). CONCLUSIONS: Induced VF in BS patients can be characterized using FFT analysis. Our data support the hypothesis that symptomatic patients have a significantly shorter VF CL than asymptomatic patients.

Is this a philosophic issue? Do patients with drug-induced Brugada type ECG have poor prognosis? (Pro).

Brugada syndrome (BS) has an intermittent or concealed type, which can be unmasked by the sodium (Na(+))-channel-blocker challenge test. The appropriate risk stratification of patients with a drug-induced Brugada-type electrocardiographic (ECG), especially those without a history of syncope or aborted sudden cardiac death, remains unclear. The prognosis of patients with BS depends on the clinical type, cardiac arrest, syncope or if asymptomatic. The ratio of the asymptomatic group varies from 56.9% to 63.6% and, furthermore, their annual cardiac event rate is relatively lower at 0.24-3.6% compared with the cardiac arrest group. Patients with a drug-induced Brugada-type ECG have a poor prognosis if they had a history of ventricular fibrillation (VF) or aborted sudden cardiac death, because their risk becomes similar to that of patients with spontaneous Brugada-type ECG. They have the disturbance of the Na(+)-channel and the electrophysiologic substrate of VF, proven by the high inducibility of VF by stimulation test even in patients without spontaneous VF. Spontaneous VF will never occur if there is no VF substrate. Implantable cardioverter-defibrillators will certainly protect them, so patients with a drug-induced Brugada-type ECG, even without a history of VF or aborted sudden cardiac death, should be considered to have a poor prognosis.

Mechanisms for the genesis of paroxysmal atrial fibrillation in the Wolff Parkinson-White syndrome: intrinsic atrial muscle vulnerability vs. electrophysiological properties of the accessory pathway.

BACKGROUND: Paroxysmal atrial fibrillation (PAF) develops in up to one-third of patients with the Wolff Parkinson-White syndrome (WPW). The reason for this high incidence of PAF in the WPW syndrome is not yet clearly understood. When PAF appears in patients with WPW syndrome who have anterograde conduction via the accessory pathway (AP), it may be life-threatening if an extremely rapid ventricular response develops degenerating into ventricular fibrillation. METHODS AND RESULTS: Several mechanisms responsible for the genesis of PAF in WPW patients were hypothesized, namely, spontaneous degeneration of atrioventricular reciprocating tachycardia into atrial fibrillation (AF), electrical properties of the APs, effects of APs on atrial architecture, and intrinsic atrial muscle vulnerability. Focal activity, multiple reentrant wavelets, and macroreentry have all been implicated in AF, perhaps under the further influence of the autonomic nervous system. AF can also be initiated by ectopic beats originating from the pulmonary veins, and elsewhere. Several studies demonstrated a decrease incidence of PAF after successful elimination of the AP, suggesting that the AP itself may play an important role in the initiation of PAF. However, PAF still occurs in some patients with the WPW syndrome even after successful elimination of the AP. There is an important evidence of an underlying atrial disease in patients with the WPW syndrome. CONCLUSIONS: Atrial vulnerability has been studied performing an atrial endocardial catheter mapping and analysing abnormal atrial electrograms. Other studies evaluated atrial refractoriness and intraatrial conduction times, suggesting an intrinsic atrial vulnerability as the mechanism of PAF and considering the AP as an innocent bystander. It is our intention to analyse the available data on this particular and interesting topic since AF has a singular prognostic significance in patients with the WPW syndrome, and its incidence is unusually high in the absence of any clinical evidence of cardiac organic disease.

Activation patterns and conduction velocity in posterolateral right atrium during typical atrial flutter using an electroanatomic mapping system.

BACKGROUND: To investigate the activation patterns and conduction velocity (CV) in the posterolateral right atrial (RA) wall during typical counterclockwise atrial flutter (AFL) using an electroanatomic mapping system. METHODS AND RESULTS: During typical AFL in 25 patients, the transverse conduction pattern and CV were classified and calculated. The line blocking transverse conduction was defined by the conduction pattern and double potentials recorded during mapping. There were 3 types (including 2 subtypes) of transverse conduction pattern based on the conduction blocks across the posterolateral RA in a line between the superior and inferior venae cava. Trans-cristal conduction activation in a horizontal direction was seen in all but 4 patients. The CV in the gap area was 0.59+/-0.21 m/s. CONCLUSIONS: Three types of transverse conduction pattern were observed during trans-ctristal conduction and the trans-ctristal CV was relatively slower than that in other parts of the RA, except for the isthmus.

Pilsicainide-induced Brugada-type ECG and ventricular arrhythmias originating from the left posterior fascicle in a case with Brugada syndrome associated with idiopathic left ventricular tachycardia.

The patient was a 50-year-old male in 2002, who was first suspected of having a Brugada-type electrocardiogram (ECG). A drug challenge test using pilsicainide was performed and unmasked a typical coved type ST elevation followed by ventricular arrhythmias (VAs) manifesting a QRS pattern with a right bundle branch block and left axis deviation. Three years later, he was transferred to the emergency room due to a wide QRS tachycardia with the same QRS morphology as the VA that previously occurred in the drug challenge test. An ECG just after the recorded termination of the tachycardia exhibited a typical Brugada-type ECG. In an electrophysiological study, ventricular fibrillation could be easily induced with reproducibility. Since the clinical tachycardia could not be sustained by an isoproterenol infusion, mapping and catheter ablation targeting the pilsicainide-induced VAs was performed. The successful ablation site was the left mid-lower septal wall where a Purkinje potential was recorded and a false tendon was attached just to it.

Differentiation of the electrophysiological effects on the atrial myocardium between the pure Na channel blocker, pilsicainide, and flecainide.

UNLABELLED: The purpose of this study was to identify the difference between the pure Na channel blocker, pilsicainide and Ic-antiarrhythmic drug, flecainide, on the atrial electrophysiological characteristics. METHODS: The subjects consisted of 24 patients (48 +/- 12 years-old: P-group) in whom pilsicainide was administrated intravenously (1 mg/kg/10 min) and 31 patients (47 +/- 15 years-old: F-group) in whom flecainide was administrated intravenously (2 mg/kg/10 min). The atrial effective refractory period (ERP-A), intra-atrial conduction time (CT), max intra-atrial conduction delay (Max CD), repetitive atrial firing zone (RAFZ), fragmented atrial activity zone (FAZ) and intra-atrial conduction delay zone (CDZ) were measured before and after the drugs. RESULTS: Pilsicainide and flecainide significantly prolonged the ERP-A (211 +/- 27 msec to 246 +/- 39 msec; p < 0.001, 217 +/- 25 msec to 244 +/- 33 msec; p < 0.001, respectively) and CT (121 +/- 33 msec to 149 +/- 43 msec; p < 0.001, 122 +/- 22 msec to 153 +/- 27 msec; p < 0.001, respectively) to the same degree. However, the Max CD was shortened by pilsicainide, but not by flecainide. The RAFZ, FAZ and CDZ decreased in the P-group (21 +/- 25 msec to 4 +/- 10 msec; p < 0.01, 24 +/- 24 msec to 14 +/- 18 msec; p < 0.05, 56 +/- 29 msec to 43 +/- 32 msec, p < 0.05, respectively), but not in the F-group. CONCLUSIONS: The effects of atrial conduction delays may differ between pilsicainide and flecainide. Further examination will be needed to explain this mechanism.

The effects of aging on atrial endocardial electrograms in patients with paroxysmal atrial fibrillation.

BACKGROUND: The prevalence of atrial fibrillation (AF) has been reported to increase with advancing age. Histologic studies in AF have demonstrated that the percentage of fibrosis and degenerative changes in the atrial muscle increase significantly with age. HYPOTHESIS: This study was undertaken to assess the influence of advancing age on atrial endocardial electrograms recorded during sinus rhythm in patients with paroxysmal atrial fibrillation (PAF), which had not been assessed previously. METHODS: Right atrial endocardial catheter mapping during sinus rhythm was performed in 111 patients with PAF to evaluate the influence of advancing age on atrial endocardial electrograms. The bipolar electrograms were recorded at 12 sites in the right atrium, and an abnormal atrial electrogram was defined as lasting > or = 100 ms, and/or showing eight or more fragmented deflections. RESULTS: In all, 1,332 right atrial endocardial electrograms were assessed and measured quantitatively. The number of abnormal atrial electrograms in patients with PAF showed a significantly positive correlation with age (r = 0.34; p < 0.0005). Patients aged > 60 years had a significantly greater mean number of abnormal electrograms (2.58 +/- 2.05) than those aged < 60 years (1.43 +/- 2.03; p < 0.004). The longest duration (r = 0.35; p < 0.0005) and the maximal number of fragmented deflections (r = 0.29; p < 0.005) of atrial electrograms among the 12 right atrial sites also showed a significantly positive correlation with age. CONCLUSIONS: Aging alters the electrophysiologic properties of the atrial muscle in patients with PAF. Elderly patients have a significantly greater abnormality of atrial endocardial electrograms than do younger ones. There is a progressive increment in the extension of altered atrial muscle with advancing age in patients with PAF.

New method of determining the atrial fibrillation cycle length during human atrial fibrillation.

INTRODUCTION: The aim of this study was to investigate the usefulness of the autocorrelation function (reversed fast Fourier transform analysis) in determining the atrial fibrillation cycle length (AFCL) during human atrial fibrillation (AF). METHODS AND RESULTS: From 30 episodes of atrial electrograms recorded for 30 seconds from the high right atrium during type I AF in 16 patients, the mean, 5th percentile (p5), and 95th percentile (p95) of the AFCLs were measured by using a computer-picked activation time. The peak, minimum, and maximum AFCLs also were measured by using the autocorrelation function. The mean AFCL was retrieved at the point of the maximum peak of the coefficient of the first positive autocorrelogram. The minimum AFCL (min AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from negative to positive, and the maximum AFCL (max AFCL) was chosen as the point where the first positive autocorrelogram crossed the baseline from positive to negative. There was a significantly strong correlation between the mean and peak AFCLs (r = 0.995, P < 0.0001), p5 and min AFCLs (r = 0.953, P < 0.0001), and p95 and max AFCLs (r = 0.98, P < 0.0001). CONCLUSION: The autocorrelation function was useful in determining the AFCLs, at least during type I AF. The min AFCL may be used as an index of the refractory period during AF when the p5 AFCL approximates the refractory period.