Yasutaka Tanabe

Comparison of Arrhythmogenicity of Atrial Pacing at Several Right Atrial Pacing Sites: Evaluation of Canine Atrial Electrograms During Atrial Pacing and Arrhythmogenicity for Atrial Fibrillation

The changes in the duration of atrial electrograms and the appearance of AF during atrial pacing were compared among five atrial pacing sites in dogs to clarify the arrhythmogenicity of atrial pacing at different atrial pacing sites. In seven mongrel dogs (15–20 kg), the right atrial surface was exposed by right thoracotomy. Atrial electrograms were recorded via bipolar electrodes with an interelectrode distance of 1.2 mm at four right atrial sites: (1) the high right atrium (HRA), (2) the mid‐right atrium (MRA), (3) the low right atrium (LRA), and (4) the center of the pectinate muscle (PM). The duration of the atrial electrograms at these four recording sites were measured during atrial pacing with fixed cycle lengths of 200, 150, and 120 ms delivered at five atrial sites: (1) the HRA, (2) the inferior vena cava (IVC), (3) the right atrial appendage (RAA), (4) Bachmans bundle (BB), and (5) the atrial septum (AS). In each dog, the atrial pacing with the 120‐ms cycle length was performed five times at each pacing site to evaluate the in‐ducibility of AF. When AF was induced, the atrial recording site which first showed a fragmented atrial electrogram was considered the initiation site of the AF. AF was induced during 9 of 35 episodes of atrial pacing at the HRA site, 11 of 35 at the IVC site, 5 of 35 at the RAA site. 3 of 35 at the BB site, and none at the AS site. The initiation site of AF was in the HRA site in 11 of 28 episodes of induced AF, in the MRA site in 9 of 28, and in the LRA site in 8 of 28. At each recording site, the shorter the paced cycle length, the longer the duration of the atrial electrogram regardless of the pacing site. During the atrial pacing with the 200‐ms cycle length, the HRA pacing resulted in the shortest duration of the atrial electrogram at each recording site in comparison with the other pacing sites. However, during atrial pacing at the two shorter paced cycle lengths, the duration of the atrial electrogram was shorter during the pacing at the BB or AS sites in comparison with the other three pacing sites, i.e., the HRA, IVC, and RAA sites. These results were the same for all atrial recording sites, but the prolongation of the atrial electrogram was most prominent at the HRA and MRA recording sites, which are most likely initiation sites of the induced AF. In the canine atria, (1) the initiation sites of AF were likely to be the HRA, MRA, or LRA sites in comparison with the PM site; and (2) the atrial pacing at the BB or AS sites was considered less arrhythmogenic for AF than the pacing at the HRA, LRA, or RAA sites.

Suppression of Electrical Storm by Biventricular Pacing in a Patient with Idiopathic Dilated Cardiomyopathy and Ventricular Tachycardia

TANABE, Y., et al. : Suppression of Electrical Storm by Biventricular Pacing in a Patient with Idiopathic Dilated Cardiomyopathy and Ventricular Tachycardia. This study presents a patient with idiopathic dilated cardiomyopathy who had suffered from multiple ICD shocks. Amiodarone and a β‐blocker failed to suppress ventricular tachycardia. His ECG showed a very wide QRS complex with an intraventricular conduction delay, so biventricular (BV) pacing was attempted. The BV pacing successfully prevented the multiple ICD shocks accompanied with an improvement in left ventricular systolic function and physical activity.(PACE 2003; 26[Pt. I]:101–102)

Acute effect of percutaneous transvenous mitral commissurotomy on ventilatory and hemodynamic responses to exercise. Pathophysiological basis for early symptomatic improvement.

BackgroundImprovement of exertional dyspnea occurs immediately after percutaneous transvenous mitral commissurotomy (PTMC), but the pathophysiological basis for this early symptomatic improvement has not been elucidated. Methods and ResultsExercise hemodynamic measurement and exercise ventilatory measurement with arterial blood gas analysis were performed in 21 patients aged 50.4+9.5 years (mean±SD) with symptomatic mitral stenosis before and a few days after PTMC. Exercise ventilatory measurement were also performed in 14 normal control subjects aged 48.9±4.9 years. After PTMC, mitral valve area increased (from 1.0±03 to 1.7±03 cm2, p<.001), mean mitral gradient (from 12.2±5.2 to 5.2±2.2 mm Hg, p<.001), and mean left atrial pressure (from 18.7±6.1 to 12.1±4.0 mm Hg, p<.001) decreased. All patients experienced significant symptomatic improvement soon after PTMC. Comparison of hemodynamic parameters at the same ergometer work rate showed a significant decrease in pulmonary artery systolic pressure (from 77±_18 to 67±+14 mm Hg, p<.001) and diastolic pressure (from 36±10 to 28±7 mm Hg, p<.001) and a significant increase in cardiac output (from 6.4±1.4 to 8.1 ± 1.9 L/min, p<.001). Despite the improvement in exercise hemodynamics and symptoms, exercise capacity determined by peak oxygen uptake (from 18.0+2.9 to 18.6+3.1 mL- kg-1 min-1) and anaerobic threshold (from 11.7±2.4 to 12.0±2.4 mL* kg-1 min-1) remained unchanged. Excessive exercise ventilation, as assessed by the slope of the regression line between expired minute ventilation and carbon dioxide output, decreased significantly from 37.2±6.7 to 33.9±5.8 (P<.001), but remained significantly higher than that in the normal subjects (27.9±3.6, p<.01). The ratio of total dead space to tidal volume and total dead space per breath during exercise decreased significantly after PTMC (P<.05). The change in excessive exercise ventilation after PTMC was correlated with the change in dead space to tidal volume ratio (r=.59) ConclusionsSignificant relief of exertional dyspnea immediately after PTMC is not accompanied by an improvement in exercise capacity. A decrease in excessive exercise ventilation due to a decrease in physiological dead space resulting from hemodynamic improvement partly contributes to the early relief of symptoms after PTMC. However, lung compliance, which was not measured in the present study, may have changed after PTMC. This change may also contribute to the symptomatic improvement.

Variable Electrocardiographic Effects of Short‐Term Quinidine Sulfate Administration in Brugada Syndrome

Quinidine, a class I antiarrhythmic agent with blocking property of transient outward current, is a possible candidate for the suppression of ventricular fibrillation in patients with Brugada syndrome; although there is a concern that its ability to these effects may be proarrhythmic. Therefore, we evaluated the effect of quinidine sulfate on ST‐segment elevation in Brugada syndrome. In 8 patients with Brugada syndrome, the magnitude of ST‐elevation at the J‐point (STJ), and the ST‐segment configuration in leads V1–V3, were compared before and on day 2 after the initiation of quinidine administration. In 3 patients, quinidine attenuated STJ by ≥0.1 mV. Of these 3 patients, ST‐segment elevation was normalized in 2 patients, while the ST‐segment configuration was unchanged in another. In another 3 patients, quinidine augmented STJ by ≥0.1 mV without any change of ST‐segment configuration, and the augmentation was returned to baseline after the discontinuation of quinidine. Quinidine exhibited no effect on the ST‐segment in the remaining 2 patients. The favorable effects of quinidine on the ST‐segment tended to be more pronounced in patients with prominent ST‐elevation at baseline. In 1 patient, quinidine was effective in eliminating both ST‐segment elevation and repetitive tachyarrhythmia episodes. In conclusion, the effects of quinidine on ST‐segment elevation were variable. Quinidine may potentially augment the ST‐segment elevation in some patients with Brugada syndrome.

Effect of Dl-Sotalol on Mortality and Recurrence of Ventricular Tachyarrhythmias:Ischemic Compared to Nonischemic Cardiomyopathy

Objective: We compared the effectiveness of sotalol on mortality and the recurrence of ventricular tachyarrhythmia (VTA) between idiopathic dilated cardiomyopathy (IDCM) and coronary artery disease (CAD).

Recovery of the right atrial effective refractory period after cardioversion of chronic atrial fibrillation

The effective refractory period was shorter in patients with than without chronic atrial fibrillation (AF). The effective refractory period was prolonged, and at 12 and 24 hours after cardioversion of AF it was the same as the subjects without AF.

Electrophysiologic study guided therapy with sotalol for life-threatening ventricular tachyarrhythmias

The aim of this study was to investigate the long‐term efficacy and safety of electrophysiologic study (EPS)‐guided sotalol administration combined with implantable cardioverter defibrillators (ICD) for ventricular tachyarrhythmias (VTA). This study enrolled 92 patients with both structural heart disease and sustained VTA. Sotalol was administered to 57 patients, and its efficacy was assessed by EPS. Long‐term treatment was continued in combination with ICD in 31 patients (57%) whose VTA was no longer inducible (responder group) and in 16 patients whose VTA remained inducible (nonresponder group). The long‐term outcomes were compared among the responder group, the nonresponder group, and 35 ICD recipients untreated with antiarrhythmic drugs (ICD‐only group). During a mean follow‐up of 44 ± 33 months, the recurrence of VTA was not significantly different between all patients treated with sotalol (30%) and patients in the ICD‐only group (46%). However, the recurrence of VTA was significantly lower in the responder (13%) than in the nonresponder (63%) or the ICD‐only groups (46%). There was no significant difference in VTA recurrence between the nonresponder and the ICD‐only groups. One patient each in the responder and the ICD‐only groups died suddenly, and all‐cause mortality was similar in the three groups. The incidence of inappropriate ICD discharges was less in the sotalol than in the ICD‐only groups. No patient had to discontinue long‐term sotalol treatment because of the adverse effects. In conclusion, sotalol reduced VTA recurrence in the responding patients and inappropriate ICD discharge. EPS may predict the efficacy of sotalol for VTA recurrence.

Activation-recovery interval as a parameter to assess the intracardiac ventricular repolarization in patients with congenital long QT syndrome

P experimental studies have reported that the activation-recovery interval (ARI) calculated from the unipolar electrogram was approximate to the local effective refractory period (ERP), but this subject has not been well studied in human intracardiac electrograms. The analysis of intracardiac ARIs in patients with congenital long QT syndrome (LQTS) may be useful and relevant to study, focusing on the arrhythmogenesis and therapeutic effects, so we examined whether the ARI calculated from the intracardiac electrograms of patients with LQTS reasonably corresponded to local refractoriness. The alteration of intracardiac ARI distribution by epinephrine and mexiletine was also studied in some of the patients.

Molecular characterization and gene disruption of a novel zinc‐finger protein, HIT‐4, expressed in rodent brain

J. Neurochem. (2010) 112, 1035–1044.

Postprandial Variations in ST‐Segment in a Patient with Brugada Syndrome and Partial Gastrectomy

A 74‐year‐old man with a history of partial gastrectomy presented with an electrocardiogram consistent with Brugada syndrome and marked meal related fluctuations in the ST segment. ST‐segment elevation was prominently attenuated at 30 minutes and increased at 120 minutes after meals. Analysis of heart rate variability revealed a relationship between postprandial heightened parasympathetic activity and increase in Brugada‐type ECG abnormality. A rapid postprandial increase in blood glucose may initially stimulate sympathetic nervous activity and secondarily increase parasympathetic tone. Food intake can be associated with fluctuations in ST‐segment elevation in patients with the Brugada syndrome.