Patients with VSA and lethal ventricular arrhythmia are a population at high risk for recurrence of cardiopulmonary arrest, and there is no reliable indicator for predicting recurrence of ventricular arrhythmia. Insertion of an ICD with medication for VSA is appropriate for this high-risk population.

on behalf of the J-RHYTHM Registry Investigators* Background--To clarify the influence of hypertension and blood pressure (BP) control on thromboembolism and major hemorrhage in patients with nonvalvular atrial fibrillation, a post hoc analysis of the J-RHYTHM Registry was performed.

Patients with vasospastic angina exhibited an increased baseline QTc dispersion compared with patients with atypical chest pain, which suggests that inhomogeneity of repolarization and susceptibility to ventricular arrhythmias are increased in patients with vasospastic angina, even when asymptomatic. The association between increased QTc dispersion and ventricular arrhythmias during the provocation test suggests that measurement of QT dispersion may help predict which patients with vasospastic angina are at high risk for ventricular arrhythmias during ischemia.

Introduction: ST segment elevation in patients with Brugada syndrome is known to fluctuate occasionally, influenced by multiple factors. Insulin has been shown to affect QT dispersion in healthy volunteers, as well as result in abnormality of ventricular repolarization in patients with congenital long QT syndrome. Methods and Results: To assess a possible role of insulin in ST segment elevation in patients with Brugada syndrome, an oral glucose tolerance test (OGTT) was administered to 20 patients with Brugada syndrome and 20 normal patients without ST‐T changes as a control group. Plasma glucose and potassium levels, immunoreactive insulin concentration (IRI), and ST segment elevation and ST‐T wave changes on 12‐lead ECG during OGTT were analyzed. Augmentation (>1 mm) of ST elevation or morphologic changes in ST‐T waves were observed frequently in response to increased IRI during OGTT [15/20 cases (75%)] in patients with Brugada syndrome but in none of the patients in the control group [0/20 cases (0%), P < 0.01 ]. The changes returned to baseline 180 minutes after the glucose load in 9 of 15 patients. Patients who showed coved‐type ST elevation before the glucose load exhibited positive ECG changes more frequently than patients with saddleback‐type elevation or transiently normalized ST segment [8/8 cases (100%) vs 7/12 (58%), P < 0.05 ]. There was no significant difference between the two groups in terms of glucose, IRI, and potassium levels during OGTT. Conclusion: The findings suggest that glucose‐induced insulin secretion is one of the contributing factors to fluctuation of ST segment elevation in patients with Brugada syndrome. (J Cardiovasc Electrophysiol, Vol. 14, pp. 243‐249, March 2003)

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