SUMMARYIt has been reported that green tea consumption reduces the risk of coronary artery disease and cardiac events. Catechin is a major constituent of Japanese green tea and an antioxidant. Lipids and oxidization of low-density lipoprotein cholesterol (LDL-C) play important roles in atherosclerosis. Therefore, we evaluated the effect of catechin intake on the lipid profile and plasma oxidized LDL. The study population consisted of 40 healthy adult volunteers (10 men, 30 women). Catechin was extracted from green tea leaves. The subjects were randomly divided into two groups, a catechin group (n = 29) and a control group (n = 11). In the catechin group, catechin (500 mg: equivalent to 6 or 7 cups of green tea) was administered orally. Venous blood samples were obtained before eating a meal at the start and after 4 weeks without any lifestyle modification. Plasma oxidized LDL assay was performed with a sandwich-type enzyme immunoassay using anti-oxidized phosphatidylcholine monoclonal antibody. The baseline lipid profiles and tea consumptions were similar between the two groups. Plasma oxidized LDL was significantly decreased after catechin administration (from 9.56 ± 9.2 to 7.76 ± 7.7 U/mL, P = 0.005), while plasma LDL-C, triglyceride, and HDL-C concentrations did not change. Catechin decreased the plasma oxidized LDL concentration without significant change in plasma LDL concentration. The mechanism of the beneficial effects of green tea on coronary artery disease might result from a decrease in plasma oxidized LDL. (Int Heart J 2007; 48: 725-732)

SUMMARYQT prolongation and torsades de pointes have been documented in patients administered cisapride and its blocking of potassium channels in myocytes has been suggested as the mechanism. An interaction with cytochrome P450 CYP3A4 inhibitor drugs like macrolide and azole antifungals is also thought to be a possible mechanism. Since mosapride has characteristics similar to cisapride, we examined the effects of mosapride on the electrocardiogram and pharmacokinetics before and after its coadministration with erythromycin. Ten healthy male volunteers were repeatedly administered mosapride 15 mg/day for 7 days followed by coadministration with erythromycin 1200 mg/day for 7 days. Coadministration with erythromycin resulted in a 1.6-fold increase in the C max of mosapride and prolongation of t 1/2 from 1.6 to 2.4 hours, indicating the inhibition of mosapride metabolism. However, there were no significant differences in the QT interval and QTc between mosapride alone and concomitant use with erythromycin. There was no correlation between the electrocardiographic parameters and plasma mosapride concentrations, and no case exceeded the upper limit of the normal range of QTc. Although there was a certain pharmacokinetic interaction between mosapride and erythromycin, their coadministration did not affect the electrocardiogram at all, indicating a reduced likelihood of severe clinical adverse events like QT prolongation and torsades de pointes. (Jpn Heart J 2003; 44: 225-234) Key words: Mosapride, Erythromycin, Drug interaction IN recent years, cardiovascular adverse effects including QT prolongation and torsades de pointes have been documented 1,2) in patients administered cisapride, a gastroprokinetic drug with serotonin 5-HT 4 receptor agonistic activity. Its blocking action on delayed rectifier potassium channels in myocytes has been suggested as the mechanism.3,4) Cisapride, which is metabolized by cytochrome P450 CYP3A4 species, undergoes inhibition of its biotransformation by CYP3A4 From

Background: The clinical and electrophysiological characteristic of ventricular premature contractions (VPCs) which trigger the incessant form of polymorphic ventricular tachycardia (VT), so-called ''electrical storm'' associated with ischemic heart disease, remains unclarified. The aim of this study was to evaluate those matters and the possible role of the Purkinje network in the emergence of an electrical storm.Methods and results: We experienced 5 patients (68 AE 5 years, mean LVEF: 29%) with electrical storms which occurred during the acute phase of an infarction in 3 patients and the remote phase in 2. The triggering VPCs were multifocal in 3 patients and monofocal in the remaining 2. Radiofrequency (RF) catheter ablation was performed for a goal of eliminating the triggering VPCs. A total of 9 different kinds of VPCs differentiated by their morphology were successfully eliminated by the RF deliveries targeting the VPCs' foci. At the successful ablation sites, Purkinje potentials preceded the QRS onset of the VPC by 67 AE 23 ms, suggesting the VPCs originated in the surviving Purkinje fibers. Moreover, the extensive RF deliveries applied at the surviving Purkinje network rendered the polymorphic VT unable to be induced by programmed stimulation which reproducibly induced it before the ablation in 2 patients.Conclusion: A surviving Purkinje network might contribute not only to the initiation of the repetitive form of lethal ventricular arrhythmias, but also to the perpetuation of the arrhythmias in patients with ischemic heart disease. (J Arrhythmia 2008; 24: 200-208)

Background: The clinical and electrophysiological characteristic of ventricular premature contractions (VPCs) which trigger the incessant form of polymorphic ventricular tachycardia (VT), so‐called “electrical storm” associated with ischemic heart disease, remains unclarified. The aim of this study was to evaluate those matters and the possible role of the Purkinje network in the emergence of an electrical storm. Methods and results: We experienced 5 patients (68 ± 5 years, mean LVEF: 29%) with electrical storms which occurred during the acute phase of an infarction in 3 patients and the remote phase in 2. The triggering VPCs were multifocal in 3 patients and monofocal in the remaining 2. Radiofrequency (RF) catheter ablation was performed for a goal of eliminating the triggering VPCs. A total of 9 different kinds of VPCs differentiated by their morphology were successfully eliminated by the RF deliveries targeting the VPCs’ foci. At the successful ablation sites, Purkinje potentials preceded the QRS onset of the VPC by 67 ± 23 ms, suggesting the VPCs originated in the surviving Purkinje fibers. Moreover, the extensive RF deliveries applied at the surviving Purkinje network rendered the polymorphic VT unable to be induced by programmed stimulation which reproducibly induced it before the ablation in 2 patients. Conclusion: A surviving Purkinje network might contribute not only to the initiation of the repetitive form of lethal ventricular arrhythmias, but also to the perpetuation of the arrhythmias in patients with ischemic heart disease.

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