ABSTRACT
We investigated the effects of purified eicosapentaenoic acid (EPA) on vascular endothelial function and free fatty acid composition in Japanese hyperlipidemic subjects. In subjects with hyperlipidemia (total cholesterol ≥220 mg/dL and/or triglycerides ≥150 mg/dL), lipid profile and forearm blood flow (FBF) during reactive hyperemia were determined before and 3 months after supplementation with 1800 mg/day EPA. Peak FBF during reactive hyperemia was lower in the hyperlipidemic group than the normolipidemic group. EPA supplementation did not change serum levels of total, HDL, or LDL cholesterol, apolipoproteins, remnant-like particle (RLP) cholesterol, RLP triglycerides, or malondialdehyde-modified LDL cholesterol. EPA supplementation did not change total free fatty acid levels in serum, but changed the fatty acid composition, with increased EPA and decreased linoleic acid, γ-linolenic acid, and dihomo-γ-linolenic acid. EPA supplementation recovered peak FBF after 3 months. Peak FBF recovery was correlated positively with EPA and EPA/arachidonic acid levels and correlated inversely with dihomo-γ-linolenic acid. EPA supplementation restores endothelium-dependent vasodilatation in hyperlipidemic patients despite having no effect on serum cholesterol and triglyceride patterns. These results suggest that EPA supplementation may improve vascular function at least partly via changes in fatty acid composition.
ABSTRACT
BACKGROUND: Antiarrhythmic agents are considered to have significant effects on the defibrillation energy requirement, so this study investigated the effects of nifekalant on defibrillation. METHODS AND RESULTS: Forty-two patients with persistent atrial fibrillation (AF) underwent electrical cardioversion via intracardiac electrode catheters prior to and after the intravenous administration of nifekalant. The success rate of the defibrillation and change in the defibrillation threshold using sequential incremental defibrillation energy deliveries was investigated. In addition, the parameters that could predict the beneficial effects of nifekalant were also assessed. Nifekalant significantly decreased the defibrillation energy requirement in 13 of the 42 cases, and nifekalant also converted AF to sinus rhythm with an identical energy to that of the last unsuccessful defibrillation in 21 of 42 cases. The success of defibrillation seemed to be dependent on significant prolongation of the intracardiac atrial electrogram intervals during AF by the nifekalant. CONCLUSIONS: Intravenous nifekalant significantly improved the electrical defibrillation efficacy in patients with persistent AF that was resistant to defibrillation, without any serious adverse effects.
