Action potential duration is prolonged in ventricular hypertrophy induced by sustained pressure overload. Since the transient outward current (I(to)) is a major factor for determining action potential duration in rat ventricular cells, we used patch-clamp techniques to compare the characteristics of I(to) in normal and hypertrophied left ventricular cells of the rat. Left ventricular pressure overload was induced by partial ligation of the abdominal aorta for 4 to 6 weeks before study. Age-matched normal rats served as controls. Pressure overload increased the heart weight-to-body weight ratio by 47.7%. I(to) was significantly smaller in hypertrophied cells than in normal cells (20.0 +/- 1.3 versus 31.0 +/- 2.1 pA/pF, respectively, at a test potential of +60 mV; P < .001). There were no differences in the steady-state inactivation, the inactivation time course, and the time course of recovery from inactivation between normal and hypertrophied cells. At the single-channel level, there were no differences in the unitary current amplitude of the single I(to) channel between normal and hypertrophied cells, and the slope conductance was 13.7 picosiemens in normal cells and 13.4 picosiemens in hypertrophied cells. The maximum open-state probability, which was estimated from the ratio of the peak of the ensemble-averaged currents to the single-channel current amplitude, was similar for normal and hypertrophied cells (0.66 +/- 0.03 and 0.69 +/- 0.04, respectively, at a test potential of +40 mV; P = NS). We conclude that diminished I(to) contributes to action potential prolongation in hypertrophied ventricular cells from pressure-overloaded rat hearts. Reduced I(to) channel density may be responsible for the diminished whole-cell I(to).

In Japan, data on the epidemiological and clinical features of atrial fibrillation (AF) are rather sparse; even less data are available on the risk of thromboembolism in nonvalvular AF. The present study enrolled 19,825 patients who visited the cardiovascular clinics of the 13 hospitals in Hokkaido, Japan, between March and July 1995. The prevalence of AF, the clinical characteristics of AF patients, and the occurrence of ischemic events were examined during the 2 year follow-up period. The prevalence of AF increased with age, and the overall prevalence was 14%. Antithrombotic therapy was used in 57% of AF patients and the incidence of ischemic events during the follow-up period was 4.6% in all AF patients. Warfarin reduced the risk of ischemic events in both the valvular and nonvalvular AF groups. A history of cerebrovascular accidents, advanced age, and the presence of underlying heart disease were each associated with a significantly increased risk of ischemic events in the nonvalvular AF group. These results show a lower incidence of ischemic events and more frequent use of antiplatelet drugs in the nonvalvular AF group. Further prospective studies are needed to determine the best preventive methods for thromboembolic complications in Japanese patients with nonvalvular AF.

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1 The aim of this study was to determine whether dierent signal transduction mechanisms underlie the Ca 2+ sensitizing eects of guanosine 5'-O-(3-thiotriphosphate) (GTP g S) and receptor agonists on b-escin-skinned smooth muscle of rabbit mesenteric artery. 2 In the homogenate of the b-escin-skinned arterial strip, C3 exoenzyme of Clostridium botulinum catalyzed the [ 32 P]-ADP-ribosylation of only one protein that had the same molecular mass as the protein detected in Western blots with anti-rho p21 antibody. Pretreatment of preparations with C3 resulted in great inhibition of GTP g S-induced Ca 2+ sensitization, although the eect of GTP g S at higher concentrations (530 mM) was not completely blocked by this treatment. In contrast, the enhancement by phenylephrine and histamine, in the presence of guanosine 5'-triphosphate, of the Ca sensitizing eects of phenylephrine and histamine were also blocked by these tyrosine kinase inhibitors. 5 These results suggest that rho p21 predominantly mediates GTP g S-induced Ca 2+ sensitization of b-escin-skinned smooth muscle of rabbit mesenteric artery, while the Ca 2+ sensitizing actions of heterotrimeric G protein-coupled receptor agonists do not involve this small G protein. However, it seems that tyrosine phosphorylation, but not PKC activation, plays an important role in both of the rho p21 protein-and heterotrimeric G protein-mediated Ca 2+ sensitization mechanisms.