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      A Single Intravenous Dose of Ivabradine, a Novel I f Inhibitor, Lowers Heart Rate but Does Not Depress Left Ventricular Function in Patients with Left Ventricular Dysfunction


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          This randomized, single-blind, placebo-controlled study investigated the effect of ivabradine, a novel heart rate-lowering agent, on echocardiographic indices of left ventricular (LV) systolic function in patients with regional (coronary artery disease) or global (cardiomyopathy) LV dysfunction. Patients were randomized on an unequal basis to receive ivabradine 0.25 mg/kg (n = 31) or placebo (n = 13) by intravenous infusion. Resting heart rate was reduced by a mean of 17.6 ± 4.7% with ivabradine and 1.5 ± 5.8% with placebo. The mean maximum decrease in LV ejection fraction was 0.2% with ivabradine and 1.7% with placebo. Fractional shortening and stroke volume were also fully preserved after ivabradine administration. Thus, a single intravenous dose of ivabradine produced a substantial reduction in resting heart rate without affecting LV function in patients with regional or global LV dysfunction.

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          Antianginal and Antiischemic Effects of Ivabradine, an I <sub>f</sub> Inhibitor, in Stable Angina

          Circulation, 107(6), 817-823
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            Properties and functional roles of hyperpolarization-gated currents in guinea-pig retinal rods.

            1. The inward rectification induced by membrane hyperpolarization was studied in adult guinea-pig rods by the perforated-patch-clamp technique. 2. CsCl blocked the rectification observed in both voltage- and current-clamp recordings at voltages negative to -60 mV, while BaCl2 blocked the inward relaxation observed at voltages positive to -60 mV. The current activated at -90 mV had a low selectivity between sodium and potassium and reversed at -31.0 mV. 3. These observations suggest that two inward rectifiers are present in guinea-pig rods: a hyperpolarization-activated (Ih) and a hyperpolarization-deactivated (Ikx) current. The functional roles of Ih and Ikx were evaluated by stimulating rods with currents sinusoidally modulated in time. 4. Rods behave like bandpass amplifiers, with a peak amplification of 1.5 at about 2 Hz. For hyperpolarizations that mainly gate Ikx, amplification and phase shifts are fully accounted for by a rod membrane analogue model that includes an inductance. For hyperpolarizations that also gate Ih, a harmonic distortion became apparent. 5. Bandpass filtering and amplification of rod signals, associated with Ih and Ikx gating by membrane hyperpolarization, are strategically located to extend, beyond the limits imposed by the slow phototransductive cascade, the temporal resolution of signals spreading to the rod synapse.
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              Kinetic and ionic properties of the human HCN2 pacemaker channel.

              Human cDNA coding for the hyperpolarization-activated "pacemaker" channel HCN2 was expressed in Phoenix cells and yielded an inward current (IhHCN2) activated on hyperpolarization. The average IhHCN2 was half-activated at -83.1 mV and its kinetics could be described by second-order Hodgkin-Huxley gating. The time constant curve was bell-shaped and peaked at -82.2 mV. With 115 mM external Na+ and 30 mM external K+, IhHCN2 reversed at -17.1 mV, and had a mean conductance of 5.6 nS. Reducing the external K+ or Na+ concentration led to a concentration-dependent reduction of the IhHCN2 conductance and to a hyperpolarizing shift of reversal potential. External Cs+ ions (5 mM) blocked IhHCN2 in a voltage-dependent way according to a Woodhull-type block model, at an electrical distance of 0.66 from the external membrane surface, and with a dissociation constant of 15 mM at 0 mV. Increasing cytoplasmic cAMP using forskolin increased IhHCN2 by shifting the current activation curve to more positive voltages (11.7 mV). Exposure of the intracellular side of inside-out macro-patches to cAMP led to a depolarizing shift of the channel open probability curve (15.2 mV with 10 microM cAMP). These results indicate that although hHCN2 channels share several properties with native cardiac f-channels, differences also exist in permeability and block properties, suggesting that native channels may not be composed simply of homomeric constructs.

                Author and article information

                S. Karger AG
                November 2003
                21 November 2003
                : 100
                : 3
                : 149-155
                aDepartment of Cardiology, Marienhof Hospital, Koblenz, bDepartments of Medicine and Cardiology, University of Bonn, Bonn, Germany
                73933 Cardiology 2003;100:149–155
                © 2003 S. Karger AG, Basel

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                Page count
                Tables: 3, References: 27, Pages: 7
                Clinical Pharmacology


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