Antiischemic, antianginal, and hemodynamic effects of ULFS 49 CL (a new heart-rate-reducing agent) in patients with angiographically proven CAD

ULFS 49 CL, a so-called sinus node inhibitor, does not affect β-adrenergic or muscarinic receptors at therapeutical plasma concentrations in man. The compound’s underlying mechanism of action to decrease heart rate can be explained by an inhibition of the if-current, which seems to be responsible for the spontaneous depolarization of the pacemaker cells in the sino-atrial node [1, 2]. Like β-blockers, the substance is expected to produce a reduction in heart rate. Through this mechanism ULFS 49 CL may result in antianginal and/or antiischemic efficacy in patients with angina pectoris. At present, no data are available on its antiischemic potential. The aim of the present multicenter trial was to investigate the antianginal, antiischemic, and hemodynamic effects of ULFS 49 CL, a new heart-rate-reducing compound, in patients with stable angina pectoris.