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ULFS 49 CL, a prototype of a novel pharmacological concept

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Sinus node inhibitors

Abstract

In patients with stable angina pectoris, ischemic attacks during exercise or other stress are caused by an imbalance between myocardial oxygen demand and oxygen supply. Current anti-ischemic drug therapy is aimed to extend exercise tolerance by an improvement of the O2-demand/supply ratio. Antianginal drugs have been traditionally categorized as vasodilators mainly increasing O2-supply (e.g., calcium-channel blockers, nitrates) and heart-rate-reducing drugs (e.g., β-adrenoceptor blockers), or combinations thereof (e.g., verapamil or diltiazem-like calcium-channel blockers). The conventional view of the mechanism of action of β-adrenoceptor blockers is relief of ischemia by a decrease of myocardial O2-demand during exercise due to reductions of heart rate and contractility. However, the benefit of the negative inotropic effect of β-adrenoceptor blockers remains in dispute. The attenuation of exercise-induced tachycardia and the preservation of an adequate diastolic perfusion time was often suggested as the only therapeutic principle of β-adrenoceptor blockers.

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© 1991 Dr. Dietrich Steinkopff Verlag GmbH & Co. KG, Darmstadt

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Lillie, C. (1991). ULFS 49 CL, a prototype of a novel pharmacological concept. In: Hjalmarson, Å., Remme, W.J. (eds) Sinus node inhibitors. Steinkopff. https://doi.org/10.1007/978-3-642-72458-9_2

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  • DOI: https://doi.org/10.1007/978-3-642-72458-9_2

  • Publisher Name: Steinkopff

  • Print ISBN: 978-3-7985-0861-3

  • Online ISBN: 978-3-642-72458-9

  • eBook Packages: Springer Book Archive

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