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
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