By Helmut Lydtin M. D., Peter Trenkwalder M. D. (auth.)
This quantity significantly and objectively analyses the literature as much as 1989 and offers a advisor to the sensible use of all calcium antagonists which were completely investigated so far. It starts with a concise overview of physiological rules as a foundation for a dialogue of the overall and particular pharmacodynamics and pharmacokinetics of calcium antagonists. distinct emphasis is given to their healing use in perform, special dosage schedules are supplied, interactions with different medicinal drugs defined, and healing choices thought of.
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Additional info for Calcium Antagonists: A Critical Review
G. felodipine) is reduced when the input rate is lowered (Edgar 1988). Similar observations have been made concerning the relationship between diltiazem and changes in the PQ interval. In dosage guidelines of any kind, especially in the case of dosages taken from clinical studies, careful attention must be given to whether the relevant data refer to normal preparations or sustained-release preparations. Here, too, the prescribing physician should always check and, where necessary, appropriately adjust the selected dosage according to the degree of therapeutic success.
Consequently, QRS duration and the H-V interval in the His bundle ECG remain unaltered. Only in the case of verapamil and, to a lesser extent, in the case of nifedipine have relative prolongations of the atrial refractory period in relation to the duration of the action potential been reported (Landmark and Amlie 1976; Seipel et al. 1983). Bepridil, a substance additio l1ally exhibiting an effect on the fast sodium channel, extends the refractory period in the atrium and the ventricle, (Rowland et al.
The relative efficacies in vitro of the various compounds are shown in Table 6. In vivo, owing to the role of autonomic counter-regulation (which depends on the dose given and the extent of individual vasoselectivity), individual substances produce different effects. Thus, while nifedipine either has no influence or even accelerates AV conduction and the effective refractory period of the AV node (Furlanello et al. 1980; Mitchell et al. 1982), verapamil (Mitchell et al. 1982; Seipel et al. 1983), diltiazem (Sugimoto et al.