Cardiac electrophysiologic properties of intravenous isradipine in patients with sick sinus syndrome.
Isradipine is a new dihydrophyridine calcium antagonist with powerful vasodilating properties. Although therapeutic concentrations do not affect myocardial contractility in vivo, in vitro studies have demonstrated a negative chronotropic action with only minor dromotropic influence. In humans with normal sinus and atrioventricular node function, even in the presence of beta-blockade, such a negative chronotropic effect could not be proved. No data are available on the effects of isradipine on a compromised sinus node. Therefore, the effect of intravenous isradipine at 0.3 microgram/kg/minute for 30 minutes was studied in seven patients with the clinical signs of a sick sinus syndrome. Mean arterial blood pressure decreased from 126 +/- 21 to 113 +/- 15 mm Hg (p less than 0.05). Spontaneous sinus cycle length decreased from 969 +/- 22 to 843 +/- 161 msec (p less than 0.05). Changes in sinoatrial conduction time, sinus node recovery time, and corrected sinus node recovery time were not significant. Changes in atrioventricular node function, as reflected by the atrioventricular node functional refractory period, the atrial-His interval, the His-ventricle interval, and Wenckebach point were not significant. Also, effective refractory periods of atrium and ventricle, and QRS duration changed but not significantly. The QT interval decreased (419 +/- 45 to 405 +/- 44 msec; p less than 0.05), and there was a slight (not significant) increase of QTc interval (429 +/- 41 to 443 +/- 37 msec; not significant). It is concluded that isradipine in hemodynamically effective doses has no depressant effect on sinus and atrioventricular node function in patients with sick sinus syndrome.[1]References
- Cardiac electrophysiologic properties of intravenous isradipine in patients with sick sinus syndrome. van Wijk, L.M., van Gelder, I., Crijns, H.J., van den Toren, E.W., Lie, K.I., Rüegg, P.C. Am. J. Med. (1989) [Pubmed]
Annotations and hyperlinks in this abstract are from individual authors of WikiGenes or automatically generated by the WikiGenes Data Mining Engine. The abstract is from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.About WikiGenesOpen Access LicencePrivacy PolicyTerms of Useapsburg
