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Biomedical subjects

R R Abendroth

Publications and source records attributed to R R Abendroth.

30 records · Page 2Linked to original sources
PubMed1980

[Demonstration of retrograde block in a patient with preexcitation syndrome by intraoperative electrophysiological studies (author's transl)].

In a patient with a WPW syndrome, the electrophysiological investigation revealed a left-sided bypass conducting only in antegrade (A-V) direction. During right ventricular stimulation, there was a complete retrograde (V-A) block. Therefore no reentry tachycardia could be initiated. The patient was operated upon because of an aortic valve lesion. During operation the bypass was localized at the free wall of the mitral annulus by epicardial mapping. Even during direct stimulation at the ventricular insertion of the bypass, no retrograde conduction to the left atrium could be demonstrated. After ablation of the bypass by surgery, intra- and postoperative electrophysiological studies showed a normal antegrade activation pattern of the ventricles. The case reported demonstrates that the "heterodromia" of an accessory bypass can markedly influence the clinical setting in the WPW syndrome.

Action Potentials↗
PubMed1980

[The electrophysiological effects of the Ca-antagonists gallopamil (D 600), dimeditiapramine (Ro 11-1781) and verapamil in man (author's transl)].

The electrophysiological effects of D 600 (D) (0.03 mg/kg i.v., 10 pts) and Ro 11-1781 (Ro) (1.0 mg kg i.v., 10 pts) were compared with those of verapamil (V) (0.1 mg/kg i.v., 20 pts). All three Ca-antagonists caused a slight shortening of the cycle length which was only significant after verapamil. There was practically no change in SNRT. As a consequence, the SNRT corrected for heart rate (CNSRT) increased insignificantly in all three groups (control C): 359.7 +/- 174.8 ms, V: 397.1 +/- 204.6 ms; C: 362.5 +/- 125.2 ms, Ro: 420.8 +/- 179.0 ms; C: 339.5 +/- 93.6 ms, D: 407.7 +/- 272.0 ms). In addition, the calculated "sinoatrial conduction time" increased insignificantly (C: 84.3 +/- 23.0 ms, V: 101.3 +/- 39.4 ms; C: 105.2 +/- 35.1 ms, Ro: 114.8 +/- 31.9 ms) or did not change (C: 105.9 +/- +/- 20.6 ms, D: 101.6 +/- 32.2 ms). The conduction time from high-to-low right atrium (HRA-A) as well as the His-ventricle time (HV) and the conduction interval from the septum to the right ventricular apex (V RVA) did not change. In contrast, the conduction time through the AV node (A-H) was significantly prolonged by all three drugs (C: 78.1 +/- 16.0 ms, V: 88,4 +/- 19.5 ms; C: 92.9 +/- 16.2 ms, Ro: 104.3 +/- 19.1 ms; C: 88.5 +/- 20.0 ms, D: 102.5 +/- 22.6 ms). The effective refractory period of the AV node (ERP AVN) was significantly prolonged by verapamil (C: 290.0 +/- 77.6 ms, V: 360.5 +/- 93.3 ms) and by D 600 (C: 266.7 +/- 72.6ms, D: 380.0 +/- 112.7 ms). Ro 11-1781 did not show any effect on this parameter. As a consequence, the Wenckebach point during high rate atrial pacing was significantly lowered by Verapamil and D 600, but only insignificantly by Ro 11-1781. The refractoriness of the right atrium and ventricle was not altered by any of the drugs. The results show that all three Ca-antagonists have similar electrophysiological effects in man after acute i.v. application. In the dose given, D 600 and verapamil are equipotent, whereas Ro 11-1781 is less effective.

Blood Pressure↗
PubMed1979

[Electrophysiological mapping during open-heart surgery (author's transl)].

Intraoperative electrophysiological mapping provides a method to identify the specialized atrioventricular conduction system and to localize the morphological origin of different tachycardiac rhythm disorders at time of surgery. The basic technical aspects and methodical implications are presented with respect to its clinical applications.

Atrioventricular Node↗
PubMed1976

[Acute myocardial infarct and pindolol. Effect of a beta sympatholytic with intrinsic sympathomimetic activity on hemodynamics and contractility].

After acute circumscribed myocardial infarction the effects of the beta-sympatholytic agent 1-(indol-4-yl-oxy)-3-isopropyl-amino-propan-2-ol (pindolol; Visken) on hemodynamics and contractility were examined. Hemodynamic changes after application of pindolol are of small extent only. Heart rate shows a rising tendency whereas systolic and diastolic aortic pressure decreases only after higher doses. Left ventricular end-diastolic pressure (LVEDP) does not change remarkably. Cardiac output is reduced by small doses of pindolol and reaches starting values again before the administration of higher doses. Changes of the contractility parameters (dp/dt)max, t-(dp/dtmax, and PEP in the sense of a beta-sympatholysis appear only in the lower range of the doses given. Thus maximum decrease of contractility is 20% measured at (dp/dt)max, which consequently reaches the starting value again. The other contractility parameters change accordingly. These typical dose-response relations between pindolol and contractility parameters are considered to be due to lacking cardiac depressive properties combined with significant so-called positive intrinsic activity. Our results show that no contraindication can be derived from the small influence of pindolol on contractility in acute myocardial infarction.

Animals↗
PubMedDate not supplied

Comparison of the antiarrhythmic efficacy of disopyramide and mexiletine against stimulus-induced ventricular tachycardia.

Programmed ventricular stimulation was used to assess the effect of oral disopyramide (600 mg/day), mexiletine (600--1000 mg/day), and a combination of both drugs in a randomized cross-over study on 12 patients with documented ventricular tachycardia and/or fibrillation. In two cases, all three types of treatment were ineffective in that ventricular tachycardia could still be initiated under the same conditions. In four cases, disopyramide and mexiletine alone were ineffective or the change in inducibility was only slight. However, when both drugs were administered in combination, ventricular tachycardia was more difficult to induce or was no longer inducible. In two other cases, disopyramide was the more effective drug. In the remaining four patients, all three types of treatment were similarly effective. In patients whose ventricular tachycardia remained inducible its rate decreased from 188 +/- 45 bpm (control) to 170 +/- 40 bpm on disopyramide, 172 +/- 31 bpm on mexiletine, and 146 +/- 39 bpm on disopyramide plus mexiletine. Long-term therapy was based on the results of acute testing. Seven patients received both disopyramide and mexiletine and tolerated this therapy well during a follow-up of 42 +/- 23 weeks. Two sudden deaths occurred, one possibly due to dose reduction and one in a patient in whom short bursts of ventricular tachycardia remained inducible during acute testing. We conclude that the combined administration of disopyramide and mexiletine is effective and safe in patients with ventricular tachycardia. It is tolerated without major side effects even during long-term therapy.

Adult↗