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[Comparative studies on the contractile and hemodynamic effects of antiarrhythmic agents (lidocaine, diphenylhydantoin, ajmaline) (author's transl)].
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The contractile and hemodynamic effects of lidocaine, diphenylhydantoin and ajmaline were compared in isolated ventricular myocardium and in patients during diagnostic cardiac catheterization. The animal experiments show that diphenylhdantoin is 3-5 times more potent as a contractility inhibitor
Ajmaline Testing and the Brugada Syndrome
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Brugada syndrome (BrS) diagnosis requires the presence of a typical type 1 ECG pattern. Owing to the spontaneous ECG variability, the real BrS prevalence in the general population remains unclear. The aim of the present study was to evaluate the prevalence of positive ajmaline challenge for BrS in a
[Comparative effects of ajmaline and lidocaine on hemodynamics in myocardial infarct].
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Haemodynamic changes after single intravenous injection of antiarhythmic doses of ajmaline (50 mg) and lidocain (100 mg) were measured comparatively in 10 patients with acute myocardial infarction, stable cardiac rhythm and without manifest left heart failure. The effects of ajmaline were
[Effect of the class IA anti-arrhythmic agents ajmaline on end-systolic pressure-volume relations (conductance technique)].
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To evaluate cardiodepressive risks of antiarrhythmic treatment with ajmaline, we monitored, in addition to conventional hemodynamic parameters, end systolic pressure-volume relations (ESPVR) to assess potential negative inotropic effects. Twelve patients (CAD without ischemia; EF = 60 +/- 3%)
Do class 1 antiarrhythmic drugs impair myocardial contractility? The class 1A example of ajmaline (conductance catheter technique).
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Antiarrhythmic drug effects may include cardiodepression. This risk is theoretically well recognized but clinically rather poorly defined. To evaluate the risks of ajmaline treatment, we monitored hemodynamic parameters and end-systolic pressure-volume relations (ES-PVR) to evaluate potential
Protective effects of antiarrhythmic agents against anoxic injury in CNS white matter.
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Irreversible anoxic injury is dependent on extracellular Ca2+ in mammalian CNS white matter, with a large portion of the pathologic Ca2+ influx occurring through reverse Na(+)-Ca2+ exchange, stimulated by increased intracellular [Na+]. This Na+ leak likely occurs via incompletely inactivated
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