ajmaline and Cardiomyopathy--Dilated

The electrophysiological and haemodynamic effects of lidocaine (100 mg) and ajmaline (50 mg) were evaluated while attempting to interrupt sustained ventricular tachycardia. The study was performed as a prospective, non-blinded, randomized investigation in 61 patients. Lidocaine terminated ventricular tachycardia in four of 31 patients, ajmaline in 19 of 30 patients (P less than 0.001). QRS and RR intervals during ventricular tachycardia were prolonged by ajmaline from 164 +/- 28 ms to 214 +/- 49 ms and from 371 +/- 86 ms to 479 +/- 137 ms (P less than 0.001), respectively; lidocaine did not influence these parameters. The duration of the return cycles after termination of ventricular tachycardia did not differ between the two groups. Lidocaine did not change cardiac output during ventricular tachycardia whereas cardiac output increased significantly under ajmaline from 3.5 +/- 1.21.min-1 to 5.5 +/- 1.91.min-1 (P less than 0.001). It is concluded that anti-arrhythmic agents such as ajmaline, which slow conduction velocity and prolong refractoriness, are more effective than lidocaine in the medical treatment of haemodynamically stable, sustained ventricular tachycardia.

Topics: Ajmaline; Cardiac Output; Cardiac Pacing, Artificial; Cardiomyopathy, Dilated; Coronary Disease; Electrocardiography; Female; Heart Rate; Heart Valve Diseases; Heart Ventricles; Hemodynamics; Humans; Lidocaine; Male; Middle Aged; Tachycardia

The Brugada sign has been associated with mutations in SCN5A and with right ventricular structural abnormalities. Their role in the Brugada sign and the associated ventricular arrhythmias is unknown.. The purpose of this study was to delineate the role of structural abnormalities and sodium channel dysfunction in the Brugada sign.. Activation and repolarization characteristics of the explanted heart of a patient with a loss-of-function mutation in SCN5A (G752R) and dilated cardiomyopathy were determined after induction of right-sided ST-segment elevation by ajmaline. In addition, right ventricular structural discontinuities and sodium channel dysfunction were simulated in a computer model encompassing the heart and thorax.. In the explanted heart, disappearance of local activation in unipolar electrograms at the basal right ventricular epicardium was followed by monophasic ST-segment elevation. The local origin of this phenomenon was confirmed by coaxial electrograms. Neither early repolarization nor late activation correlated with ST-segment elevation. At sites of local ST-segment elevation, the subepicardium was interspersed with adipose tissue and contained more fibrous tissue than either the left ventricle or control hearts. In computer simulations entailing right ventricular structural discontinuities, reduction of sodium channel conductance or size of the gaps between introduced barriers resulted in subepicardial excitation failure or delayed activation by current-to-load mismatch and in the Brugada sign on the ECG.. Right ventricular excitation failure and activation delay by current-to-load mismatch in the subepicardium can cause the Brugada sign. Therefore, current-to-load mismatch may underlie the ventricular arrhythmias in patients with the Brugada sign.

Topics: Adolescent; Ajmaline; Anti-Arrhythmia Agents; Brugada Syndrome; Cardiomyopathy, Dilated; Chromatography, High Pressure Liquid; Computer Simulation; Electrocardiography; Electrophysiologic Techniques, Cardiac; Female; Genetic Predisposition to Disease; Heart Transplantation; Humans; In Vitro Techniques; Lamin Type A; Muscle Proteins; Mutation; NAV1.5 Voltage-Gated Sodium Channel; Sodium Channels; Ventricular Dysfunction, Right

Topics: Action Potentials; Ajmaline; Anti-Arrhythmia Agents; Brugada Syndrome; Cardiomyopathy, Dilated; Computer Simulation; Electrocardiography; Electrophysiologic Techniques, Cardiac; Humans; Sodium Channels; Ventricular Dysfunction, Right

The hemodynamic effect of the intravenous application of ajmaline (50 mg) was studied during persistent ventricular tachycardia. With the onset of ventricular tachycardia an increase of heart rate up to 177 +/- 40 bpm and a simultaneous decrease of cardiac output from 7.1 +/- 2.7 l/min to 3.4 +/- 1.1 l/min (p less than 0.001) could be demonstrated. Ajmaline prolonged the QRS interval and slowed the ventricular tachycardia rate to 133 +/- 28 bpm. Simultaneously, an increase of cardiac output to 5.9 +/- 2.3 l/min (p less than 0.001) could be documented. A significant correlation between the increase of cardiac output and the change of ventricular tachycardia rate was found. A drug-induced termination of ventricular tachycardia by ajmaline was possible in 60% of patients. Intravenous application of ajmaline during persistent ventricular tachycardia leads to a hemodynamic improvement caused by the reduction of the tachycardia rate. This temporary stabilization of the hemodynamic status is important for emergency treatment of ventricular tachycardia.

Topics: Adult; Aged; Ajmaline; Cardiac Output; Cardiomyopathy, Dilated; Coronary Disease; Heart Rate; Humans; Infusions, Intravenous; Middle Aged; Tachycardia