ajmaline and Tachycardia

Topics: Adult; Aged; Ajmaline; Electrocardiography; Heart Arrest; Humans; Male; Middle Aged; Tachycardia; Verapamil

Antiarrhythmic treatment is based on the hypothesis that ventricular premature beats (VPBs), in the presence of underlying cardiac disease and impaired ventricular function, may predispose to sudden cardiac death. The effectiveness of treatment, however, has not been proven. For acute treatment of paroxysmal ventricular tachycardia, on comparison of the effectiveness of lidocaine and ajmaline, some new aspects have been rendered. VENTRICULAR PREMATURE BEATS (VPB): Isolated VPBs can be found in 40 to 75% of healthy subjects; if their number is substantial, investigation is warranted. For VPBs with subjective symptoms, beta-receptor blockers or specific antiarrhythmic agents, if necessary in combination, may be given. In several studies it has been shown that the prognosis of patients with frequent and complex VPBs, that is couplets and salvos, without heart disease is not compromised. In one long-term study over an average of 6.5 years, sudden death was observed in only one of 70 subjects who had 566 VPBs/24 hours, 60% additionally couplets and 26% salvos in the Holter ECG. Accordingly, treatment for the sake of prognosis is not warranted. For patients with mitral valve prolapse or only mildly impaired ventricular function and asymptomatic arrhythmias, treatment is not necessary since it has not been shown to be beneficial. Coronary artery disease is the most frequent cause of ventricular arrhythmias and sudden death. In numerous studies in patients after myocardial infarction, a relationship has been recognized between frequent and complex VPBs and overall mortality as well as sudden death. Particularly at risk are patients with very frequent and complex VPBs with additional impairment of ejection fraction to less than 30 to 40% but this group only accounts for 10% of patients after infarction. Only in one interventional study, carried out with aprindine, there was a significant reduction in overall mortality from 12.5 to 7.8% with an adverse reaction rate, however, of 21%. In high-risk patients with a low ejection fraction and numerous, complex VPBs as well, in a further study with aprindine, after one year, there was no decrease in overall mortality as compared with the placebo group. The cause for the insufficient effectiveness of the antiarrhythmic agents in various interventional studies has been attributed to a limited number of patients, rigid dosing regimens, inadequate suppression of VPBs and a high incidence of adverse reactions. In the multicen

Topics: Ajmaline; Anti-Arrhythmia Agents; Electrocardiography; Follow-Up Studies; Heart Ventricles; Humans; Lidocaine; Tachycardia

Topics: Adolescent; Adrenergic beta-Antagonists; Adult; Aged; Ajmaline; Amiodarone; Anilides; Aprindine; Atrial Fibrillation; Benzofurans; Digitalis Glycosides; Disopyramide; Encainide; Female; Humans; Lidocaine; Male; Middle Aged; Procainamide; Quinidine; Tachycardia; Verapamil; Wolff-Parkinson-White Syndrome

The more recent antiarrhythmic drugs sometimes with more complex action extend the therapeutic possibilities. In addition, numerous other substances are in clinical trial. An ideal antiarrhythmic agent with a reliable action, persistent effective levels, easily absorbable and with few side effects is not found among them. The indication for therapy in ventricular extrasystole is made on the grounds of an ominous ECG criteria and a presumed clinical threat. Controversial results of lidocaine therapy of acute mayocardial infarction are possibly due to pharmacokinetic factors. For "inhomogeneous repolarization" with increased tendency to ventricular fibrillation inducing drugs should be avoided. Malignant cardiac rhythm irregularities possible leading to sudden death require systemic therapeutical testing. In this case, combinations of antiarrhythmic drugs have the highest effectiveness.

Topics: Action Potentials; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Bretylium Compounds; Calcium; Cardiac Complexes, Premature; Digoxin; Disopyramide; Electrophysiology; Humans; Lidocaine; Mexiletine; Myocardial Infarction; Phenytoin; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Verapamil

Topics: Adult; Aged; Ajmaline; Animals; Arrhythmias, Cardiac; Atropine; Bretylium Compounds; Cardiac Complexes, Premature; Coronary Care Units; Dogs; Electrocardiography; Female; Heart Block; Humans; Isoproterenol; Lidocaine; Male; Myocardial Infarction; Pacemaker, Artificial; Phenytoin; Procainamide; Quinidine; Tachycardia; Ventricular Fibrillation

Topics: Adult; Ajmaline; Atropine; Cardiac Catheterization; Digitalis Glycosides; Electric Stimulation; Electrocardiography; Heart; Heart Atria; Heart Conduction System; Humans; Male; Methods; Pacemaker, Artificial; Procainamide; Propranolol; Quinidine; Tachycardia; Vagus Nerve; Wolff-Parkinson-White Syndrome

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 efficacy of ajmaline (50-75 mg i.v.) or lidocaine (100-200 mg i.v.) in terminating persistent, haemodynamically stable ventricular tachycardia (VT) was compared in a prospective, randomized trial of 31 patients. There were no significant differences as to age, underlying heart disease, ejection fraction and rate of ventricular tachycardia between the two treatment groups. Ajmaline terminated VT in 10 of the 15 patients receiving it, lidocaine in only 2 of 16 (P less than 0.01). The frequency of VT was not significantly changed by lidocaine, while mean cycle length during VT changed under ajmaline from 369 +/- 82 ms to 452 +/- 11 ms (P less than 0.01). In contrast to lidocaine, QRS duration under ajmaline lengthened from 166 +/- 18 ms to 200 ms +/- 28 ms (P less than 0.01), but return cycles after tachycardia termination were similar (ajmaline, 863 +/- 296 ms; lidocaine, 917 +/- 367 ms). Both drugs were equally well tolerated, but in this series ajmaline was more effective in the acute treatment of persistent VT.

Topics: Ajmaline; Clinical Trials as Topic; Electrocardiography; Emergencies; Humans; Lidocaine; Prospective Studies; Random Allocation; Recurrence; Tachycardia; Time Factors

In an open randomized therapeutic study, 20 patients known to have frequent ventricular premature beats (VPB) and/or ventricular pairs (VP) were treated with both 2 X 200 mg flecainide (F) and 4 X 20 mg prajmalium-bitartrate (P) for 3 months each. There was a drug-free interval of one week between the two therapy phases. 24-hour long-term ECG-registrations were carried out before the start of the therapy phases as well as 1 week, 1 month, 2 months and 3 months after the initiation of antiarrhythmic therapy. After one week, the group as a whole evidenced a VPB reduction of 94% under F and only 57% under P (p less than or equal to 0.05). The percentage of individual patients in whom there was a statistically significant VPB reduction was also higher under F than under P (65% vs. 40%). In the group as a whole, there was a VP reduction of 99% under F and 88% under P (p less than or equal to 0.05) after one week. Of the 13 individuals with frequent VP (over 16 VP/24 h), a significant reduction was seen in 77% under F and only 38% under P. The difference between the two antiarrhythmic agents registered after one week was also observed in the further course of therapy but could no longer be statistically confirmed for the ventricular pairs. An aggravation of ventricular arrhythmias was observed in 2 patients under F and in 3 under P.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Ajmaline; Cardiac Complexes, Premature; Clinical Trials as Topic; Electrocardiography; Female; Flecainide; Heart Ventricles; Humans; Male; Middle Aged; Prajmaline; Random Allocation; Tachycardia

Topics: Acute Coronary Syndrome; Ajmaline; Angioplasty, Balloon, Coronary; Antibodies, Monoclonal, Murine-Derived; Antineoplastic Combined Chemotherapy Protocols; Chest Pain; Contraindications; Coronary Angiography; Cyclophosphamide; Dizziness; Doxorubicin; Dyspnea; Heart Neoplasms; Humans; Lymphoma, Follicular; Male; Middle Aged; Prednisone; Rituximab; Tachycardia; Tomography, X-Ray Computed; Ultrasonography; Vincristine

Bradycardic (heart rate<50/min) and tachycardic heart rhythm disturbances (100/min) require rapid therapeutic strategies. Supraventricular tachycardias (SVT) are sinus tachycardia, atrial tachycardia, AV-nodal reentrant tachycardia and tachycardia due to accessory pathways. Mostly SVT are characterized by small QRS complexes (QRS width<0.12 ms). It is essential to evaluate the arrhythmia history, to perform a good physical examination and to exactly analyze the 12-lead electrocardiogram. An exact diagnosis is then possible in >90% of SVT patients. Ventricular tachycardias have a broad QRS complex (>or=0.12 s), ventricular flutter and ventricular fibrillation are associated with chaotic electrophysiologic findings. For acute therapy, we will present the new concept of the "5A" that includes adenosine, adrenaline, ajmaline, amiodarone and atropine. Additional "B, C and D strategies" include betablocking agents, cardioversion as well as defibrillation. The "5A" concept allows a safe and effective antiarrhythmic treatment of all bradycardic and tachycardic arrhythmias as well as asystolia.

Topics: Adenosine; Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Atropine; Bradycardia; Defibrillators, Implantable; Electric Countershock; Electrocardiography; Emergencies; Epinephrine; Heart Rate; Humans; Pacemaker, Artificial; Signal Processing, Computer-Assisted; Tachycardia

Topics: Adenosine; Ajmaline; Diagnosis, Differential; Electrocardiography; Family Practice; Hemodynamics; Humans; Patient Care Team; Tachycardia

Ajmaline, a reserpine derivative, is an effective class I antiarrhythmic agent. Herein we report two cases of ajmaline-induced abnormal QT prolongation accompanied by polymorphic ventricular tachycardia of the torsade de pointes type. Since ajmaline is increasingly used for the acute termination of wide complex tachycardia and as a diagnostic tool after syncope and in patients with idiopathic ventricular tachyarrhythmias, our observations suggest that caution should be exercised with regard to the effects of the drug on the QT interval and its potency to induce proarrhythmia of the torsade de pointes type.

Topics: Ajmaline; Anti-Arrhythmia Agents; Atrial Flutter; Electrocardiography; Female; Humans; Long QT Syndrome; Male; Middle Aged; Tachycardia; Tachycardia, Ventricular; Torsades de Pointes

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

Up to now lidocain was regarded as remedy of first choice in life-threatening ventricular arrhythmias. According to more recent investigations in the emergency situation ajmalin showed itself superior to lidocain in the treatment of ventricular tachycardias. For the prophylaxis of primary ventricular fibrillation lidocain is still recommended, though despite numerous studies an effectiveness is not verified. The treatment of the primary ventricular fibrillation should always be performed by defibrillation as far as possible. The earlier it is performed the more successful is the measure. If a defibrillator is not at disposal an attempt with lidocain or ajmalin can bie made.

Topics: Ajmaline; Combined Modality Therapy; Electric Countershock; Electrocardiography; Emergencies; Heart Ventricles; Humans; Lidocaine; Myocardial Infarction; Tachycardia; Ventricular Fibrillation

120 cases of class IC antiarrhythmic overdose, including propafenone, flecainide, ajmaline and prajmaline overdose, were evaluated with respect to clinical course, therapy and outcome. Whereas drug overdose in general has an overall mortality of less than 1%, intoxication with antiarrhythmic drugs of class IC was associated with a mean mortality of 22.5%. Nausea, which occurred within the first 30 minutes after ingestion, was the earliest symptom. Spontaneous vomiting probably led to self-detoxication in about half the patients. Cardiac symptoms including bradycardia and, less frequently, tachyrhythmia occurred after about 30 minutes to 2 hours. Therapeutic measures included administration of activated charcoal, gastric lavage and a saline laxative, catecholamines, and in some patients, hypertonic sodium bicarbonate, insertion of a transvenous pacemaker and hemoperfusion. Fatal outcome was mainly due to cardiac conduction disturbances progressing to electromechanical dissociation or asystolia. Resuscitation, which had to be performed in 29 patients, was successful in only two of them. No correlation was found between fatal outcome, the type of antiarrhythmic, and ingested dose. Since a specific treatment is not available and resuscitive procedures including sodium bicarbonate and insertion of a pacemaker are of limited therapeutic value, early diagnosis and primary detoxification are most important for prevention of fatal outcome.

Topics: Ajmaline; Anti-Arrhythmia Agents; Bicarbonates; Bradycardia; Drug Overdose; Flecainide; Hemoperfusion; Humans; Hypertonic Solutions; Nausea; Prajmaline; Propafenone; Resuscitation; Retrospective Studies; Sodium; Sodium Bicarbonate; Tachycardia; Vomiting

We report a case of bidirectional tachycardia (BT) found on Holter recording (H-ECG), likely due to antiarrhythmic therapy with lorajmine. The patient, who was not on digitalis therapy and had good myocardial function, was investigated for presyncope. H-ECG revealed frequent premature ventricular complexes (PVC). Disopyramide, lorajmine and amiodarone (in succession) were ineffective in controlling the arrhythmias. During therapy with lorajmine (600 mg/die) H-ECG showed numerous symptomless episodes of BT. Two forms of BT were found. In the first one the PVC had a right bundle branch block (BBB) pattern in lead CM1 and alternating polarity (Rs-rS) in lead CM5, whereas in the second one an alternating right and left BBB pattern in CM1 was found. PVC were subsequently controlled with flecainide. In a 4-year follow-up period the patient underwent several H-ECGs, both with and without antiarrhythmic drugs; however, BT episodes were found only during lorajmine therapy. Thus, this drug was likely responsible for the appearance of BT episodes.

Topics: Aged; Ajmaline; Electrocardiography, Ambulatory; Humans; Male; Tachycardia

A 23-year-old woman was hospitalized because of life-threatening monomorphic ventricular tachycardia (VT) of 150 beats/min. An intravenous bolus of lidocaine was without effect but 25 mg ajmaline converted the tachycardia to sinus rhythm. A total of 70 mg ajmaline was subsequently infused because of frequent ventricular premature systoles. During this treatment polymorphic VT with very wide QRS complexes developed, but spontaneously disappeared after ajmaline had been discontinued. The case demonstrates the need for taking into account the potential risk of a proarrhythmic effect of anti-arrhythmic drugs.

Topics: Adult; Ajmaline; Arrhythmias, Cardiac; Electrocardiography; Female; Humans; Infusions, Intravenous; Lidocaine; Sotalol; Tachycardia

1. The pharmacokinetics and the dromotropic action (increased PQ interval) of intravenously administered ajmaline (2 mg kg-1) were studied in hyperthyroid rats with sinus tachycardia. The hyperthyroidism was induced by intraperitoneal injection of 3,5,3'-triiodo-L-thyronine (0.5 mg kg-1) for 4 days. 2. The change in the ajmaline concentration in whole blood could be described by a biexponential equation. The steady state distribution volume of ajmaline decreased from 4.81 l kg-1 in control rats to 3.80 l kg-1 in hyperthyroid rats and the total body blood clearance was slightly higher in hyperthyroid rats than in control rats. 3. Ajmaline exhibited a saturable binding to rat plasma proteins, and one kind of binding site was found in the observed range of concentrations. The binding capacity was 2 fold higher in hyperthyroid rats than in control rats. 4. On the basis of the plasma unbound concentration, ajmaline exhibited an increased negative dromotropic activity in hyperthyroid rats compared with control rats. 5. A positive correlation was found between the pacing rate and the dromotropic action of ajmaline on atrioventricular conduction in isolated perfused hearts. There was no significant difference in the rate-dependence of the effect of ajmaline on the heart between control and hyperthyroid rats. 6. Our findings suggest that the increased dromotropic activity of ajmaline is mainly due to the increased heart rate in hyperthyroid rats.

Topics: Ajmaline; Animals; Heart; Hyperthyroidism; In Vitro Techniques; Male; Protein Binding; Rats; Rats, Inbred Strains; Tachycardia; Triiodothyronine

Thirty-five patients with bundle branch block (BBB) and unexplained syncope underwent electrophysiologic study (EPS) including programmed ventricular stimulation and ajmaline administration (1 mg/kg, IV) to induce infra-His block. A prolonged HV interval (greater than 55 ms) was present in 16 of the 35 patients. Ajmaline-induced HV block occurred in 12 patients (complete HV block in 10, and 2:1 HV block in two). Monomorphic ventricular tachycardia (VT) was inducible in nine (25.7%) and polymorphic VT in two patients (5.7%). Left ventricular ejection fraction (LVEF) was less than 40% in five patients (45.5%) with inducible VT. Two patients had an unexpected co-existence of inducible HV block and VT. The remaining 14 patients (40%) had no detectable abnormality. The incidence of inducible VT was higher (45% vs 13.3%), and the presence of negative studies was lower (30% vs 53.3%) in patients with structural heart disease (n = 20), when compared to those with no significant heart disease (n = 15) (differences not significant [NS]). During a mean follow-up period of 16.5 +/- 9.2 months, all the patients with inducible HV block have been asymptomatic after having received permanent pacemakers. Patients with inducible monomorphic VT (except one with poor left ventricular function who died suddenly) have also been asymptomatic on antiarrhythmic drugs. Of the remaining patients, seven with normal EPS, two with prolonged HV intervals but no inducible HV block (despite being given permanent pacemakers) and one patient with polymorphic VT on antiarrhythmic drugs continue to have recurrent syncope. Approximately 60% of patients with BBB and unexplained syncope have clinically significant electrophysiologic abnormalities.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adult; Aged; Ajmaline; Bundle-Branch Block; Cardiac Pacing, Artificial; Electric Stimulation; Electrophysiology; Female; Heart Block; Heart Conduction System; Humans; Male; Middle Aged; Monitoring, Physiologic; Prospective Studies; Syncope; Tachycardia

The fitness of patients with Wolff-Parkinson-White syndrome to indulge in sporting activities is a practical cardiology problem. The major risk is sudden death due to atrial fibrillation deteriorating to ventricular fibrillation. This risk is small or even theoretical, but signing a fitness certificate engages the clinician's responsibility. Non invasive complementary examinations are useful. Echocardiography may detect a heart disease that would preclude any sport. Exercise tests explore the behaviour of the accessory pathway and rarely trigger off arrhythmias. Holter recordings mainly investigate disorders of the atrial rhythm. The decision concerning fitness may be based on clinical symptoms. Exercise-induced tachycardia is a classical contra-indication to competitive sports. In patients whose tachycardia is unrelated to exercise, fitness may be discussed according to the results of exercise tests and of the electrophysiological study. A refractory period which would be considered as rather prolonged at rest does not protect against fast ventricular rate during passage to atrial fibrillation. If pre-excitation disappears during the exercise test in an asymptomatic patient, then competitive sports can be authorized without limitations. If not, only surgical excision or fulguration would provide full protection against a potentially dangerous fibrillation. It is concluded that Wolff-Parkinson-White syndrome contra-indicates competitive sports in most cases. Games played outside competitions remain possible in the absence of symptoms or when arrhythmias are well controlled by medical treatment.

Topics: Ajmaline; Electrocardiography; Exercise Test; Humans; Monitoring, Physiologic; Physical Fitness; Sports; Tachycardia; Wolff-Parkinson-White Syndrome

Topics: Acetanilides; Ajmaline; Electrocardiography; Female; Heart Block; Humans; Isoproterenol; Middle Aged; Tachycardia; Trimecaine

A 55-year old male patient, with dizzy spells during everyday activity and a complete right bundle branch block as the sole electrocardiographic abnormality, reproducibly demonstrated tachycardia-dependent Mobitz Type II- and 2:1 second degree atrioventricular block. An electrophysiologic study revealed a provocable block within the distal portion of the bundle of His without evidence of a split His potential. Because of the truly tachycardia-dependent AV-block, beta-blocker medication was initiated to prevent high sinus rates during everyday activity. This therapy abolished symptoms totally.

Topics: Ajmaline; Bundle of His; Bundle-Branch Block; Cardiac Pacing, Artificial; Electrocardiography; Heart Block; Humans; Male; Middle Aged; Purkinje Fibers; Tachycardia

We prospectively evaluated and followed-up 45 patients with syncope in whom conventional cardiovascular and neurological investigations did not reveal the cause. All patients underwent electrophysiologic studies to assess the function of the sinus node and the integrity of atrioventricular conduction. These included the ajmaline test and the inducibility of supraventricular or ventricular tachycardia. Seven patients (15.5%) had evidence of sinus node dysfunction, 8 patients (17.7%) had evidence of infra-His atrioventricular block after ajmaline administration and 5 patients (11.1%) had inducible ventricular tachycardia. The remaining 25 patients (55.5%) had non-diagnostic studies. All patients with sinus node dysfunction and inducible infra-His atrioventricular block were asymptomatic during a mean follow-up period of 14.3 +/- 9.5 months after implantation of a permanent pacemaker. Patients with inducible ventricular tachycardia (except 1 with poor left ventricular function who died) were likewise asymptomatic while receiving laboratory guided anti-arrhythmic drug therapy. Twenty-five patients with non-diagnostic studies who were treated empirically are alive but the symptoms persist in 14 (56%). Provocative electrophysiological studies are of diagnostic and therapeutic utility in a significant number of patients with recurrent syncope of "unknown cause".

Topics: Adult; Aged; Ajmaline; Cardiac Catheterization; Electrocardiography; Female; Heart Block; Heart Conduction System; Humans; Male; Middle Aged; Pacemaker, Artificial; Sinoatrial Node; Syncope; Tachycardia

Topics: Ajmaline; Cardiomyopathies; Humans; Tachycardia

Bepridil has been shown to block both slow- and fast-channel activity in the heart. Electrophysiologic studies in man demonstrate that oral and intravenous bepridil prolongs sinus cycle length, PR interval and QT interval, without apparently changing the QRS interval. In addition, the drug depresses atrioventricular (AV) nodal conduction, resulting in an increased AH interval. Refractoriness in the AV node, atrium and ventricle is increased. There is usually little or no change in the HV interval. The antiarrhythmic properties of bepridil have been noted in patients with supraventricular tachycardia, ventricular premature complexes (VPCs) and sustained ventricular tachycardia (VT). In 17 patients, intravenous bepridil was compared with either verapamil or ajmaline. AV nodal reentrant tachycardia was terminated in all patients with bepridil and verapamil. However, ajmaline was somewhat more effective than bepridil in patients with AV reentry (8 of 8 versus 5 of 8). In 12 of these 17 patients, oral bepridil (500 mg/day for 3 days) suppressed the induction of tachycardia or slowed its rate. In 3 studies of oral bepridil for VPCs, the drug was effective in 68%, 69% and 70% of patients. Another group of studies evaluated bepridil in a total of 30 patients with sustained VT. Intravenous bepridil terminated VT in 17 of 26 patients. The induction of VT by programmed ventricular stimulation was also prevented in 7 of 17 patients. Although torsade de pointes has been reported, its incidence appears to be low.

Topics: Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bepridil; Calcium Channel Blockers; Electrocardiography; Electrophysiology; Heart Conduction System; Heart Rate; Humans; Pyrrolidines; Tachycardia; Verapamil

Bepridil (2 mg/kg intravenously) was given to 20 patients with atrioventricular (AV) reentrant tachycardia and its effects were compared with those of verapamil (0.15 mg/kg intravenously) in 8 patients and ajmaline (0.75 mg/kg intravenously) in 12. After baseline electrophysiologic measurements, the drugs were given during sustained AV reentrant tachycardia (8 patients had dual AV nodal pathways and 12 had an accessory AV pathway). Verapamil terminated AV reentrant tachycardia in 7 patients and bepridil terminated it in 6. In 8 of the patients who received ajmaline, AV reentrant tachycardia was terminated and in 6 of this group bepridil did so. Bepridil was more successful in terminating AV reentrant tachycardia in those with dual AV nodal pathways than in those with an accessory AV pathway. Bepridil slowed sinus rate by 10% (p less than 0.0001), whereas verapamil did not change it significantly. Both verapamil and bepridil administration prolonged AV nodal conduction (39% and 44%, respectively), lengthened AV nodal effective refractory period (18% and 17% respectively) and increased the Wenckebach cycle length of the AV node (24% and 25%, respectively) to a significant degree (p less than 0.05). Bepridil also lengthened atrial and ventricular effective refractory periods (p less than 0.01) and QT interval (p less than 0.0001) in the group as a whole; in those receiving ajmaline and bepridil only atrial refractoriness was significantly altered (p less than 0.05). After treatment for 3 to 5 days with oral bepridil, 19 patients underwent repeat study.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Ajmaline; Anti-Arrhythmia Agents; Atrioventricular Node; Bepridil; Electrophysiology; Humans; Pyrrolidines; Tachycardia; Verapamil

A patient with primary myocardial disease and left bundle-branch block who developed marked QT prolongation and torsade de pointes following an intravenous injection of ajmaline during an electrophysiologic study is reported. The patient could be resuscitated successfully 1 h after the onset of tachycardia.

Topics: Ajmaline; Bundle-Branch Block; Cardiomyopathies; Humans; Male; Middle Aged; Tachycardia

Recently a unique clinical entity has been suggested in subjects without apparent heart disease presenting with recurrent ventricular tachycardia (VT) characterized by RBBB + LAH electrocardiographic pattern, relatively slow rate, induction by atrial stimulation, and interruption by verapamil. According to these characteristics, three cases (2 M and 1 F, aged 18, 33 and 66 years) are presented in this study. They have had palpitations from one to twenty years, but not syncopal episodes. During VT the cycle length ranged from 300 to 480 msec. VT was terminated both by verapamil and by ajmaline. VT was inducible in 3/3 cases by incremental atrial pacing when cycle length of pacing became similar to that of spontaneous VT; in 2/3 cases VT was induced by programmed right atrial stimulation and in 2/3 cases by programmed ventricular stimulation. Serial electrophysiological studies for pharmacological and therapeutic evaluation applied to 1/3 cases showed: amiodarone given orally (200 mg/die) for two months prevented the induction of VT while verapamil, propranolol, mexiletine, and propafenone tested intravenously were ineffective. In the remaining two patients amiodarone, tested only intravenously, was not effective to prevent the induction of VT but lengthened its cycle length. All patients received amiodarone orally (200 mg/die) and were followed for 2,7 and 8 years respectively. Two of them had no more episodes of VT and one, while asymptomatic, continued to present with. The electrophysiological mechanism of this form of VT cannot be identified with certainty, but many data suggest a reentry in the posterior fascicle of left bundle branch as the most probable mechanism.(ABSTRACT TRUNCATED AT 250 WORDS)

Topics: Adolescent; Adult; Aged; Ajmaline; Amiodarone; Bundle-Branch Block; Female; Humans; Male; Tachycardia; Verapamil

Intraindividual comparison of the acute response to intravenous quinidine and to intravenous ajmaline was performed in 23 patients with sustained ventricular tachycardia (VT) who underwent serial electrophysiological studies. In each patient, sustained VT could be reproducibly initiated by programmed ventricular stimulation during control studies. Inducibility of sustained VT was prevented after quinidine in 6 of the 23 patients (26%) and after ajmaline in 8 of the same 23 cases (35%). Agreement between the effects of both drugs was not significant: 2 patients had a similar response to both quinidine and ajmaline and 11 patients did not have a response to either of the two drugs, resulting in a total of only 13 patients (57%) who had a similar response to both drugs. In the 11 non-responders with inducible sustained VT before and after both drugs, quinidine and ajmaline caused qualitatively and quantitatively similar alterations of VT characteristics including a significant prolongation of the interval between the initiation extrastimulus and the first beat of VT by 38 and 42% (P less than 0.01), an increase in VT cycle length by 15 and 22% (P less than 0.01) and a prolongation of the QRS duration during VT by 15 and 18% (P less than 0.01), respectively. In all 23 patients, quinidine and ajmaline caused a quantitatively similar prolongation of ventricular refractoriness by 11 and 9% (P less than 0.05), of the QRS duration at sinus rhythm by 10 and 15% (P less than 0.01) and of the QTc interval by 13 and 10% (P less than 0.05), respectively. Thus, ajmaline and quinidine appear to have similar electrophysiological effects on both normal myocardium and on indirect parameters of reentry; in individual patients with sustained VT, however, such electrophysiological similarities do not result in significant agreement of preventive responses.

Topics: Adult; Aged; Ajmaline; Cardiac Pacing, Artificial; Electrocardiography; Female; Heart Conduction System; Heart Ventricles; Humans; Infusions, Parenteral; Male; Middle Aged; Quinidine; Tachycardia; Ventricular Fibrillation

Cardiac arrhythmia causing sudden cardiac death is a serious worldwide public health problem. Antiarrhythmic agents have been available for therapy, but the conventional agents cause a high degree of intolerable side effects. The recent development of many new experimental antiarrhythmic agents has increased our capacity to effectively treat cardiac arrhythmias. Using a multifaceted approach of programmed electrical stimulation studies, drug level determinations, exercise testing and 24-hour ambulatory Holter monitoring, it can reasonably be decided which patient needs therapy and if therapy is going to be effective. Both aspects of the sudden death equation, ectopy frequency (triggering mechanism) and the ability to propagate sustained ventricular tachycardia (substrate), may be examined. Careful follow-up is needed to determine continued drug efficacy and the presence of side effects that may compromise patient compliance with therapy. If side effects intervene that may cause continued therapy to be intolerable, changing the antiarrhythmic agent, as opposed to decreasing the dosage to an ineffective range, may be appropriate. A comprehensive approach to arrhythmia management may begin to reduce the high incidence of sudden death due to fatal arrhythmias.

Topics: Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anilides; Anti-Arrhythmia Agents; Aprindine; Benzeneacetamides; Bepridil; Bethanidine; Bretylium Tosylate; Death, Sudden; Disopyramide; Encainide; Flecainide; Humans; Lidocaine; Mexiletine; Moricizine; Phenothiazines; Piperidines; Procainamide; Propafenone; Propiophenones; Pyrrolidines; Quinidine; Tachycardia; Tocainide; Verapamil

The conservative management of supraventricular tachycardias is briefly surveyed and described. For exact treatment a description of different ways of origin of tachycardias such as focal activity or reentry-mechanisms is given. A diagram at the end shows the site of influence of different antiarrhythmic drugs in the atria and the AV-node as well as the accessory pathways in preexcitation. A list of antiarrhythmics according to their classification of Vaughan Williams and of Tournboul completes this survey.

Topics: Adrenergic beta-Antagonists; Ajmaline; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Flutter; Digitalis Glycosides; Electrocardiography; Humans; Propafenone; Propiophenones; Tachycardia; Verapamil

By induced polymorphism (I.P.) we mean the electrical induction during endocavitary electrophysiologic study (E.E.S.) either of two or more morphologically distinct types of Sustained Ventricular Tachycardia (S.V.T.) (i.e. different bundle branch block patterns or with shifting of QRS by greater than or equal to 90 degrees) or of one type of sustained ventricular tachycardia other than the spontaneous one. Twenty-two patients with clinical sustained ventricular tachycardia, in whom at least one episode of sustained ventricular tachycardia was induced during endocavitary electrophysiologic study, were divided into 2 groups depending on the presence or not of induced polymorphism: Group I consisted of 13 patients with induced polymorphism; Group II consisted of 9 patients without induced polymorphism. All the patients of the Group I had chronic ischemic heart disease (C.I.H.D.); 12/13 previously had myocardial infarction. Only 1 patient of the Group II had chronic ischemic heart disease. Intraventricular conduction defect was present in 9 patients of the Group I and in 2 of the Group II. An overall of 26 sustained ventricular tachycardia episodes were induced in patients of the Group I: 9 with RBBB, 10 with LBBB and 7 with "bizarre" QRS morphology. Sustained ventricular tachycardia reinduction was attempted in 10 patients of the Group I after acute drug testing (Ajmaline, Propafenone, Amiodarone): sustained ventricular tachycardia was no longer inducible in 6, but in 3 of those 4 in whom it was, a marked increase in polymorphism was observed as compared to pre-test pattern. Of the 11 alive patients of Group I, 10 are on Amiodarone alone or in combination with other antiarrhythmic drugs. We conclude as follows: different morphological types of sustained ventricular tachycardia can be quite commonly induced during endocavitary electrophysiologic study; according to our cases induced polymorphism is observed only in patients with chronic ischemic heart disease; patients with induced polymorphism often have intraventricular conduction defect; induced polymorphism furtherly accounts for reentry as the mechanism of sustained ventricular tachycardia in patients with chronic ischemic heart disease; a prevalent morphology of the endocavitary electrophysiologic study induced sustained ventricular tachycardia in patients with chronic ischemic heart disease was not observed at least in our patients; Amiodarone is the drug of choice for the treatment of induced polymorp

Topics: Adult; Aged; Ajmaline; Amiodarone; Electric Stimulation; Electrocardiography; Electrophysiology; Female; Heart Block; Heart Ventricles; Humans; Male; Middle Aged; Propafenone; Propiophenones; Tachycardia

Topics: Ajmaline; Heart Block; Humans; Male; Middle Aged; Tachycardia

The authors report the case of a patient with ajmaline hepatitis. The clinical presentation suggested angiocholitis; serum bilirubin concentration and the activity of alkaline phosphatase were markedly increased; serum transaminase activity was moderately increased; the prothrombin time remained normal. After interruption of the drug, the outcome was favorable, with complete recovery within 2 months. Histologic examination of a liver specimen obtained early after the onset of jaundice showed inflammatory cells in the portal tracts and mild hepatocytic lesions. Electron microscopy disclosed dilatation of the endoplasmic reticulum. The microfilamentous network of the hepatocytes was reduced and disorganized. Biliary canaliculi were enlarged with absent or blunted microvilli. There was evidence for passage of bile products from the biliary caniculi into the space of Disse. These aspects are reminiscent of those observed in animals after the administration of cytochalasin B. It is suggested that ajmaline may, in some patients, trigger an immune response which then alters the microfilamentous network of the hepatocytes, and may, thereby, produce cholestasis.

Topics: Aged; Ajmaline; Biopsy, Needle; Chemical and Drug Induced Liver Injury; Humans; Liver; Male; Microscopy, Electron; Tachycardia

Programmed stimulation can now be safely performed for the evaluation of therapy for recurrent ventricular tachyarrhythmia. The initiation of ventricular tachycardia appears closely related to its actual spontaneous clinical occurrence. Serial electrophysiologic studies can be performed and are effective in prospectively evaluating the response to antiarrhythmic drugs. The efficacy of therapy based on the results of programmed stimulation appears to be good. On the other hand, Amiodarone can be effective in the chronic treatment as well as in patients with ineffective acute drug test.

Topics: Adult; Aged; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Drug Evaluation; Female; Humans; Male; Mexiletine; Middle Aged; Propafenone; Propiophenones; Tachycardia

Topics: Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Benzofurans; Drug Therapy, Combination; Humans; Quinidine; Tachycardia; Verapamil; Wolff-Parkinson-White Syndrome

The authors report the cases of 4 patients with jaundice following the administration of ajmaline. The disease had a pseudo- angiocholitic onset with fever, chills and pruritus in the 4 patients and abdominal pains in 2 patients. Serum transaminase activity and serum alkaline phosphatase activity were increased in the 4 patients. Blood eosinophilia was found in 3 patients. Liver lesions included predominantly centrilobular cholestasis, mild hepatocytic lesions, and portal inflammation. After the interruption of the drug administration, recovery occurred in the 4 patients. Two patients resumed the intake of ajmaline; transient hepatitis recurred in these 2 patients.

Topics: Adult; Aged; Ajmaline; Chemical and Drug Induced Liver Injury; Female; Humans; Male; Middle Aged; Tachycardia

Six patients including three females with WPW syndrome (three with type A and three with type B) presenting with recurrent paroxysmal tachyarrhythmia were subject to electrophysiological studies. Apart from basal parameters, rapid atrial and ventricular pacing was done which confirmed electrophysiological characteristics of bundle of Kent operation. A single intravenous bolus of ajmaline 50 mg. was effective in blocking the bundle of Kent in all patients within 30 seconds of injection with the effect persisting for 15 minutes in one and from 25 to 60 minutes in the others. The most dramatic effect was prolongation of the HV interval with normalization of QRS complex with a marginal effect on the AH interval. The drug was also effective in breaking narrow QRS tachycardia in two patients and broad QRS tachycardia in one patient. Long-term oral therapy with ajmaline has proved effective in preventing recurrent tachyarrhythmias. We conclude that ajmaline is specifically effective and safe in the treatment of the WPW syndrome.

Topics: Adult; Ajmaline; Bundle of His; Electrocardiography; Electrophysiology; Female; Heart Block; Heart Conduction System; Humans; Male; Middle Aged; Tachycardia; Time Factors; Wolff-Parkinson-White Syndrome

Topics: Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Arrhythmia, Sinus; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Cardiac Pacing, Artificial; Digoxin; Disopyramide; Electric Countershock; Humans; Phenytoin; Procainamide; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Verapamil

Topics: Adult; Aged; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Drug Tolerance; Electrocardiography; Female; Humans; Male; Middle Aged; Tachycardia

We present a case of overdosage of ajmaline in an infant. The appearance of atactic gait and clonic tonic seizures were followed by loss of consciousness, apnea, supraventricular tachycardia, left bundle-branch block, and a prolonged Q-T interval. Cardiopulmonary resuscitation, gastric lavage, and forced diuresis were followed by complete recovery. Continuous electrocardiographic monitoring is mandatory in these cases, and the use of a cardiac pacemaker, respirator, and therapy with antiarrhythmic agents should be considered.

Topics: Accidents, Home; Administration, Oral; Ajmaline; Apnea; Arrhythmias, Cardiac; Ataxia; Bundle-Branch Block; Consciousness Disorders; Diuresis; Electrocardiography; Female; Gastric Lavage; Humans; Infant; Monitoring, Physiologic; Resuscitation; Seizures; Sodium Chloride; Tablets; Tachycardia

Three patients with reentrant tachycardia are described who had an accessory pathway with a very long conduction time that was incorporated in the tachycardia circuit. The accessory pathway was able to conduct in one direction only, in retrograde manner in two patients and in anteriograde manner in the remaining patient. Evidence is presented that reveals that in the first two patients the accessory pathway was septally located, had completely bypassed the normal atrioventricular (A-V) conduction system, had properties of decremental conduction, and had an atrial exit close to the coronary sinus and a ventricular exit relatively far from the atrioventricular A-V ring. In the third patient, who manifested wide QRS complex during tachycardia, the ventricular end of the accessory pathway seemed to be located close to the right ventricular apex. The atrial end of the pathway could not be localized exactly.

Topics: Adult; Ajmaline; Atropine; Bundle-Branch Block; Cardiac Pacing, Artificial; Child; Electrocardiography; Female; Heart Conduction System; Humans; Male; Physical Exertion; Tachycardia; Tachycardia, Paroxysmal; Time Factors; Wolff-Parkinson-White Syndrome

Topics: Action Potentials; Adrenergic beta-Antagonists; Ajmaline; Amiodarone; Anti-Arrhythmia Agents; Aprindine; Calcium; Disopyramide; Electrophysiology; Humans; Lidocaine; Mexiletine; Myocardial Infarction; Phenytoin; Procainamide; Quinidine; Tachycardia; Verapamil

The electrophysiological effects of ajmaline (1 mg/Kg i.v.) on sinus node were evaluated in 63 control subjects and in 12 pts with sick sinus syndrome (S.S.S.). In the control group the mean spontaneous cycle length (S.C.L.) was found significatively (less less than 0.001) reduced (8,?%), and corrected sinus node recovery time (C.S.N.R.T.) significatively (p less than 0.01) prolonged (30,2%) by the drug. In the patients with S.S.S. the S.C.L. was prolonged by 16% but not significatively and the C.S.N.R.T. by 60,7% (p less than 0.05). In 8/12 pts, with S.S.S. spontaneous sinoatrial blocks appeared or were more frequently observed following ajmaline injection. The use of ajmaline as a unic pharmacologic test for the differential diagnosis of symptomatic bradycardia in patients with atrioventricular associated conduction defects is discussed.

Topics: Adult; Aged; Ajmaline; Arrhythmias, Cardiac; Bradycardia; Female; Heart Block; Humans; Male; Middle Aged; Tachycardia

In two patients with supraventricular tachyarrhythmias with atrioventricular block, therapy with lidocaine and ajmaline decreased the atrioventricular block and caused paradoxic acceleration of the ventricular rate. Appropriate treatment of this hazardous result of therapy with antiarrhythmic drug is reviewed.

Topics: Aged; Ajmaline; Arrhythmias, Cardiac; Electrocardiography; Heart Block; Heart Conduction System; Heart Rate; Heart Ventricles; Humans; Lidocaine; Male; Tachycardia

A case of a 39 years old woman on therapy with Monodicloroacetilajmaline for repetitive crises of Ventricular Tachycardia is shown. We have observed neurological symptoms by central compromission of 3rd, 4th, 6th pair of cranial nerves, cutaneous symptoms and a neurodisletic crisis. We particularly analyse the dosage of the drug in relation to the progression of symptoms and also the possible pathogenesis. Symptoms disappeared completely about 20 days after withdrawal of the drug.

Topics: Adult; Ajmaline; Female; Humans; Nervous System Diseases; Tachycardia

Topics: Ajmaline; Arrhythmias, Cardiac; Humans; Lidocaine; Procaine; Quinidine; Tachycardia

Topics: Adrenergic beta-Antagonists; Ajmaline; Anti-Arrhythmia Agents; Atrial Fibrillation; Atrial Flutter; Cardiac Complexes, Premature; Humans; Lidocaine; Quinidine; Tachycardia; Tachycardia, Paroxysmal; Verapamil

A report is given on a patient in whom during treatment and prophylactic measures of paroxysmal tachycardias after intravenous application of ajmalin large attacks of fever with chills developed. The oral application evoked subfebrile temperatures and weakness. The drug-fever which was to be ascertained by exposition and omitting experiments was falsely explained for many years.

Topics: Ajmaline; Allergens; Diagnostic Errors; Drug Hypersensitivity; Fever; Haptens; Humans; Male; Middle Aged; Shivering; Tachycardia

1. In the isolated left atrium of the guinea pig ajmaline and di-monochloracetylajmaline (DCAA) show almost the same activity concerning prolongation of the functional refractory period. 2. In contrast to this N-propylajmaline (NPA) is much more effective than ajmaline. 3. NPA as compared to ajmaline and DCAA, however, shows a considerably smaller difference between the concentrations prolonging refractory period (I) and those decreasing contractility (II) in the guinea pig atrium (EC25). The quotient from I and II is 0.4 with NPA, 1.2 with ajmaline and 1.6 with DCAA. 4. Differences in efficacy similar to those observed in the guinea pig atrium are also found in experimental cardiac arrhythmias in the intact animal. NPA is much more effective than ajmaline regarding inhibition of extrasystoles, ventricular tachycardia and ventricular flutter due to aconitine infusion in the rat. In this experimental model DCAA shows slightly less activity than ajmaline; this difference is statistically significant.

Topics: Aconitine; Aconitum; Ajmaline; Animals; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Electrocardiography; Guinea Pigs; Heart; Heart Atria; Heart Rate; In Vitro Techniques; Male; Myocardial Contraction; Rats; Tachycardia; Ventricular Fibrillation

For the practicing physician the medicamentous treatment of the patients with infarction is the main problem of the secondary prevention in the prehospital phase as well as in the after-treatment. In these cases in the acute phase not the myocardial insufficiency is in the centre of the out-patient care, but the therapy of the disturbances of cardiac rhythm, which mainly cause the high lethality in the early phase. Therefore, uncomplicated infarctions, in whch care must be taken only for a sedation of sympathico-adrenergic reactions and a volume reduction of the heart, should be differed from complicated cases. However, an immediate transport to the hospital must be guaranteed. If there appear a contraction insufficiency of the left ventricle or threatening disturbances of the rhythm, additionally glycosides and saluretics must be administered as well as an aimed antiarrhythmic therapy must be initiated. The necessary medicamentous measures are described dependent upon the diagnosis of brady- and tachycardiac disturbances of the rhythm. The author enters briefly the problems of volume substitution, treatment of acidosis as well as the administration of beta-sympathicolytics and gluco-corticoids. - In the after-treatment of infarctions anticoagulants are the only medicaments to be prescribed, when findings completely without complications are present. If, however, there are signs of activity of the coronary heart disease in the post-infarction phase, a basic therapy with a glycoside and anticoagulants as well as an individually to be varied additive therapy with nitro-preparations, beta-sympathicolytics, saluretics, anti-hypertensive agents and antiarrhythmic agents are necessary.

Topics: Acidosis; Adrenergic beta-Antagonists; Aftercare; Ajmaline; Ambulatory Care; Anticoagulants; Arrhythmias, Cardiac; Atropine; Cardiac Complexes, Premature; Cardiac Glycosides; Glucocorticoids; Heart Block; Heart Failure; Hospitalization; Humans; Lidocaine; Meperidine; Metaproterenol; Morphine; Myocardial Infarction; Nitroglycerin; Tachycardia

Topics: Ajmaline; Anti-Arrhythmia Agents; Aprindine; Arrhythmia, Sinus; Arrhythmias, Cardiac; Bradycardia; Humans; Isoproterenol; Lidocaine; Myocardial Infarction; Pacemaker, Artificial; Phenytoin; Procainamide; Propranolol; Quinidine; Tachycardia; Verapamil

Topics: Administration, Oral; Ajmaline; Aniline Compounds; Animals; Anti-Arrhythmia Agents; Cardiac Complexes, Premature; Diethylamines; Disopyramide; Dogs; Heart Ventricles; Humans; Indans; Injections; Injections, Intravenous; Myocardial Infarction; Practolol; Procainamide; Propranolol; Quinidine; Tachycardia

Topics: Aconitum; Ajmaline; Animals; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Azepines; Benzoates; Cardiac Complexes, Premature; Dogs; Electrocardiography; Epinephrine; Heart Block; Male; Ouabain; Tachycardia

Topics: Acute Disease; Adult; Aged; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Blood Pressure; Carbamates; Coronary Disease; Drug Resistance; Electrocardiography; Female; Heart Rate; Heart Ventricles; Humans; Hypertension; Infusions, Parenteral; Lidocaine; Male; Middle Aged; Myocardial Infarction; Phenytoin; Procainamide; Quaternary Ammonium Compounds; Quinidine; Tachycardia

Topics: Adult; Aged; Ajmaline; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Coronary Disease; Female; Heart Diseases; Humans; Injections, Intravenous; Male; Middle Aged; Tachycardia

Topics: Adult; Ajmaline; Electrocardiography; Electrophysiology; Female; Heart Atria; Heart Block; Heart Conduction System; Heart Ventricles; Humans; Male; Middle Aged; Procainamide; Quinidine; Refractory Period, Electrophysiological; Tachycardia; Wolff-Parkinson-White Syndrome

Topics: Adrenergic beta-Antagonists; Ajmaline; Arrhythmia, Sinus; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Bradycardia; Cardiac Complexes, Premature; Digitalis Glycosides; Humans; Hypnotics and Sedatives; Reserpine; Tachycardia

Topics: Ajmaline; Arrhythmias, Cardiac; Atrial Fibrillation; Bradycardia; Caffeine; Cardiac Complexes, Premature; Digitalis Glycosides; Heart Block; Humans; Lidocaine; Metaproterenol; Phenytoin; Procainamide; Tachycardia; Ventricular Fibrillation; Verapamil

Topics: Adrenergic beta-Antagonists; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atropine; Bradycardia; Humans; Lidocaine; Metaproterenol; Phenytoin; Procainamide; Quinidine; Tachycardia; Verapamil

Topics: Adrenergic beta-Agonists; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Bradycardia; Digitalis; Electrocardiography; Heart; Hemodynamics; Humans; Lidocaine; Phenytoin; Phytotherapy; Plants, Medicinal; Plants, Toxic; Procainamide; Propranolol; Quinidine; Tachycardia

Topics: Adult; Aged; Ajmaline; Electrocardiography; Heart Conduction System; Humans; Male; Middle Aged; Tachycardia; Wolff-Parkinson-White Syndrome

Topics: Ajmaline; Animals; Cardiac Glycosides; Dogs; Female; Male; Methods; Phenytoin; Propranolol; Tachycardia

Topics: Ajmaline; Apgar Score; Arrhythmias, Cardiac; Cesarean Section; Digoxin; Electrocardiography; Extraction, Obstetrical; Female; Fetus; Heart Block; Humans; Infant; Infant, Newborn; Lanatosides; Pregnancy; Prenatal Diagnosis; Tachycardia; Tachycardia, Paroxysmal; Ventricular Fibrillation; Verapamil; Wolff-Parkinson-White Syndrome

Topics: Adrenergic beta-Antagonists; Ajmaline; Atrial Fibrillation; Atrial Flutter; Atropine; Bradycardia; Cardiac Complexes, Premature; Heart Block; Humans; Lidocaine; Metaproterenol; Phenytoin; Procainamide; Quinidine; Tachycardia; Verapamil

Topics: Aged; Ajmaline; Cardiac Catheterization; Electric Countershock; Electrocardiography; Female; Heart Atria; Heart Conduction System; Heart Ventricles; Humans; Myocardial Infarction; Tachycardia

Topics: Adrenergic beta-Antagonists; Ajmaline; Anti-Arrhythmia Agents; Arrhythmias, Cardiac; Atrial Fibrillation; Atrial Flutter; Bradycardia; Digitalis Glycosides; Humans; Phenytoin; Procainamide; Quinidine; Sympatholytics; Tachycardia

Topics: Adrenergic beta-Antagonists; Ajmaline; Analgesics; Arrhythmias, Cardiac; Bradycardia; Child; Child, Preschool; Digitalis Glycosides; Electric Countershock; Electrocardiography; Humans; Infant; Infant, Newborn; Infant, Newborn, Diseases; Metaproterenol; Pacemaker, Artificial; Sparteine; Tachycardia; Tachycardia, Paroxysmal

Topics: Adult; Ajmaline; Anuria; Bicarbonates; Bundle-Branch Block; Electrocardiography; Female; Humans; Isoproterenol; Lidocaine; Plants, Medicinal; Rauwolfia; Shock, Septic; Suicide; Tachycardia; Time Factors; Ventricular Fibrillation

Topics: Aged; Ajmaline; Alkaloids; Drug Therapy; Female; Geriatrics; Humans; Injections; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal

Topics: Ajmaline; Alkaloids; Humans; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal; Tachycardia, Ventricular

Topics: Ajmaline; Atrial Fibrillation; Atrial Flutter; Cardiac Complexes, Premature; Humans; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal; Toxicology

Topics: Ajmaline; Cardiac Complexes, Premature; Humans; Hypnotics and Sedatives; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal

Topics: Ajmaline; Electrocardiography; Heart Arrest; Heart Block; Humans; Iatrogenic Disease; Injections, Intravenous; Rauwolfia; Tachycardia; Tachycardia, Supraventricular; Toxicology

Topics: Ajmaline; Drug Therapy; Electrocardiography; Humans; Myocardial Infarction; Rauwolfia; Tachycardia; Tachycardia, Ventricular

Topics: Ajmaline; Pacemaker, Artificial; Procainamide; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal; Tachycardia, Ventricular; Therapeutics

Topics: Ajmaline; Arrhythmias, Cardiac; Cardiac Complexes, Premature; Drug Therapy; Emergency Treatment; Humans; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal

Topics: Ajmaline; Alkaloids; Atrial Flutter; Cardiac Complexes, Premature; Humans; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal

Topics: Ajmaline; Myocardial Infarction; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal; Tachycardia, Ventricular

Topics: Ajmaline; Electrocardiography; Humans; Niacin; Nicotinic Acids; Rauwolfia; Tachycardia; Tachycardia, Paroxysmal

Topics: Ajmaline; Arrhythmias, Cardiac; Brugada Syndrome; Cardiac Catheterization; Cardiac Complexes, Premature; Cardiac Conduction System Disease; Digitalis Glycosides; Emergency Treatment; Heart Conduction System; Humans; Rauwolfia; Tachycardia

Topics: Ajmaline; Anemia; Anti-Arrhythmia Agents; Arrhythmia, Sinus; Arrhythmias, Cardiac; Atrial Fibrillation; Cardiac Complexes, Premature; Heart Failure; Humans; Hypertension; Hyperthyroidism; Rauwolfia; Tachycardia

Topics: Ajmaline; Heart; Hypnotics and Sedatives; Rauwolfia; Tachycardia