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PubMed1992

[The prospective evolution of the efficacy of antiarrhythmia therapy in paroxysmal supraventricular tachycardia in patients with the ventricular pre-excitation syndrome].

Evolution of the effectiveness of antiarrhythmic drugs used in 240 patients with preexcitation syndrome to arrest episodes of paroxysmal supraventricular tachycardia was analysed prospectively. The first intravenous administration was effective in 97, 93.3, 80.9, 75, 70.3, 60, 48% of cases for novocainamid, verapamil, cordarone, disopyramide, ajmaline, ethacizine, mexitil and inderal, respectively. When observed in prospective evolution for 10-14 years, overall group efficacy dropped from 81.3% at first administration to 21.4%.

Adolescent↗
PubMed1992

[Does the appearance of pro-arrhythmic response to anti-arrhythmic drugs have prognostic significance?].

Study was undertaken to assess whether proarrhythmic response to antiarrhythmic drug is a risk factor for cardiac death in patients (pts) with ischaemic heart disease (IHD). In 782 pts with IHD and frequent and/or complex ventricular ectopic beats (VEB) 1041 drug tests guided by 24 hour Holter monitoring were conducted. The following drugs were assessed: propranolol, disopyramide, mexiletine, amiodarone. Pro-arrhythmia was defined according to Velebit: 1/greater than or equal to 4-fold increase in VEBs, 2/greater than or equal to 10-fold increase in repetitive forms of 3/new occurrence of ventricular tachycardia or ventricular fibrillation (VT/VF). Proarrhythmic effect was observed in 8.4% of pts and in 7.9% of drug tests. The frequency with individual drugs ranged from 5.7% to 9%. No drug was completely free of this type of reaction. Antiarrhythmic drugs inducing arrhythmogenic response were eliminated. Pts were followed-up for a mean of 22 months (range 1-49). Chronic antiarrhythmic treatment was conducted. Pts were discharged taking the agent deemed most effective for suppression of arrhythmia. Follow-up visits were made every 6-12 months. All cases of death were verified. In long-term observation cardiac death and sudden death occurred in 53 and 32 pts. With actuarial analysis (Kaplan-Meler method, log rank test) there was significant difference in cardiac death (p less than 0.05) of pro-arrhythmia (+) compared with ++pro-arrhythmia (-) pts at yr (11% v 4%, 7% v 3%) and 3 yr (24% x 11%, 16% v 7%). The relative importance of baseline clinical variables in predicting survival was assessed with a stepwise Cox regression.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed2006

Echocardiography in the treatment of hypertrophic cardiomyopathy.

Echocardiography is the best technique to diagnose, evaluate, follow-up and guide the treatment of hypertrophic cardiomyopathy (HCM). Diagnosis of HCM depends on left ventricular wall thickness >/=15 mm. Also noted are mitral valve systolic anterior motion, anteriorly positioned mitral valve leaflet coaptation, anomalous anterior insertion of papillary muscles, and diastolic dysfunction. Resting left ventricular outflow tract (LVOT) gradient occurs in 25% of patients and provocable gradients may be demonstrated in more than half of patients. Echocardiography is important for sudden death risk assessment; patients with a wall thickness more than 30 mm have a higher risk of sudden cardiac death, as often as 2%/year. Two thirds of the symptomatic obstructed patients can be successfully managed long term with medical treatment alone (beta-blockers, disopyramide, verapamil) guided by transthoracic echocardiography (TTE) response and follow-up. Obstructed patients, who fail medical therapy, are usually offered invasive treatment: surgical septal myectomy, alcohol septal ablation, or DDD pacemaker. Preoperative TTE is a necessary guide for the surgeon in planning the operation. It gives the surgeon precise measurements of septal thickness, mitral valve leaflets length and floppiness and papillary muscle anomalies. Intraoperative transesophageal echocardiography is a very important tool for evaluating surgical results. Persistent SAM, resting outflow gradient more than 30 mm Hg or more than 50 mmHg with provocation, moderate to severe mitral regurgitation are indications for immediate revision. For patients >40 years old, and also not suitable for surgery because of comorbidities, alcohol septal ablation is viable alternative therapy for relief of obstruction and improvement of symptoms. Echocardiography is a valuable tool to choose the site of ablation (using myocardial contrast echocardiography), as well as for evaluation of results.

Cardiomyopathy, Hypertrophic↗
PubMed1991

Antiarrhythmic treatment of atrial arrhythmias.

Atrial premature beats seldom require an antiarrhythmic treatment; reassurance and suppression of coffee, alcohol, and tobacco generally suffice. Acute atrial fibrillation is best treated by electrical cardioversion if it induces acute cardiovascular decompensation. If it is not poorly tolerated, the arrhythmia may be treated with digitalis at doses sufficient to keep the ventricular response rate at 70-90/min. This therapy may restore sinus rhythm, but conversion to sinus rhythm often requires the combined use of digitalis with a beta-blocker or class I antiarrhythmic drug (quinidine, disopyramide, procainamide, propafenone, or flecainide). Digitalis must be avoided in the presence of a preexcitation, and class IA agents, which facilitate atrioventricular (AV) nodal transport, must never be used without digitalis. Chemical cardioversion may also be achieved by i.v. amiodarone. Long-term prevention of recurrences after cardioversion or in the presence of recurrent paroxysmal atrial fibrillation requires digitalis combined with a class I agent, or a beta-blocker, preferably sotalol. Amiodarone is also very efficacious. Special mention should be made of atrial fibrillations of vagal or sympathetic origin, which are best treated by amiodarone, or beta-blockade (nadolol), respectively. In the presence of chronic established atrial fibrillation, digitalis in combination with a beta-blocking agent or a calcium antagonist, such as verapamil or diltiazem, may be useful to slow the ventricular response rate. If successful control cannot be obtained, catheter ablation of the AV node with implantation of a rate-responsive pacemaker must be contemplated. The therapeutic approach in patients with chronic atrial fibrillation, whether or not associated, is similar to atrial flutter.(ABSTRACT TRUNCATED AT 250 WORDS)

Animals↗
PubMed1991

Negative inotropic effects of antiarrhythmic drugs: a clinical point of view.

From a clinical point of view, the negative inotropic effects of antiarrhythmic drugs lead to the following questions: Do antiarrhythmic drugs induce or worsen congestive heart failure (CHF)? Which patients are at increased risk of developing CHF with antiarrhythmic drugs? Which antiarrhythmic drugs are most likely to induce CHF clinically? The present review of the recent literature demonstrates that antiarrhythmic drugs may induce or worsen CHF in a small number of patients. This is true for all antiarrhythmic drugs, but only disopyramide (and flecainide) are antiarrhythmic drugs with a relevant rate of clinical CHF. Patients with a history of heart failure, a low left ventricular ejection fraction, and cardiomyopathy are at increased risk of developing CHF with antiarrhythmic drugs, especially if the drugs are administered intravenously and in high doses.

Animals↗
PubMed1991

[Idiopathic atrial fibrillation: clinical and therapeutic problems].

Atrial fibrillation (AF) is defined as idiopathic when no one heart disease can be documented by clinical examination or by laboratory investigations. Epidemiological studies have shown that almost one third of all the cases of AF are idiopathic and that their incidence increases with age. Idiopathic AF may have different clinical manifestations: the paroxysmal form, characterised by long-lasting episodes, the transient recurrent form, characterised by frequent self-terminating episodes, or, less commonly, the chronic form. According to the literature, the risk of thromboembolic complications in idiopathic AF is not elevated and certainly lower than in AF associated with heart disease. By a clinical evaluation patients in whom an electrical cardioversion is necessary for reestablishing the sinus rhythm can be identified, considering that definite contraindications to electrical cardioversion exist. For prophylaxis of recurrences of AF the classical treatment with class 1A antiarrhythmic drugs (disopyramide or quinidine) is not very effective and not well tolerated; recently class 1C antiarrhythmic drugs have been employed with better results. In patients without heart failure their employment appears sufficiently safe. Amiodarone is certainly very effective but considering the serious side effects, its use must be limited to selected cases. Moreover non-pharmacological treatments (catheter ablation and surgery) have been developed recently for selected cases of AF refractory to antiarrhythmic drugs.

Adult↗
PubMed1991

[Recurrent ventricular tachyarrhythmias primarily diagnosed as epilepsy].

In Denmark, 6,000-10,000 persons die annually from sudden cardiac death. The majority of these die on account of ventricular fibrillation. A patient is presented here who suffered from recurrent lipothymic seizures which were primarily diagnosed as epilepsy. On account of absence of paraclinical documentation and because of suspected depression, treatment with a cyclic antidepressive agent was commenced, which further increases the tendency to sudden cardiac death. The patient was then brought to hospital with Lidocaine-resistant ventricular fibrillation which responded partly to Ajmalin and partly to Disopyramide. The lipothymic seizures were then interpreted as being precipitated by intermittent malignant episodes of cardiac arrhythmia. During the subsequent six months, the patient has felt well and has been free from lipothymic seizures while receiving 200 mg Mexiletin thrice daily. Attention is drawn to the value of Holter monitoring in the investigation of lipothymic seizures. Lidocaine (despite the existence of resistant cases) must still be considered to be the preparation of first choice on account of extensive knowledge about and confidence in the preparation.

Aged↗
PubMed1975

[Comparative evaluation of new drugs used in the treatment of cardiac arrhythmia].

The paper summarizes the experience gained in treating 830 patients with various cardiac rhythm disorders by employing new antirhythmic agents (propranolol, practolol, pindolol, alprenolol, oxyprenolol, benzoral, verapamil, lidocaine, imaline, sparteine, pulsonorma, disopyramide and quinidine durules). Comparative data on the efficacy of these agents are presented and indications and counterindications for their use are discussed.

Administration, Oral↗
PubMedDate not supplied

[Wolff-Parkinson-White syndrome with orthodromic supraventricular tachycardia associated with a "hyper-conductor" atrio-ventricular node. A therapeutic challenge].

One case of Wolff-Parkinson-White Syndrome with paroxysmal supraventricular tachycardia related to orthodromic atrioventricular reentry using an accessory pathway for retrograde conduction an a rapidly conducting AV node for anterograde conduction is present. The pharmacological therapy with Digoxin, Propranolol, Quinidine, Disopyramide and Propafenone was not effective. An electrophysiologic study showed a reciprocating tachycardia induced by spontaneous ventricular beats. Both the effective refractory period of the AV node and the anterograde effective refractory period of the accessory pathway were minor or equal to 220 msec which made the control of the arrhythmia difficult. Amiodarone was able to suppress the premature ventricular beats, depress conduction and prolong refractoriness in both, the AV node and accessory pathway to prevent recurrences of atrioventricular reentry. In this patient a false positive test with ajmaline was documented. The electrophysiologic study showed the association of Wolff-Parkinson-White Syndrome with an enhanced atrioventricular nodal-conduction and allowed the selection of an appropriate antiarrhythmic agent.

Adult↗
PubMed1986

[Effectiveness of ethacizin in ventricular arrhythmias refractory to prior anti-arrhythmia drug therapy].

Using Holter ECG monitoring, the efficiency of the new drug ethacizin was assessed on an individual basis in 48 patients with ventricular arrhythmias refractory to past treatments (group 1) and in 46 patients who responded to at least one of the available antiarrhythmic drugs (group 2). Ethacizin proved effective in 63% of first-group patients and in all second-group patients, with an overall response rate of 81%. The efficiency of ethacizin, ethmozin, and disopyramide was 100, 73 and 69%, respectively, in the same patients. It is suggested that separate assessments of new antiarrhythmic drugs are preferable in patients with treatment-resistant ventricular arrhythmias and those responding to at least one of the drugs available.

Adolescent↗
PubMed1986

[Choice of a class I intravenous anti-arrhythmic drug in severe ventricular arrhythmias].

In the choice of a Class I intravenous antiarhythmic medication for the treatment of threatening ventricular extrasystoles, one must take into account the speed of action of the product, its effects on hemodynamics and conduction as well as its efficacy. The rapidity of action implies the ability to reach, without delay, a therapeutic plasma level which will depend upon the distribution volume and the dose injected. An effective plasma level may be quickly reached following the intravenous administration of lidocain, disopyramide, lorcainide, tocainide and flecainide. All antiarhythmic medications have an unfavorable effect on hemodynamics; xylocain and ajmaline seem to depress the least the left ventricular function, followed by lorcainide. Unfavorable effects on the atrio-ventricular conduction are observed with substances of type IC; the duration of QRS may be affected as well by antiarhythmic medications IA and IC, with a lengthening of QT being mostly noted type IA medications. Comparison of the efficacy of antiarhythmic medications requires a strict methodology and the current data from the literature do not permit to assert with certainty the superiority of one antiarhythmic medication over the others.

Anti-Arrhythmia Agents↗
PubMed1988

[Use of combinations of group I anti-arrhythmia drugs in patients with refractory arrhythmias].

The efficiency of various combinations of antiarrhythmic agents (quinidine, etmozin, disopyramide, mexitil, and allapinine) was assessed in 24 cases of frequent ventricular and supraventricular extrasystoles, where treatment with one of the above listed drugs had been ineffective. Combined use of the drugs produced anti-arrhythmic effect in 22 of the patients. Mechanisms of the combined action are discussed.

Adult↗
PubMed1989

[Calcium metabolism and transmembrane potential of thrombocytes in patients with frequent ventricular extrasystole treated with anti-arrhythmia drugs].

The effect of antiarrhythmic drugs on platelet calcium metabolism in peripheral blood has been examined. Anti-arrhythmic agents (ethmozine, ethacizine, quinidine, disopyramide, amiodarone), used extensively for the control of various heart rhythm disorders, as well as calcium antagonists (verapamil were shown to have a calcium-blocking property. It is demonstrated that the rate of reduction in the total number of extrasystoles in the presence of antiarrhythmic drugs is correlated to the magnitude of their in vitro calcium-blocking effect. It can be assumed that the action of antiarrhythmic drugs is in part mediated by their effect on calcium currents; at the same time, disorders of Ca2+ transport in myocardial cells are a cause of developing arrhythmias. The ability of antiarrhythmic drugs to affect platelet calcium ion currents may be used for preliminary assessment of the efficiency of antiarrhythmic drugs, used clinically to control heart rhythm disorders.

Action Potentials↗
PubMed1989

[Safety of long-term therapy with a combination of various anti-arrhythmia agents].

Safety and the effectiveness of combined therapy of arrhythmia was studied in 27 patients in prolonged (up to 4 months) administration of a combination of medicinal agents specially chosen during pharmacodynamic investigation. The obtained anti-arrhythmic effect was stable and there were no new side effects in prolonged administration of combinations of ethmozine with chinidin, ritmilen, obsidan, cordaron (amiodaron) and of allapinin with chinidin, ritmilen (disopyramide) and obsidan (propronalol). Tolerance to drugs was adequate and the ECG parameters remained unaffected.

Anti-Arrhythmia Agents↗
PubMed1989

[Successful treatment of stress-induced therapy refractory ventricular tachycardia with verapamil].

A 51-year-old woman was admitted to the hospital for further elucidation of a syncope of unknown origin and exercise-induced tachycardias with broad QRS-complex. The tachycardia was induced by bicycle exercise stress testing, had a frequency of 165/min, showed an inferior axis and left bundle branch block. Organic heart disease was excluded by right and left heart catheterization and selective coronary angiography. A nodoventricular bundle or an atrio-ventricular bundle was excluded by an extensive electrophysiologic study, therefore the documented tachycardia was probably of ventricular origin. However, it was not possible to induce a ventricular tachycardia by programmed ventricular stimulation with up to three extrastimuli even after the infusion of isoprenaline. Sotalol (2 x 160 mg/die) and the combined treatment with mexiletine (2 x 360 mg/die) and disopyramide (2 x 250 mg/die) did not prevent the induction of the tachycardia by exercise testing. The combination of sotalol and flecainide (2 x 100 mg/die) evoked complex ventricular arrhythmias at rest not noted before, and it was therefore withdrawn as well. After all antiarrhythmic drugs were withdrawn verapamil was given in a dose of 3 x 120 mg and this therapy reproduceably prevented the induction of ventricular tachycardia by exercise testing.

Anti-Arrhythmia Agents↗
PubMed1989

[The effect of cardiac insufficiency on pharmacokinetics].

Heart failure may have repercussions on the different stages of pharmacokinetics. Following intramuscular or oral administration, drug absorption may be slowed down by the fall in cardiac output and by peripheral vasoconstriction. Tissue distribution is altered by changes in the plasma protein binding of drugs and by redistribution of cardiac output to the brain and heart, resulting in changes in the apparent volume of distribution. Excretion through the liver is influenced by the decrease of hepatic blood flow and metabolic capacities. Lowering of the renal blood flow alters the glomerular and tubular excretion processes. These hepatic and renal dysfunctions result in a reduction of total plasma clearance. The effects of heart failure on the pharmacokinetics of digitalis compounds seem to consist merely of a delay in digestive tract absorption. More studies have been devoted to the fate of antiarrhythmic agents. Blood concentrations of lidocaine are raised in patients with heart failure; this is accounted for by the redistribution of local blood flows, the increase in plasma protein binding observed after myocardial infarction and the reduced hepatic clearance. A fall in the volume of distribution and total clearance of quinidine has been described. Data concerning disopyramide are discordant, but reduction of the free drug fraction and variations in total clearance have been observed after myocardial infarction. Alterations in the total clearance of prazosin, nitroglycerin and theophylline have been reported by several authors.(ABSTRACT TRUNCATED AT 250 WORDS)

Anti-Arrhythmia Agents↗
PubMed1989

[Atrial flutter with 1:1 AV conduction during intravenous flecainide treatment].

Acute drug treatment of recent onset atrial flutter may reduce the ventricular rate by increasing block in the A-V node (digitalis/verapamil) or act by directly affecting the atria by reducing the atrial rate or converting flutter to sinus rhythm (1a and 1c antiarrthythmic drugs). Treatment that reduces the atrial rate may cause 1:1 A-V conduction. Quinidine and disopyramide are well known for increasing A-V conduction to 1:1 in some patients, because of their anticholinergic effect on the A-V node. Flecainide, a 1c antiarrhythmic drug, slows down atrial conduction, reducing flutter rate by 1/3. Clinical studies have shown flecainide to be effective in converting atrial fibrillation, atrial tachycardia, A-V reentry and A-V nodal reentry tachycardias to sinus rhythm. The effect on atrial flutter has been less impressive. Flecainide prolongs A-V conduction and increases Wenckebach cycle length. In spite of this, 1:1 A-V conduction may occur during treatment with intravenous flecainide for atrial flutter. We present a case where this is demonstrated and review the literature.

Aged↗
PubMed1989

[Bidirectional tachycardia during therapy with lorajmine].

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.

Aged↗