antiarrhythmic/infarction

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An antiarrhythmic effect of a chymase inhibitor after myocardial infarction.

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Chymase plays an important role in the regulation of local angiotensin (Ang) II formation in the cardiac tissue. We recently found that cardiac chymase was activated significantly and survival rate markedly improved by treatment with chymase inhibitors after myocardial infarction (MI) in hamsters.

Effects of azimilide, a new class III antiarrhythmic drug, on reentrant circuits causing ventricular tachycardia and fibrillation in a canine model of myocardial infarction.

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BACKGROUND Azimilide blocks the slow (I(Ks)) and fast (I(Kr)) components of the delayed rectifier potassium channel. It also has blocking effects on sodium (I(Na)) and calcium currents (I(CaL)). Its effects on reentrant circuits in infarct border zones causing ventricular tachyarrhythmias are

Class I and III antiarrhythmic drugs for prevention of sudden cardiac death and management of postmyocardial infarction arrhythmias. A review.

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BACKGROUND The aim of the present paper is to review the evolution of concepts regarding the use of Class I and III antiarrhythmic drugs (AADs) in myocardial infarction over the past four decades. METHODS Results of animal experiments carried out by the authors and papers published between 1970 and

Comparative antiarrhythmic efficacy of amiodarone and dronedarone during acute myocardial infarction in rats.

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The effects of dronedarone, a non-iodinated derivative of amiodarone, on ventricular tachycardia and ventricular fibrillation post-myocardial infarction are not well established. Fifty-five Wistar rats were randomly allocated to a 2-week oral treatment with either vehicle (n=18), amiodarone (30

Comparison of antiarrhythmic effects of oral prajmalium bitartrate and intravenous lidocaine in acute myocardial infarction.

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In 35 patients with acute myocardial infarction premature ventricular complexes were quantified from stored continuous electrocardiographic tape recordings using a semiautomated arrhythmia detection system. Seventeen patients, separated at random, received no antiarrhythmic drug and formed the

[Tetrodotoxin potentiation of the antiarrhythmic action of lidocaine in the late stage of experimental myocardial infarct].

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Lidocaine (4--12 mg/kg) and the specific fast sodium current blocker tetrodotoxin (TTX) (1--6 mg/kg, i. v.) reduced ventricular arrhythmias that occurred 24 h after coronary artery ligation in dogs. Infusion of a mixture of subthreshold doses of lidocaine and TTX decreased ventricular arrhythmias to

Antiarrhythmic and arrhythmogenic actions of methyl lidocaine during the recovery phase after canine myocardial infarction.

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Programmed electrical stimulation was used to evaluate the electrophysiologic and antiarrhythmic actions of methyl lidocaine in both conscious and anesthetized dogs, 4-7 days after myocardial infarction. When administered to animals demonstrating sustained ventricular tachycardia (n = 6), methyl

Comparative investigation of the antiarrhythmic effect of propafenone (Rytmonorm) and lidocaine in patients with ventricular arrhythmias during acute myocardial infarction.

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Propafenone, a new class I antiarrhythmic drug, given as a bolus injection followed by oral medication, or lidocaine were given to 20 consecutive patients admitted with chest pain suggesting acute myocardial infarction and showing high grades, i.e. multiform, pairs or R-on-T premature ventricular

[The comparative hemodynamic effects of antiarrhythmic drugs in acute myocardial infarction (comparison of propafenone and lidocaine) (author's transl)].

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Hemodynamic changes after single intravenous injection of antiarrhythmic doses of propafenone (70 mg) and lidocaine (100 mg) were measured comparatively in 11 patients with acute myocardial infarction, stable cardiac rhythm and without evidence of manifest left heart failure. The effects of

The persistent sodium current blocker riluzole is antiarrhythmic and anti-ischaemic in a pig model of acute myocardial infarction.

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BACKGROUND The potential of the cardiac persistent sodium current as a target for protection of the myocardium from ischaemia and reperfusion injury is gaining increasing interest. We have investigated the anti-ischaemic and antiarrhythmic effects of riluzole, a selective INaP blocker, in an open

Synergistic interaction between class I antiarrhythmic drugs and halothane in depressant effects on ventricular activation in a canine myocardial infarction model.

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Previous studies have showed that halothane has depressed ventricular activation in a canine myocardial infarction model. It is also well known that class I antiarrhythmic drugs depress ventricular activation in the infarcted myocardium. In the present study, we examined whether some

Effects of SUN-1165, N-(2,6-dimethylphenyl)-8-pyrrolizidine acetamide hydrochloride hemihydrate, a new class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the refractory period in canine myocardial infarction.

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Effects of SUN-1165, a class I antiarrhythmic drug, on ventricular arrhythmias, intraventricular conduction, and the effective refractory period (ERP) were examined in a canine model of myocardial infarction and compared with those of lidocaine. The antiarrhythmic effects were examined on the

Prophylactic antiarrhythmic therapy in acute myocardial infarction.

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Safe, effective prophylaxis of arrhythmias in acute myocardial infarction (AMI) is an important clinical goal. Despite rescue squads, out-of-hospital ventricular fibrillation (VF) has a poor prognosis. Even in-hospital VF has an important morbidity and mortality. Successful prophylactic therapy may

Antiarrhythmic efficacy, pharmacokinetics and clinical safety of tocainide in convalescent myocardial infarction patients.

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The antiarrhythmic efficacy and pharmacokinetics of tocainide, an oral analog of lidocaine, was evaluated in 18 hospitalized convalescing myocardial infarction patients. Holter ECG tapes were recorded daily during two-day placebo therapy preceding and succeeding two days of tocainide treatment. Left

Electrophysiologic interaction between class I antiarrhythmic drugs and volatile anesthetics in depressant effects on ventricular activation in a canine myocardial infarction model.

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Previous studies showed that volatile anesthetics depressed ventricular delayed activation in a canine myocardial infarction model. It is well known that class I antiarrhythmic drugs depress the ventricular activation in the infarcted myocardium. In the present study, we examined the

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