Suppression of ventricular ectopic depolarizations by flecainide acetate, a new antiarrhythmic agent.

Hodges, Morrison; Haugland, J. Mark; Granrud, Gregory; Conard, Gordon J.; Asinger, Richard W.; Mikell, Frank L.; Krejci, Jeananne

doi:10.1161/01.cir.65.5.879

Cited by 136 publications

(32 citation statements)

References 25 publications

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“…Deficiency of the CYP2D6 Flecainide Flecainide is very well absorbed orally with negligible hepatic first pass effect [76]. Elimination halfisozyme ( poor metabolizers) results in impaired metabolism but only of the R-enantiomer [89], the life ranges from 7 to 15 h in healthy volunteers and averages about 10 h in patients with cardiac disease [77].…”

Section: Class Ic Drugs (Flecainide Propafenone)mentioning

confidence: 99%

Therapeutic drug monitoring: antiarrhythmic drugs

Campbell

Williams

2001

Brit J Clinical Pharma

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Antiarrhythmic agents are traditionally classified according to Vaughan Williams into four classes of action. Class I antiarrhythmic agents include most of the drugs traditionally thought of as antiarrhythmics, and have as a common action, blockade of the fast-inward sodium channel on myocardium. These agents have a very significant toxicity, and while they are being used less, therapeutic drug monitoring (TDM) does significantly increase the safety with which they can be administered. Class II agents are antisympathetic drugs, particularly the b-adrenoceptor blockers. These are generally safe agents which do not normally require TDM. Class III antiarrhythmic agents include sotalol and amiodarone. TDM can be useful in the case of amiodarone to monitor compliance and toxicity but is generally of little value for sotalol. Class IV antiarrhythmic drugs are the calcium channel blockers verapamil and diltiazem. These are normally monitored by haemodynamic effects, rather than using TDM. Other agents which do not fall neatly into the Vaughan Williams classification include digoxin and perhexiline. TDM is very useful for monitoring the administration (and particularly the safety) of both of these agents.

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Section: Class Ic Drugs (Flecainide Propafenone)mentioning

confidence: 99%

Therapeutic drug monitoring: antiarrhythmic drugs

Campbell

Williams

2001

Brit J Clinical Pharma

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“…The absence of trend of change in any of the baseline haemodynamic variables during the control period confirmed the haemodynamic stability of each group. The therapeutic ranges for plasma levels of lignocaine, disopyramide and flecainide are 1-5 ,ug ml-', 2-5 ,ug ml-' and 200-800 ng ml-1 respectively (Bigger, 1980;Grossman et al, 1969;Niarchos, 1976;Koch-Weser, 1979;Anderson et al, 1981;Duran et al, 1982;Hellestrand et al, 1982;Hodges et al, 1982). These were achieved throughout the study, with plasma disopyramide close to the upper limit.…”

Section: Discussionmentioning

confidence: 88%

“…Flecainide, a new class 1C antiarrhythmic agent is an effective broad spectrum anti-arrhythmic (Hellestrand et al, 1982;Hodges et al, 1982;Anderson et al, 1981;Duff et al, 1981;Duran et al, 1982;Anderson et al, 1984). In common with other class 1 agents it induces mild depression of cardiac function in stable coronary artery disease (Legrand et al, 1983;Serruys et al, 1983;Josephson et al, 1984).…”

Section: Introductionmentioning

confidence: 99%

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction

1987

Journal of Cardiothoracic Anesthesia

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1 A prospective study evaluated the comparative haemodynamic effects of three Class I antiarrhythmics (lignocaine Class 1B, disopyramide Class 1A and flecainide Class 1C) in 30 patients with uncomplicated acute myocardial infarction. Three groups, each of 10 patients, were allocated to lignocaine (Group I) 1.5 mg kg-' i.v. loading dose over 10 min followed by infusion at 3 mg kg-' h-', disopyramide (Group II) or flecainide (Group III), both administered as a 1.0 mg kg-' i.v. loading bolus over 10 min followed by a 1.6 mg kg-' h-1 infusion for 120 min.2 The plasma levels of each drug were in the described therapeutic range. Lignocaine decreased cardiac index (-0.31 min-' m-2 (9%); P < 0.05) and stroke volume index (-5 ml m-2 (11%); P < 0.01). Systemic blood pressure, heart rate and systemic vascular resistance index were unchanged. There was a small increase (+3 mm Hg (30%); P < 0.01) in pulmonary artery occluded pressure (PAOP).3 Both disopyramide and flecainide increased systemic blood pressure; the maximum increases for mean blood pressure were + 10 mm Hg (11%) and + 4 mm Hg (4%) respectively. Both drugs reduced cardiac index (-0.5 1 min-' m-2 (16%): -0.4 1 min-' m-2 (11%)) and stroke volume index (-11 mIm-2 (25%): -5 mI m-2 (11%)). There were increases in heart rate (+ 13: +5 beats min-1) pulmonary artery occluded pressure (+2: + 3 mm Hg) and systemic vascular resistance index (+696: +275 dyn s cm-5 m2).4 Thus greatest and least haemodynamic depression followed disopyramide and lignocaine respectively with flecainide occupying an intermediate position. Disopyramide also resulted in progressive haemodynamic depression; this contrasted with early depression of parameters but with subsequent return towards control values following lignocaine and flecainide. 5 This study suggested a haemodynamic basis favouring lignocaine, flecainide and disopyramide in that order for the management of arrhythmias in patients with acute myocardial infarction.

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“…13-15 Parameters related to myocardial contractility, such as peak positive dP!dt and Vmax, decrease after intravenous administration of 2 mg/kg of flecainide. l4 Increases in pulmonary wedge pressure and left* ventricular end-diastolic pressure have been observed, together with decreases in cardiac index (7 to l2%] and left ventricular ejection fraction (7 …”

Section: Discussionmentioning

confidence: 96%

Effect of flecainide on regional left ventricular wall motion after acute intravenous, acute oral and chronic oral administration late after coronary artery bypass grafting

Vanhaleweyk

Katen

Brower

et al. 1986

The American Journal of Cardiology

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Epicardial marker motion was measured in 14 patients before flecainide administration, immediately after an intravenous dose of 2 mg/kg over 15 minutes (maximum' 150 mg) and 15 minutes thereafter. Platinum epicardial markers had been implanted more than 4 years earlier at the time of coronary artery bypass grafting. Maximal and minimal marker separation (Lmax and Lmin) during the cardiac cycle were measured and regional shortening fraction (Lmax -Lmin)/Lmax) was determined as a per: centage. After intravenous flecainide, a significant increase in end-diastolic (immediately after 2.8%; after 15 minutes 2.1% ) and end-systolic (3.8 % and 3.2% ) regional dimensions was observed, together with a decrease in regional myocardial shortening (9.3% and 9.0%). One week later, after a single oral dose of 200 mg of flecainide, Lmax and Lmin had increased 2.4 % and 2.7 % , while regional myocardial shortening did not differ significantly, from baseline values. In 19 patients measurements were repeated after 8 weeks of chronic oral treatment with 300 mg/day. Despite plasma flecainide levels similar to those after intravenous administration, no significant changes.in'end-diastolic and end-systolic dimensions or regional shortening fraction were observed. Thus, acute intravenous or oral flecainide administration increases regional end-diastolic and end-systolic dimensions, but only intravenous administration decreases regional shortening fraction. Values during chronic administration indicate that regional myocardial function is more affected at the time of rising or acutely changing flecainide plasma levels than when stable plasma levels are achieved.( Am J Cardiol 1988;58:470-475) F lecainide acetate, an antiarrhythmic agent that slows atrial, nodal and ventricular conduction and increases atria1 and ventricular refractoriness,1-4 is effective in suppressing ventricular arrhythmias and reentrant tachycardias related to anomalous atrioventricular pathways4-l2A myocardial depressant effect after intravenous administration of flecainide in humans has been reported,13-l5 whereas echocardiographic measures of From the Thoraxcenter, University Hospital "Dijkzigt," Rotterdam, The Netherlands. Manuscript

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Suppression of ventricular ectopic depolarizations by flecainide acetate, a new antiarrhythmic agent.

Cited by 136 publications

References 25 publications

Therapeutic drug monitoring: antiarrhythmic drugs

Therapeutic drug monitoring: antiarrhythmic drugs

Comparative haemodynamic effects of intravenous lignocaine, disopyramide and flecainide in uncomplicated acute myocardial infarction

Effect of flecainide on regional left ventricular wall motion after acute intravenous, acute oral and chronic oral administration late after coronary artery bypass grafting

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