Hemodynamic effects of mexiletine

Shanks, R. G.

doi:10.1016/0002-8703(84)90176-5

Cited by 18 publications

(8 citation statements)

References 24 publications

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“…Unlike disopyramide, procainamide, and a new antiarrhythmic drug SUN-1 165, mexiletine exacerbated neither epinephrine-induced arrhythmias by inducing ventricular fibrillation nor digitalis-and coronary ligation-induced arrhythmias (25,54). As shown in Table 2, lidocaine in our study at plasma concentrations of less than 5 pg/ml, surprisingly and in spite of its known effectiveness in the myocardial infarction-related arrhythmias, did not suppress coronary ligation-and epinephrine-induced arrhythmias (2628).…”

mentioning

confidence: 56%

Mexiletine

Hashimoto¹

1986

Cardiovascular Drug Reviews

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mentioning

confidence: 56%

Mexiletine

Hashimoto¹

1986

Cardiovascular Drug Reviews

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“…Our data agree with those of previous studies that show effective suppression of ventricular arrhythmia by intravenous mexiletine with modest toxicity in 60% to 80% of patients.Y:":" Intravenous mexiletine in the dose range we used has rarely adversely affected hemodynamic function or induced adverse cardiac electrophysiologic effects. 13 Despite more stringent criteria for efficacy than used in previous reports, in two thirds of our subjects there was suppression of arrhythmia despite the previous failure of a variety of other antiarrhythmics.…”

Section: Discussionmentioning

confidence: 99%

Conversion from intravenous to oral mexiletine in the acute management of repetitive ventricular arrhythmia

Horowitz

Greenspan

Spielman

et al. 1985

Clin Pharmacol Ther

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We evaluated the safety and efficacy of intravenous mexiletine and a method for converting from intravenous to oral mexiletine therapy. Fifteen patients with repetitive ventricular ectopy (13 had ventricular tachycardia) received intravenous mexiletine at a rate of 10 mg/min for 30 to 60 minutes. Ventricular ectopy was suppressed with minimal side effects in 10 of 15 subjects. Oral mexiletine was begun immediately after completion of the intravenous infusion at a dose of 10 mg/kg/24 hr in the 10 responders to intravenous therapy. In eight, the oral dose was effective in suppressing the arrhythmia, but it induced side effects in three of them. In one of these three, dose reduction resulted in adequate arrhythmia control with acceptable toxicity. In the two who did not respond to the original dose, a larger dose (15 mg/kg/24 hr) induced arrhythmia control with acceptable side effects in one subject. Thus rapid control of nonsustained repetitive ventricular arrhythmia can be achieved with intravenous mexiletine in about two thirds of patients, and conversion to oral therapy can often be achieved smoothly without significant arrhythmia recurrence.

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“…Seventy-three of the 114 patients (43 mexiletine, 26 quinidine, 4 both drugs) underwent long-term follow-up study. Data regarding concurrent arrhythmia therapy are shown in Table IV.…”

Section: Long-term Observations Of Arrhythmia Controlmentioning

confidence: 99%

“…Forty-two patients received both drugs, whereas 36 patients were given mexiletine, and 36 patients received quinidine only. During acute drug testing, mexiletine was more effective than quinidine in controlling ve and Vf (54 vs. 32 patients, respectively, P < .001) and resulted in fewer proarrhythmic events (4 vs. 13, respectively, P < .05). Mean duration offollow-up for mexiletine (27 ± 14 mol and quinidine (21 ± 14 .mol did not differ.…”

mentioning

confidence: 97%

Mexiletine Versus Quinidine as First‐Line Antiarrhythmia Therapy: Results From Consecutive Trials

Frank

Watkins

et al. 1991

The Journal of Clinical Pharma

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The efficacy of mexiletine and quinidine in controlling ventricular couplets (VC) and ventricular tachycardia (VT) was compared in 156 trials (78 for each drug) in 114 consecutive patients. Forty-two patients received both drugs, whereas 36 patients were given mexiletine, and 36 patients received quinidine only. During acute drug testing, mexiletine was more effective than quinidine in controlling VC and VT (54 vs. 32 patients, respectively, P less than .001) and resulted in fewer proarrhythmic events (4 vs. 13, respectively, P less than .05). Mean duration of follow-up for mexiletine (27 +/- 14 mo) and quinidine (21 +/- 14 mo) did not differ. Long-term success was more frequent with mexiletine administration than quinidine administration (33/47 vs. 10/30 patients, respectively, P less than .01). The incidence of sudden death during follow-up with the two drugs did not differ overall, but more patients with ejection fraction greater than or equal to 40% died suddenly while taking quinidine than while receiving mexiletine (4/17 vs. 0/24, P less than .02). Mexiletine is as effective as quinidine for treating VC and VT and appears to be less proarrhythmic. It should be considered as an initial choice in the management of VC and VT.

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Hemodynamic effects of mexiletine

Cited by 18 publications

References 24 publications

Mexiletine

Mexiletine

Conversion from intravenous to oral mexiletine in the acute management of repetitive ventricular arrhythmia

Mexiletine Versus Quinidine as First‐Line Antiarrhythmia Therapy: Results From Consecutive Trials

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