Broad-Complex Tachycardia After Intrayenous Cimetidine

Dickey, William; Symington, Mark

doi:10.1016/s0140-6736(87)91931-3

Cited by 4 publications

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“…These findings are in accordance with data from postmarketing surveillance studies of famotidine and of the older H2-receptor antagonists cimetidine and ranitidine.40-43 However, single case reports have shown that cardiac function may be compromised and arrhythmias could develop during therapy with H2-receptor antagonists, mostly after rapid intravenous injection of cimetidine or ranitidine. [44][45][46][47] The effects of quinidine, an amphophilic substance penetrating cellular membranes and residing in the myocardial cell membrane, can be explained by nonspecific inhibition of transmembranous sodium, calcium, and potassium transport leading to negative inotropic properties. [48][49][50][51] The decrease in cardiac VOLUME 5 1 NUMBER 3 Hemodynamic effects of quinidine and famotidine 3 3 1 performance after famotidine administration has not been clarified up to now.…”

Section: Discussionmentioning

confidence: 99%

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Kirch

Halabi

Hinrichsen

1992

Clin Pharmacol Ther

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In a randomized, placebo-controlled, double-blind study, 12 patients with congestive heart failure (New York Heart Association class II) were successively treated for 1 week each with placebo, 40 mg famotidine, and 1000 mg quinidine. On the seventh treatment day, heart rate, blood pressure, systolic time intervals, impedance cardiography, and Doppler ultrasound were measured. Heart rate and blood pressure were not markedly altered by either drug. By contrast, quinidine and famotidine significantly decreased stroke volume and cardiac output in impedance cardiography and Doppler ultrasound (p less than 0.05). A high correlation between both noninvasive methods was found for cardiac output and stroke volume (r = 0.93 and r = 0.97 for stroke volume 1 1/2 hours after quinidine and placebo administration, respectively). In addition, the mechanocardiographic ratio of the preejection period to the left ventricular ejection time in systolic time intervals increased significantly 1 1/2 and 3 hours after administration of quinidine and famotidine (p less than 0.05). In conclusion, both quinidine and famotidine exert similar negative effects on cardiac performance, with no significant differences in hemodynamic parameters emerging between the antiarrhythmic agent and the H2-receptor antagonist.

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Section: Discussionmentioning

confidence: 99%

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Kirch

Halabi

Hinrichsen

1992

Clin Pharmacol Ther

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Clinically Important Adverse Effects and Drug Interactions with H₂‐Receptor Antagonists: An Update

Sax¹

1987

Pharmacotherapy

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The H2‐receptor antagonists cimetidine, ranitidine, and famotidine are well tolerated, with a low frequency and similar spectrum of adverse effects. The occasional problematic effects that have been associated with these agents include central nervous system symptoms (mental confusion, headache, and depression), rare cases of thrombocytopenia, and cardiovascular events related to the rate of intravenous infusion. Severe renal and hepatic impairment appear to be associated with a higher occurrence of central nervous system effects. Because the H2‐receptor antagonists elevate gastric pH, bind to and inhibit the hepatic cytochrome P‐450 enzyme system, and undergo renal tubular secretion, competition with other drugs sharing these pathways has resulted in a number of drug interactions, most of which are not clinically significant. The interaction that occurs with theophylline and warfarin when the cytochrome P‐450 enzyme system is inhibited by cimetidine and ranitidine requires monitoring. Recent data suggest that administering cimetidine 800 mg at bedtime has less effect on the serum concentrations of warfarin and theophylline than other dosing regimens. Evidence to date indicates that famotidine does not bind to cytochrome P‐450 to a significant extent, and interactions with drugs metabolized by this system have not been reported; however, clinical experience with this agent is very limited.

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Pharmacological control of gastric acid secretion: Molecular and cellular aspects

et al. 1992

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Broad-Complex Tachycardia After Intrayenous Cimetidine

Cited by 4 publications

References 2 publications

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Clinically Important Adverse Effects and Drug Interactions with H₂‐Receptor Antagonists: An Update

Pharmacological control of gastric acid secretion: Molecular and cellular aspects

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Broad-Complex Tachycardia After Intrayenous Cimetidine

Cited by 4 publications

References 2 publications

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Hemodynamic effects of quinidine and famotidine in patients with congestive heart failure

Clinically Important Adverse Effects and Drug Interactions with H2‐Receptor Antagonists: An Update

Pharmacological control of gastric acid secretion: Molecular and cellular aspects

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Product

Resources

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Clinically Important Adverse Effects and Drug Interactions with H₂‐Receptor Antagonists: An Update