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Comparative Evaluation of the Hemodynamic Effects of Oral Cimetidine, Ranitidine, and Famotidine as Determined by Echocardiography
Author(s) -
Welage Lynda S.,
DunnKucharski Valerie A.,
Berardi Rosemary R.,
Shea Michael J.,
Dechert Ronald E.,
Bleske Barry E.
Publication year - 1995
Publication title -
pharmacotherapy: the journal of human pharmacology and drug therapy
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.227
H-Index - 109
eISSN - 1875-9114
pISSN - 0277-0008
DOI - 10.1002/j.1875-9114.1995.tb04349.x
Subject(s) - ranitidine , cimetidine , famotidine , medicine , placebo , hemodynamics , ejection fraction , crossover study , histamine h2 receptor , anesthesia , cardiology , antagonist , receptor , heart failure , alternative medicine , pathology
Study Objective . To evaluate the influence of cimetidine, ranitidine, famotidine, and placebo on cardiac performance as determined by echocardiography. Design . Randomized, four‐way crossover trial. Setting . Echocardiography laboratory at a university hospital. Participants . Twelve healthy volunteers. Interventions . Volunteers received oral treatment with placebo, cimetidine 800 mg, ranitidine 300 mg, or famotidine 40 mg once/day for 7 days. Measurements and Main Results . On the seventh day of each study phase, 2 hours after administration of the final dose, each subject underwent cardiac echocardiography and Doppler flow studies. No significant differences were detected in ejection fraction, peak flow velocity, or percentage fractional shortening among the treatment phases. A large degree of variability in ejection fraction was observed, with some subjects experiencing marked decreases. Conclusion . The histamine‐2 (H 2 )‐receptor antagonists had no effect on the hemodynamic variables as determined by echocardiography. The variability in the hemodynamic response may in part explain the conflicting results reported in the literature. It also raises the question as to whether certain individuals are more sensitive to the potential cardiac effects of H 2 ‐receptor antagonists.