Caffeine as a possible cause of ventricular arrhythmias during the healing phase of acute myocardial infarction.
Caffeine (300 mg) was administered to each of 70 patients a mean (+/- standard error of the mean) of 7 +/- 1 days after the onset of acute myocardial infarction to determine its effects on ventricular arrhythmias. The study was designed as a randomized, double-blind, within-patient comparison between caffeine and placebo. Continuous Holter electrocardiographic recording for 4 hours showed no significant differences in the proportion of patients who had ventricular ectopic activity or the total number and complexity of ventricular premature complexes after caffeine vs placebo. Caffeine increased mean blood pressure from 116 +/- 2/70 +/- 1 mm Hg to a maximum of 125 +/- 3/78 +/- 2 mm Hg (p less than 0.001) at 4 hours. Plasma epinephrine increased (p less than 0.01) from 58 +/- 4 pg/ml to a maximum 88 +/- 6 pg/ml 3 hours after caffeine ingestion, whereas the plasma norepinephrine level did not change. Although caffeine caused significant hemodynamic and humoral responses in this population of relatively caffeine-naive postinfarction patients, it did not increase the occurrence or severity of ventricular arrhythmias.
D001145:Arrhythmias, Cardiac / Q000139:chemically induced*; D001794:Blood Pressure / Q000187:drug effects; D002110:Caffeine / Q000633:toxicity*; D005117:Cardiac Complexes, Premature / Q000139:chemically induced; D004311:Double-Blind Method; D004562:Electrocardiography; D005260:Female; D006801:Humans; D008297:Male; D008875:Middle Aged; D008991:Monitoring, Physiologic; D009203:Myocardial Infarction / Q000150:complications*; D011897:Random Allocation; D013617:Tachycardia, Supraventricular / Q000139:chemically induced
D002110:Caffeine