Myers M G, Harris L, Leenen F H, Grant D M
Am J Cardiol. 1987 May 1;59(12):1024-8. doi: 10.1016/0002-9149(87)90842-3.
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.
在70例急性心肌梗死患者发病后平均（±平均标准误）7±1天，给每位患者服用300毫克咖啡因，以确定其对室性心律失常的影响。该研究设计为咖啡因与安慰剂之间的随机、双盲、患者自身对照试验。连续4小时的动态心电图记录显示，服用咖啡因组与服用安慰剂组相比，出现室性异位活动的患者比例、室性早搏的总数及复杂性均无显著差异。咖啡因使平均血压在4小时时从116±2/70±1毫米汞柱升至最高125±3/78±2毫米汞柱（p<0.001）。血浆肾上腺素在摄入咖啡因3小时后从58±4皮克/毫升升至最高88±6皮克/毫升（p<0.01），而血浆去甲肾上腺素水平未发生变化。虽然咖啡因在这群相对较少接触咖啡因的心肌梗死后患者中引起了显著的血流动力学和体液反应，但并未增加室性心律失常的发生率或严重程度。
