Rossinen J, Partanen J, Koskinen P, Toivonen L, Kupari M, Nieminen M S
Department of Medicine, Helsinki University Central Hospital, Finland.
Heart. 1996 Jun;75(6):563-7. doi: 10.1136/hrt.75.6.563.
To evaluate the effect of acute alcohol ingestion on myocardial ischaemia in patients with coronary heart disease and stable angina.
Randomised crossover study using fruit juice with and without ethanol.
Division of cardiology in a university hospital.
20 patients with stable exertional angina and > or = 50% luminal diameter narrowing of at least one major coronary artery.
Each patient was studied on two separate days, once after administration of 1.25 g of ethanol per kilogram of body weight diluted to 15% in juice, and once after an equivalent volume of juice; both tests were in the evening and lasted 90 minutes. The patients were scheduled to have 8 periods of walking for 10 min according to a time table. An ambulatory electrocardiogram and the occurrence of anginal attacks were recorded and blood pressure and blood ethanol concentration were measured until the next morning.
The blood ethanol concentration (mean (SD)) rose to 28.8 mmol/l (1.3 (0.4)/1000). Alcohol raised the systolic blood pressure from 132 (16) to 141 (14) mm Hg (P < 0.05 compared with juice). The mean heart rate increased from 57 (7) to 64 (8) beats/min (P < 0.05) for 13 hours after ethanol ingestion compared with juice. The total duration of ischaemia during the ethanol test was 3.5 (median, range 0-80) min, compared with 0 (range 0-67) min for the juice test (P < 0.05). The difference resulted mainly from more silent ischaemia after ethanol ingestion (2.3 (0-80) v 0 (0-67) min; P < 0.05). The ST segment depression time integral increased during the ethanol test (4.4 (0-170) mm x min) relative to that during the juice test (0 (0-103) mm x min; P < 0.01) and especially during the following 13 hours after alcohol (3.5 (0-123) mm x min) compared with juice (0 (0-67) mm x min; P < 0.005). There were no changes in the number, duration, or ST segment depression time integral of the episodes of symptomatic angina, indicating that ethanol augmented the appearance of silent ischaemia.
Acute heavy ethanol drinking aggravates myocardial ischaemia in patients with stable angina pectoris.
评估急性摄入酒精对冠心病稳定型心绞痛患者心肌缺血的影响。
采用含乙醇和不含乙醇的果汁进行随机交叉研究。
大学医院的心脏病科。
20例稳定型劳力性心绞痛患者,至少一支主要冠状动脉管腔直径狭窄≥50%。
每位患者在两个不同日期接受研究,一次是给予每千克体重1.25克乙醇并稀释至15%于果汁中,另一次是给予等量的果汁;两次测试均在晚上进行,持续90分钟。患者按照时间表安排进行8次10分钟的步行。记录动态心电图及心绞痛发作情况,并测量血压和血液乙醇浓度直至次日早晨。
血液乙醇浓度(均值(标准差))升至28.8 mmol/l(1.3(0.4)/1000)。酒精使收缩压从132(16)mmHg升至141(14)mmHg(与果汁相比,P<0.05)。与果汁相比,摄入乙醇后13小时内心率均值从57(7)次/分钟增至64(8)次/分钟(P<0.05)。乙醇测试期间心肌缺血总时长为3.5(中位数,范围0 - 80)分钟,而果汁测试为0(范围0 - 67)分钟(P<0.05)。差异主要源于摄入乙醇后更多的无症状性心肌缺血(2.3(0 - 80)对0(0 - 67)分钟;P<0.05)。乙醇测试期间ST段压低时间积分相对于果汁测试增加(4.4(0 - 170)mm·min)(P<0.01),尤其是在摄入酒精后的接下来13小时内(3.5(0 - 123)mm·min),与果汁测试(0(0 - 67)mm·min)相比(P<0.)。有症状性心绞痛发作的次数、持续时间或ST段压低时间积分无变化,表明乙醇增加了无症状性心肌缺血的出现。
急性大量饮酒会加重稳定型心绞痛患者的心肌缺血。