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进食后心肌缺血增加并非由内皮功能障碍所致。

Increased myocardial ischemia after food is not explained by endothelial dysfunction.

作者信息

Edwards Colin, Stewart Ralph A H, Ramanathan Krishnan, West Teena M, French John K, White Harvey D

机构信息

Cardiovascular Research Unit, Green Lane Hospital, Auckland, New Zealand.

出版信息

Am Heart J. 2002 Nov;144(5):E8. doi: 10.1067/mhj.2002.125624.

Abstract

BACKGROUND

Recent studies suggest that a high-fat meal can impair endothelial function. The aim of this study was to determine whether greater myocardial ischemia after either a low-fat or a high-fat meal is associated with an increase in brachial artery endothelial dysfunction.

METHODS

Twenty subjects with coronary artery disease and > or =1-mm ST-segment depression during exercise were studied. In a randomized, double-blind, crossover design, ST-segment changes during treadmill exercise and brachial artery diameter and flow-mediated dilation were measured before and 3 hours after a low-fat milkshake meal or the same meal supplemented with 64 grams of cooked fat.

RESULTS

After the low-fat but not the high-fat meal, resting brachial artery diameter decreased (before meal 4.72 +/-0.50 mm, after low fat meal 4.62 +/-0.49 mm, P =.001; after high fat meal 4.70 +/-0.51 mm, not significant). High-flow brachial artery diameter was similar before (4.81 +/- 0.48 mm) and after the low-fat (4.82 +/- 0.48 mm) and high-fat (4.84 +/- 0.48 mm) meals (P >.05 for all). Brachial artery flow-mediated dilation was not impaired after either meal. Exercise duration decreased more after the low-fat meal (mean change 39 seconds, 95% CI -14 to -63 seconds, P =.004) than after the high-fat meal (-7 seconds, 95% CI +19 to -34 seconds, not significant). ST-segment depression during equivalent exercise was greater after compared with before both meals (before meals 1.03 +/- 0.69 mm, after low fat 1.27 +/- 0.80 mm, P =.03; after high fat 1.24 +/- 0.74 mm, P =.04).

CONCLUSIONS

Increased myocardial ischemia after food is caused by mechanisms other than endothelial dysfunction and by meal components other than cooked fat.

摘要

背景

近期研究表明,高脂餐会损害内皮功能。本研究旨在确定低脂餐或高脂餐后心肌缺血加重是否与肱动脉内皮功能障碍增加有关。

方法

对20名患有冠状动脉疾病且运动时ST段压低≥1毫米的受试者进行了研究。采用随机、双盲、交叉设计,在食用低脂奶昔餐或添加64克熟脂肪的同一餐之前和之后3小时,测量跑步机运动期间的ST段变化以及肱动脉直径和血流介导的扩张。

结果

低脂餐后而非高脂餐后,静息肱动脉直径减小(餐前4.72±0.50毫米,低脂餐后4.62±0.49毫米,P = 0.001;高脂餐后4.70±0.51毫米,无显著差异)。高脂餐前后高流量肱动脉直径相似(分别为4.81±0.48毫米和4.84±0.48毫米),低脂餐前后也相似(分别为4.81±0.48毫米和4.82±0.48毫米)(所有P>0.05)。两餐之后肱动脉血流介导的扩张均未受损。低脂餐后运动持续时间的减少幅度(平均变化39秒,95%置信区间-14至-63秒,P = 0.004)大于高脂餐后(-7秒,95%置信区间+19至-34秒,无显著差异)。与两餐之前相比,同等运动期间的ST段压低在两餐之后均更大(餐前1.03±0.69毫米,低脂餐后1.27±0.80毫米,P = 0.03;高脂餐后1.24±0.74毫米,P = 0.04)。

结论

进食后心肌缺血增加是由内皮功能障碍以外的机制以及熟脂肪以外的膳食成分引起的。

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