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严重狭窄远端冠状动脉血流餐后激增的缺失:餐后心绞痛的一种可能机制。

Absence of postprandial surge in coronary blood flow distal to significant stenosis: a possible mechanism of postprandial angina.

作者信息

Chung Woo-Young, Sohn Dae-Won, Kim Yong-Jin, Oh Seil, Chai In-Ho, Park Young-Bae, Choi Yun-Shik

机构信息

Clinical Research Institute and Division of Cardiology, Department of Internal Medicine, Seoul National University College of Medicine, Seoul, South Korea.

出版信息

J Am Coll Cardiol. 2002 Dec 4;40(11):1976-83. doi: 10.1016/s0735-1097(02)02533-0.

Abstract

OBJECTIVES

This study was designed to investigate a possible mechanism of postprandial angina.

BACKGROUND

Postprandial angina has been recognized for more than two centuries; however, its mechanism is still controversial. The most widely accepted mechanism involves increased myocardial oxygen demand after food intake. Recently, the redistribution in coronary blood flow (CBF) was suggested as a possible mechanism.

METHODS

Twenty young, healthy volunteer controls and 20 patients with significant stenosis in the left anterior descending (LAD) or left main coronary artery were enrolled in the study. Coronary blood flow was evaluated in the distal LAD by using transthoracic Doppler echocardiography before and 15, 30, 45, and 60 min after food intake. In the CBF curve, the time velocity integral of diastolic flow (Dtvi) and the product of Dtvi and heart rate (HR) were measured. In six patients, these measurements were repeated after successful coronary intervention.

RESULTS

In the healthy volunteer controls, Dtvi and Dtvi x HR increased after food intake with a peak value at 15 min, which indicates the presence of postprandial surge in the CBF. Fasting values and peak values at 15 min were significantly different (Dtvi: 15.1 +/- 4.9 cm/s vs. 18.9 +/- 5.9 cm/s, p = 0.04, Dtvi x HR: 862.2 +/- 261.5 cm/min vs. 1,174.2 +/- 307.5, p = 0.002). In contrast with the controls, despite postprandial increase in double product (HR x blood pressure), Dtvi and Dtvi x HR in the patient group decreased after food intake, with a nadir value at 45 min. Fasting values and nadir values at 45 min were significantly different (Dtvi: 24.0 +/- 19.6 cm/s vs. 19.3 +/- 17.1 cm/s, p < 0.001, Dtvi x HR: 1,449.6 +/- 1,044.0 cm/min vs. 1,273.4 +/- 1,000.9 cm/min, p = 0.002). In six patients, the CBF pattern resumed the normal pattern of postprandial surge in the CBF after successful coronary intervention.

CONCLUSIONS

Results of our study suggest that "steal phenomenon" may play a role in the mechanism of postprandial angina.

摘要

目的

本研究旨在探究餐后心绞痛可能的机制。

背景

餐后心绞痛已被认识超过两个世纪;然而,其机制仍存在争议。最被广泛接受的机制是进食后心肌需氧量增加。最近,冠状动脉血流(CBF)的重新分布被认为是一种可能的机制。

方法

本研究纳入了20名年轻健康的志愿者作为对照,以及20名左前降支(LAD)或左主干冠状动脉存在明显狭窄的患者。在进食前以及进食后15、30、45和60分钟,使用经胸多普勒超声心动图评估LAD远端的冠状动脉血流。在CBF曲线中,测量舒张期血流的时间速度积分(Dtvi)以及Dtvi与心率(HR)的乘积。在6名患者中,冠状动脉介入成功后重复进行这些测量。

结果

在健康志愿者对照组中,进食后Dtvi和Dtvi×HR增加,在15分钟时达到峰值,这表明存在餐后CBF激增。空腹值与15分钟时的峰值有显著差异(Dtvi:15.1±4.9厘米/秒对18.9±5.9厘米/秒,p = 0.04;Dtvi×HR:862.2±261.5厘米/分钟对1,174.2±307.5,p = 0.002)。与对照组相反,尽管患者组进食后双乘积(HR×血压)增加,但Dtvi和Dtvi×HR在进食后下降,在45分钟时达到最低点。空腹值与45分钟时的最低点有显著差异(Dtvi:24.0±19.6厘米/秒对19.3±17.1厘米/秒,p < 0.001;Dtvi×HR:1,449.6±1,044.0厘米/分钟对1,273.4±1,000.9厘米/分钟,p = 0.002)。在6名患者中,冠状动脉介入成功后,CBF模式恢复为餐后CBF激增的正常模式。

结论

我们的研究结果表明,“窃血现象”可能在餐后心绞痛的机制中起作用。

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