Torres M A, Picano E, Parodi G, Sicari R, Veglia F, Giorgetti A, Marzullo P, Parodi O
CNR Institute of Clinical Physiology, Pisa, Italy.
J Am Coll Cardiol. 1997 Jul;30(1):65-70. doi: 10.1016/s0735-1097(97)88333-7.
We sought to elucidate the flow-function relation in chronic postischemic dysfunction during vasodilator stress.
In patients with ischemia and regional dysfunction, stress echocardiography can elicit three responses in the dysfunctioning segments: no change, improvement or worsening. The physiology underlying these responses is unclear.
Seventeen patients with ischemia and left ventricular dysfunction underwent evaluation of regional function by two-dimensional echocardiography and myocardial blood flow by positron emission tomography and 13N-ammonia. Flow (ml/min per g) and function (regional wall motion score [RWMS] from 1 = normal to 4 = dyskinetic) were evaluated both at rest and after dipyridamole (0.56 mg/kg body weight over 4 min).
In 45 normal segments, rest to dipyridamole flow increased from 0.83 +/- 0.22 (mean +/- 1 SD) to 1.87 +/- 0.90 (p < 0.01) with a hyperkinetic contraction pattern. Among dysfunctioning segments, responders (n = 11) showed an upsloping flow-function curve during stress (i.e., increased function [RWMS rest 2.5 +/- 0.5 vs. dipyridamole 1.2 +/- 0.4] and increased flow [rest 0.69 +/- 0.30 vs. dipyridamole 1.89 +/- 1.43, p < 0.01]); nonresponders (n = 20) had a flat flow-function curve during dipyridamole (i.e., fixed function [RWMS rest and dipyridamole 2.6 +/- 0.5] and no flow increase [rest 0.64 +/- 0.24 vs. dipyridamole 0.87 +/- 0.51, p = NS): Ischemic segments (n = 9) exhibited a downsloping flow-function curve during dipyridamole (i.e., worsened function [RWMS rest 2 +/- 0.5, dipyridamole 3.1 +/- 0.6] and no significant flow change [rest 0.67 +/- 0.29 vs. dipyridamole 0.79 +/- 0.23, p = NS]).
Myocardial segments with rest dysfunction and a contractile reserve elicitable by a vasodilator stress more often exhibit residual flow reserve, whereas segments with a fixed or worsening mechanical response during stress show a flat flow response.
我们试图阐明血管扩张剂负荷试验期间慢性缺血后功能障碍中的血流-功能关系。
在有缺血和局部功能障碍的患者中，负荷超声心动图可在功能障碍节段引发三种反应：无变化、改善或恶化。这些反应背后的生理学机制尚不清楚。
17例有缺血和左心室功能障碍的患者接受了二维超声心动图评估局部功能，以及正电子发射断层扫描和13N-氨评估心肌血流。在静息状态和双嘧达莫（0.56mg/kg体重，4分钟内）负荷后评估血流（每克每分钟毫升数）和功能（局部室壁运动评分[RWMS]，从1=正常到4=运动障碍）。
在45个正常节段中，静息至双嘧达莫负荷时血流从0.83±0.22（平均值±1标准差）增加到1.87±0.90（p<0.01），收缩模式为运动增强。在功能障碍节段中，反应者（n=11）在负荷时显示血流-功能曲线上升（即功能改善[RWMS静息时2.5±0.5对比双嘧达莫负荷时1.2±0.4]且血流增加[静息时0.69±0.30对比双嘧达莫负荷时1.89±1.43，p<0.01]）；无反应者（n=20）在双嘧达莫负荷期间血流-功能曲线平坦（即功能固定[RWMS静息和双嘧达莫负荷时2.6±0.5]且血流无增加[静息时0.64±0.24对比双嘧达莫负荷时0.87±0.51，p=无显著性差异]）：缺血节段（n=9）在双嘧达莫负荷期间显示血流-功能曲线下降（即功能恶化[RWMS静息时2±0.5，双嘧达莫负荷时3.1±0.6]且血流无显著变化[静息时0.67±0.29对比双嘧达莫负荷时0.79±0.23，p=无显著性差异]）。
静息时功能障碍且血管扩张剂负荷可诱发收缩储备的心肌节段更常表现出残余血流储备，而负荷时机械反应固定或恶化的节段显示血流反应平坦。
