Micari Antonio, Pascotto Marco, Jayaweera Ananda R, Sklenar Jiri, Goodman N Craig, Kaul Sanjiv
Division of Cardiovascular Medicine, Oregon Health and Science University, Portland, OR 97239, USA.
J Ultrasound Med. 2006 Aug;25(8):1009-19. doi: 10.7863/jum.2006.25.8.1009.
We tested the hypothesis that the cyclic variation in ultrasonic myocardial integrated backscatter (IBS) is due to cardiac contraction-induced changes in the number of patent myocardial microvessels.
We performed experiments in open-chest dogs in which we increased the number of patent myocardial microvessels without changing cardiac contraction. We achieved this either by direct intracoronary administration of adenosine (group 1; n = 10) or by producing a noncritical coronary stenosis (group 2; n = 7).
At baseline, IBS was lowest in systole and highest in diastole. This cyclic variation in IBS was closely associated with the phasic changes in myocardial blood volume that were measured with myocardial contrast echocardiography. During adenosine administration, the diastolic IBS increased from -18.8 +/- 6.5 to -17.5 +/- 6.1 dB (P = .002), with an associated increase in the difference between the systolic and diastolic IBS from 3.8 +/- 1.1 to 4.6 +/- 1.0 dB (P = .009). After a noncritical stenosis was produced, diastolic IBS also increased from -26.6 +/- 8.3 to -25.2 +/- 7.3 dB (P = .001), with an associated increase in the difference between the systolic and diastolic IBS from 3.7 +/- 1.2 to 5.0 +/- 1.0 dB (P = .02). No change in IBS was noted in the bed that did not receive adenosine or the bed that had a stenosis.
The variation in IBS during the cardiac cycle is closely associated with the phasic changes in myocardial blood volume seen during cardiac contraction. When the number of patent myocardial arterioles is increased via adenosine or placement of a noncritical stenosis, diastolic IBS increases with a concomitant increase in IBS cyclic variation. These results may have important clinical applications for the noninvasive diagnosis of noncritical coronary stenosis at rest.
我们验证了以下假设,即超声心肌背向散射积分(IBS)的周期性变化是由于心脏收缩引起的心肌微血管开放数量的改变。
我们在开胸犬身上进行实验,在不改变心脏收缩的情况下增加心肌微血管开放数量。我们通过直接冠状动脉内注射腺苷(第1组;n = 10)或制造非临界冠状动脉狭窄(第2组;n = 7)来实现这一点。
在基线时,IBS在收缩期最低,在舒张期最高。IBS的这种周期性变化与心肌对比超声心动图测量的心肌血容量的相位变化密切相关。在注射腺苷期间,舒张期IBS从-18.8±6.5 dB增加到-17.5±6.1 dB(P = 0.002),收缩期和舒张期IBS的差值从3.8±1.1 dB增加到4.6±1.0 dB(P = 0.009)。制造非临界狭窄后,舒张期IBS也从-26.6±(此处原文似乎有误,推测应为8.3)dB增加到-25.2±7.3 dB(P = 0.001),收缩期和舒张期IBS的差值从3.7±1.2 dB增加到5.0±1.0 dB(P = 0.02)。未接受腺苷的床或有狭窄的床中IBS未观察到变化。
心动周期中IBS的变化与心脏收缩期间心肌血容量的相位变化密切相关。当通过腺苷或放置非临界狭窄增加心肌小动脉开放数量时,舒张期IBS增加,同时IBS周期性变化增加。这些结果可能对静息状态下非临界冠状动脉狭窄的无创诊断具有重要的临床应用价值。