Department of Cardiology, ICaR-VU, VU University Medical Center, Amsterdam, the Netherlands.
Department of Vascular Medicine, Academic Medical Center, Amsterdam, the Netherlands.
JACC Cardiovasc Interv. 2016 Mar 28;9(6):602-13. doi: 10.1016/j.jcin.2016.01.001.
The aim of this study was to determine the effects of an acute myocardial infarction (AMI) on baseline and hyperemic flow in both culprit and nonculprit arteries.
An impaired coronary flow reserve (CFR) after AMI is related to worse outcomes. The individual contribution of resting and hyperemic flow to the reduction of CFR is unknown. Furthermore, it is unclear whether currently used experimental models of AMI resemble the clinical situation with respect to coronary flow parameters.
Intracoronary Doppler flow velocity measurements were obtained in culprit and nonculprit arteries immediately after successfully revascularized ST-segment elevation myocardial infarction (n = 40). Stable patients without obstructive coronary artery disease served as control subjects and were selected by propensity-score matching (n = 40). Similar measurements in an AMI porcine model were taken both before and immediately after 75-min balloon occlusion of the left circumflex artery (n = 11).
In the culprit artery, CFR was 36% lower than in matched control subjects (Δ = -0.9; 1.8 ± 0.9 vs. 2.8 ± 0.7; p < 0.001) with consistent observations in swine (Δ = -0.9; 1.5 ± 0.4 vs. 2.4 ± 0.9 for after and before AMI, respectively; p = 0.04). An increased baseline and a decreased hyperemic flow contributed to the reduction in CFR in both patients (baseline flow: Δ = +5 and hyperemic flow: Δ = -7 cm/s) and swine (baseline flow: Δ = +8 and hyperemic flow: Δ = -6 cm/s). Similar changes were observed in nonculprit arteries (CFR: 2.8 ± 0.7 vs. 2.0 ± 0.7 for STEMI patients and control subjects; p < 0.001). CFR significantly correlated with infarct size as a percentage of the left ventricle in both patients (r = -0.48; p = 0.001) and swine (r = -0.61; p = 0.047).
CFR in both culprit and nonculprit coronary arteries decreases after AMI with contributions from both an increased baseline flow and a decreased hyperemic flow. The decreased CFR after AMI in culprit and nonculprit vessels is not a result of pre-existing microvascular dysfunction, but represents a combination of post-occlusive hyperemia, myocardial necrosis, hemorrhagic microvascular injury, compensatory hyperkinesis, and neurohumoral vasoconstriction.
本研究旨在确定急性心肌梗死（AMI）对罪犯和非罪犯动脉基础和充血血流的影响。
AMI 后冠状动脉血流储备（CFR）受损与预后较差有关。休息和充血血流对 CFR 降低的个体贡献尚不清楚。此外，目前用于 AMI 的实验模型是否与冠状动脉血流参数方面的临床情况相似尚不清楚。
在成功再通 ST 段抬高型心肌梗死（STEMI）后，立即在罪犯和非罪犯动脉中进行冠状动脉内多普勒血流速度测量（n = 40）。选择无阻塞性冠状动脉疾病的稳定患者作为对照，并通过倾向评分匹配（n = 40）进行选择。在左回旋支动脉闭塞 75 分钟前后，对 AMI 猪模型进行类似的测量（n = 11）。
罪犯动脉的 CFR 比匹配的对照组低 36%（Δ=-0.9；1.8±0.9 比 2.8±0.7；p<0.001），猪的观察结果一致（Δ=-0.9；AMI 前后分别为 1.5±0.4 比 2.4±0.9；p=0.04）。基线增加和充血性血流减少导致患者（基线流量：Δ=+5 和充血性流量：Δ=-7 cm/s）和猪（基线流量：Δ=+8 和充血性流量：Δ=-6 cm/s）CFR 降低。非罪犯动脉也观察到类似的变化（CFR：STEMI 患者和对照组分别为 2.8±0.7 比 2.0±0.7；p<0.001）。在患者（r=-0.48；p=0.001）和猪（r=-0.61；p=0.047）中，CFR 与左心室梗死面积百分比均呈显著相关。
AMI 后罪犯和非罪犯冠状动脉的 CFR 降低，基础血流增加和充血性血流减少均有贡献。罪犯和非罪犯血管 AMI 后 CFR 降低不是预先存在的微血管功能障碍的结果，而是闭塞后充血、心肌坏死、出血性微血管损伤、代偿性过度收缩和神经激素血管收缩的综合结果。
