Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease.
Hemodynamic and metabolic correlates of dipyridamole-induced myocardial thallium-201 perfusion abnormalities in multivessel coronary artery disease.
复制标题
多支冠状动脉疾病中双嘧达莫诱导的心肌铊 201 灌注异常的血流动力学和代谢相关性。
DOI：
10.1016/0002-9149(94)90174-0
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发表时间：
1994
期刊：
影响因子：
--
通讯作者：
Feldman,MD
中科院分区：
文献类型：
--
作者：
McLaughlin,DP;Beller,GA;Linden,J;Ayers,CR;Ripley,ML;Taylor,H;Watson,DD;Feldman,MD
在冠状动脉疾病（CAD）患者中，潘生丁应激导致可逆性铊-201（Tl-201）缺陷的机制尚不清楚。先前的实验动物研究已经证明了冠状动脉盗血的特征是响应于潘生丁输注的狭窄远端的内膜下血流的绝对减少。因此，本研究的目的是确定是否可逆的TI-201的缺陷，反应潘生丁输注是心肌缺血或继发于血流储备的区域差异。在23例患者中进行了双嘧达莫（0.56 mg/kg）Tl-201成像，其中获得了系列心电图、血流动力学、主动脉和冠状窦乳酸盐和冠状窦腺苷测量值。所有患有CAD的患者都有Tl-201再分布（3.8 ± 2.0个缺陷/患者），所有没有CAD的患者都有正常扫描。两组的平均主动脉压相似，对潘生丁没有反应（非CAD 103 ± 11 vs CAD 99 ± 15 mm Hg，p = NS）。肺毛细血管楔压在基线时相似（非CAD 11 ± 4 vs CAD 13 ± 5 mm Hg，p = NS），对药物无反应（非CAD 14 ± 3 vs CAD 15 ± 7 mm Hg，p = NS）。基线时乳酸提取分数相似（非CAD 0.22 ± 0.09 vs CAD 0.17 ± 0.14，p = NS），并且两组的下降幅度相似（非CAD 0.08 ± 0.06 vs CAD 0.05 ± 0.12，p = NS）。CAD患者的冠状窦腺苷浓度在基线时显著较高（非CAD 16 ± 4 vs CAD 35 ± 13 ng/ml，p = 0.034），可能是为了维持静息冠状动脉血流量，并且在双嘧达莫治疗后两组的腺苷浓度显著增加，增加百分比相当（非CAD 35 ± 10 vs CAD 69 ± 35 ng/ml，p = 0.0001）。在这组多支血管CAD患者中，潘生丁诱导的Tl-201灌注异常与血流动力学和代谢标准的显著心肌缺血无关，似乎更能指示血流储备异常。
The mechanisms responsible for the development of reversible thallium-201 (Tl-201) defects with dipyridamole stress in patients with coronary artery disease (CAD) is not well understood. Previous experimental animal studies have demonstrated coronary steal characterized by an absolute decrease in subendocardial flow distal to a stenosis in response to dipyridamole infusion. Accordingly, the purpose of this study was to determine if reversible Tl-201 defects in response to dipyridamole infusion are reflective of myocardial ischemia or secondary to regional differences in flow reserve. Dipyridamole (0.56 mg/kg) Tl-201 imaging was performed in 23 patients in whom serial electrocardiographic, hemodynamic, aortic and coronary sinus lactate, and coronary sinus adenosine measurements were obtained. All patients with CAD had Tl-201 redistribution (3.8 ± 2.0 defects/patient), and all patients without CAD had normal scans. Mean aortic pressure was similar in both groups and did not change in response to dipyridamole (non-CAD 103 ± 11 vs CAD 99 ± 15 mm Hg, p = NS). Pulmonary capillary wedge pressure was similar at baseline (non-CAD 11 ± 4 vs CAD 13 ± 5 mm Hg, p = NS) and did not change in response to the drug (non-CAD 14 ± 3 vs CAD 15 ± 7 mm Hg, p = NS). Lactate extraction fraction was similar at baseline (non-CAD 0.22 ± 0.09 vs CAD 0.17 ± 0.14, p = NS) and decreased similarly in both groups (non-CAD 0.08 ± 0.06 vs CAD 0.05 ± 0.12, p = NS). Coronary sinus adenosine concentration was significantly higher at baseline in patients with CAD (non-CAD 16 ± 4 vs CAD 35 ± 13 ng/ml, p = 0.034), presumably to maintain resting coronary blood flow, and increased significantly with a comparable percent increase in both groups after dipyridamole (non-CAD 35 ± 10 vs CAD 69 ± 35 ng/ml, p = 0.0001). In this group of patients with multivessel CAD, dipyridamole-induced Tl-201 perfusion abnormalities were not associated with significant myocardial ischemia by hemodynamic and metabolic criteria and appeared to be more indicative of abnormal flow reserve.