Fatkin D, Loupas T, Low J, Feneley M
Cardiology Department and Victor Chang Cardiac Research Institute, St Vincent's Hospital, Darlinghurst, Australia.
Circulation. 1997 Aug 5;96(3):889-96. doi: 10.1161/01.cir.96.3.889.
Spontaneous echocardiographic contrast (SEC) is a pattern of blood echogenicity that has been attributed to ultrasonic backscatter from blood cell aggregates that form under low shear conditions. Patients with left atrial SEC have an increased thromboembolic risk. This study examined the role of red cell and platelet aggregates in the pathogenesis of SEC in human blood and the effects on SEC of antithrombotic therapy and red cell disaggregatory agents.
Blood echogenicity was examined with the use of quantitative videodensitometry over a controlled range of flow velocities in an in vitro model characterized by nonlaminar flow conditions. One hundred ninety study samples were prepared from single fresh blood donations (40 to 120 mL) from 24 healthy volunteers and 11 patients. Whole blood echogenicity was unaltered by depletion of platelets, stimulation of platelet aggregation with adenosine diphosphate, or inhibition of platelet aggregation with aspirin. Low flow-related echogenicity increased with increasing hematocrit (P<.001) but was abolished when red cells were lysed selectively with saponin (P<.001). In the presence of red cells, low flow-related echogenicity increased with increasing fibrinogen concentration (P<.001) and with plasma paraproteins. Low flow-related echogenicity in whole blood was unaltered by heparin and warfarin but was reduced in a dose-dependent manner by dextran 40 (40 mg/mL, 70% reduction, P<.001) and poloxamer 188 (8 mg/mL, 47% reduction, P<.001), which inhibited red cell aggregation.
These results support protein-mediated red cell aggregation as the mechanism of SEC in human blood. Inhibition of red cell aggregation, indexed by resolution of SEC, may provide an alternative to anticoagulant and antiplatelet therapy to reduce cardiac thromboembolic risk.
自发超声心动图造影（SEC）是一种血液回声模式，其归因于在低剪切条件下形成的血细胞聚集体产生的超声背向散射。左心房SEC患者的血栓栓塞风险增加。本研究探讨了红细胞和血小板聚集体在人类血液SEC发病机制中的作用以及抗血栓治疗和红细胞解聚剂对SEC的影响。
在以非层流条件为特征的体外模型中，通过定量视频密度测定法在可控的流速范围内检测血液回声。从24名健康志愿者和11名患者的单次新鲜血液捐献（40至120 mL）中制备了190个研究样本。血小板耗竭、用二磷酸腺苷刺激血小板聚集或用阿司匹林抑制血小板聚集均未改变全血回声。低流量相关回声随血细胞比容增加而增加（P<0.001），但用皂苷选择性裂解红细胞后则消失（P<0.001）。在有红细胞存在的情况下，低流量相关回声随纤维蛋白原浓度增加而增加（P<0.001），并与血浆副蛋白有关。全血中的低流量相关回声不受肝素和华法林影响，但右旋糖酐40（40 mg/mL，降低70%，P<0.001）和泊洛沙姆188（8 mg/mL，降低47%，P<0.001）以剂量依赖方式降低，这两种药物可抑制红细胞聚集。
这些结果支持蛋白质介导的红细胞聚集是人类血液中SEC的机制。以SEC消退为指标的红细胞聚集抑制可能为降低心脏血栓栓塞风险提供一种替代抗凝和抗血小板治疗的方法。
