Lack of elevation of platelet factor IV in plasma from patients with myocardial infarction.
Lack of elevation of platelet factor IV in plasma from patients with myocardial infarction.
复制标题
心肌梗塞患者血浆中血小板因子 IV 缺乏升高。
DOI：
10.1016/s0735-1097(84)80389-7
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发表时间：
1984
影响因子：
24
通讯作者：
Sobel,BE
中科院分区：
文献类型：
--
作者：
Jaffe,AS;Lee,RG;Perez,JE;Geltman,EM;Wilner,GD;Sobel,BE
血小板因子IV和β-血栓球蛋白是血小板颗粒的蛋白质成分。血浆中这些蛋白水平的升高已被用作血小板脱颗粒的敏感指标。体内释放蛋白后，血小板因子IV的清除速度比β-血栓球蛋白快得多。虽然在脑梗塞患者中观察到了血小板因子IV的升高，但其反映冠状动脉血栓形成等致病现象的意义尚未明确评估。因此，对52例急性心肌梗死患者在严酷的条件下连续采集的血浆样本进行前瞻性评估。脑梗死组入院时血小板第四因子水平正常，平均6.3±3.3 ng/ml，与44例无再发脑梗死者胸痛患者(5.7±2.7 ng/ml)和25例正常人(4.3±1.6 ng/ml)相近。在住院期间，尽管有反复的胸痛、左室血栓的形成或有记录的再发梗死，但在住院期间，血小板第四因子通常不会增加。然而，侵入性手术后，血小板第四因子持续升高，占体内由于血小板激活而增加的总共110例中的104例，这从持续升高的β-血栓球蛋白水平反映出来。因此，尽管急性心肌梗死，血小板因子IV的值一般保持正常。罕见的增加反映了由于采样伪影或体内由于侵入性操作引起的血小板扰动而导致的体外血小板脱颗粒。它们不能为冠状动脉血栓形成提供一个明确的标准。
Platelet factor IV and beta-thromboglobulin are protein constituents of platelet granules. Elevated levels of these proteins in plasma have been used as sensitive indicators of platelet degranulation. Clearance of platelet factor IV is much faster than that of beta-thromboglobulin after release of the proteins in vivo. Although increases of platelet factor IV have been observed in patients with infarction, the implication that they reflect pathogenetic phenomena such as coronary thrombosis has not been assessed explicitly. Accordingly, plasma samples obtained serially from 52 patients with acute myocardial infarction under rigorous conditions verified to minimize platelet degranulation in vitro were evaluated prospectively. Correlative studies were performed to detect left ventricular mural thrombus, and coronary thrombosis was assessed independently in selected patients with indium-Ill platelet scintigraphy.Platelet factor IV was normal at the time of admission in patients with infarction, averaging 6.3 ± 3.3 ng/ml, similar to values in 44 other patients with chest pain without subsequent infarction (5.7 ± 2.7 ng/ml) and in 25 normal subjects (4.3 ± 1.6 ng/ml). Platelet factor IV generally did not increase during hospitalization in patients with infarction despite recurrent chest pain, development of left ventricular thrombus or documented recurrent infarction. However, platelet factor IV increased consistently after invasive procedures, accounting for 104 of the total of 110 increases due to platelet activation in vivo as reflected by persistence of elevated levels of beta-thromboglobulin. Thus, platelet factor IV values generally remain normal despite acute myocardial infarction. Rare increases that occur reflect platelet degranulation in vitro due to sampling artifact or perturbations of platelets in vivo due to invasive procedures. They do not provide a definitive criterion of coronary thrombosis.