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起搏诱导的心肌缺血对冠状动脉循环中血小板活化和纤维蛋白形成的影响。

Effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation in the coronary circulation.

作者信息

Nichols A B, Gold K D, Marcella J J, Cannon P J, Owen J

出版信息

J Am Coll Cardiol. 1987 Jul;10(1):40-5. doi: 10.1016/s0735-1097(87)80157-2.

Abstract

The effect of pacing-induced myocardial ischemia on platelet activation and fibrin formation was investigated in seven patients with severe proximal lesions of the left anterior descending coronary artery to determine if acute ischemia activates the coagulation system. Fibrin formation was assessed from plasma levels of fibrinopeptide A. Platelet activation was assessed by levels of platelet factor 4, beta-thromboglobulin and thromboxane B2. Plasma levels were measured before, during and after acute myocardial ischemia induced by rapid atrial pacing. Blood samples were collected from the ascending aorta and from the great cardiac vein through heparin-bonded catheters. The occurrence of anterior myocardial ischemia was established by electrocardiography and by myocardial lactate extraction. No significant transmyocardial gradients in the levels of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 were found at rest, during ischemia or in the recovery period, and levels in the great cardiac vein did not change in response to ischemia. These data indicate that pacing-induced myocardial ischemia does not result in release of fibrinopeptide A, platelet factor 4, beta-thromboglobulin or thromboxane B2 into the coronary circulation, and imply that acute ischemia does not induce platelet activation or fibrin formation in the coronary circulation.

摘要

研究了七例左前降支冠状动脉严重近端病变患者中,起搏诱发的心肌缺血对血小板活化和纤维蛋白形成的影响,以确定急性缺血是否会激活凝血系统。通过纤维蛋白肽A的血浆水平评估纤维蛋白形成。通过血小板因子4、β-血小板球蛋白和血栓素B2的水平评估血小板活化。在快速心房起搏诱发急性心肌缺血之前、期间和之后测量血浆水平。通过肝素结合导管从升主动脉和大心静脉采集血样。通过心电图和心肌乳酸提取确定前壁心肌缺血的发生。在静息时、缺血期间或恢复期,未发现纤维蛋白肽A、血小板因子4、β-血小板球蛋白或血栓素B2水平存在显著的跨心肌梯度,并且大心静脉中的水平对缺血无反应。这些数据表明,起搏诱发的心肌缺血不会导致纤维蛋白肽A、血小板因子4、β-血小板球蛋白或血栓素B2释放到冠状动脉循环中,这意味着急性缺血不会在冠状动脉循环中诱导血小板活化或纤维蛋白形成。

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