Wilensky R L, Bourdillon P D, Vix V A, Zeller J A
Krannert Institute of Cardiology, Department of Medicine, Indianapolis, Indiana 46202-4800.
J Am Coll Cardiol. 1993 Mar 1;21(3):692-9. doi: 10.1016/0735-1097(93)90102-7.
We examined the relation between the level of urinary fibrinopeptide A and the presence of angiographic intracoronary thrombus in patients with unstable angina to determine whether this marker predicts active thrombus formation.
Although it is known that thrombus plays a role in acute ischemic syndromes, a noninvasive method to predict its presence in individual patients with unstable angina has not been determined. Fibrinopeptide A is a polypeptide cleaved from fibrinogen by thrombin and thus is a sensitive marker of thrombin activity and fibrin generation.
Angiographic thrombus, graded 0 to 4, and the presence of ST segment depression or T wave inversions, or both, on the electrocardiogram (ECG) were related to fibrinopeptide A levels in 24 patients with rest angina of new onset, 18 with crescendo angina, 19 with stable angina and 9 with chest pain but without coronary artery disease. All patients had chest pain within the 24 h of sample acquisition.
The angiographic incidence of thrombus was significantly higher in patients with new onset of rest angina (67%, p < 0.001) and crescendo angina (50%, p < 0.001) as were fibrinopeptide A levels (p = 0.002). Fibrinopeptide A levels correlated significantly (p < 0.001) with the presence of a filling defect (grade 4 intracoronary thrombus) or contrast staining (grade 3). All patients with fibrinopeptide A > or = 8 ng/mg creatinine showed grade 3 to 4 thrombus and 15 of 16 patients with levels > or = 6.0 ng/mg creatinine exhibited angiographic evidence of thrombus (13 with grades 3 to 4). Patients with reversible ST changes on the ECG had significantly higher levels of fibrinopeptide A (p < 0.001), and ST changes correlated significantly with the presence of angiographic thrombus (p < 0.001). Nonetheless, a significant minority of patients with unstable angina had neither angiographic nor biochemical evidence of thrombus.
Elevated fibrinopeptide A levels in unstable angina reflected active intracoronary thrombus formation and were present in patients with angina of new onset as well as crescendo angina. Reversible ST changes are accompanied by thrombin activity and angiographic thrombus formation. However, a sizable percentage of patients with unstable angina had no evidence of thrombus and these patients may have had transient platelet aggregation without fibrin thrombus formation.
我们研究了不稳定型心绞痛患者尿纤维蛋白肽A水平与冠状动脉造影显示的冠状动脉内血栓形成之间的关系,以确定该标志物是否能预测活动性血栓形成。
尽管已知血栓在急性缺血综合征中起作用,但尚未确定一种非侵入性方法来预测不稳定型心绞痛个体患者中血栓的存在。纤维蛋白肽A是一种由凝血酶从纤维蛋白原上裂解下来的多肽,因此是凝血酶活性和纤维蛋白生成的敏感标志物。
对24例新发静息性心绞痛患者、18例进行性加重性心绞痛患者、19例稳定性心绞痛患者和9例有胸痛但无冠状动脉疾病的患者,将冠状动脉造影血栓(分级为0至4级)以及心电图(ECG)上ST段压低或T波倒置或两者同时存在的情况与纤维蛋白肽A水平进行关联分析。所有患者在采集样本的24小时内均有胸痛症状。
新发静息性心绞痛患者(67%,p<0.001)和进行性加重性心绞痛患者(50%,p<0.001)的冠状动脉造影血栓发生率显著高于其他患者,纤维蛋白肽A水平也显著升高(p=0.002)。纤维蛋白肽A水平与充盈缺损(4级冠状动脉内血栓)或造影剂染色(3级)的存在显著相关(p<0.001)。所有纤维蛋白肽A≥8 ng/mg肌酐的患者均显示3至4级血栓,16例纤维蛋白肽A水平≥6.0 ng/mg肌酐的患者中有15例有冠状动脉造影血栓证据(13例为3至4级)。心电图上有可逆性ST段改变的患者纤维蛋白肽A水平显著更高(p<0.001),且ST段改变与冠状动脉造影血栓的存在显著相关(p<0.001)。然而,相当一部分不稳定型心绞痛患者既没有冠状动脉造影证据也没有生化证据表明存在血栓。
不稳定型心绞痛患者纤维蛋白肽A水平升高反映了冠状动脉内活动性血栓形成,新发心绞痛以及进行性加重性心绞痛患者中均存在这种情况。可逆性ST段改变伴有凝血酶活性和冠状动脉造影血栓形成。然而,相当比例的不稳定型心绞痛患者没有血栓证据,这些患者可能仅有短暂的血小板聚集而无纤维蛋白血栓形成。