Daniel W C, Meidell R S, Hillis L D, Lange R A
Department of Internal Medicine, Cardiovascular Division, University of Texas Southwestern Medical Center, Dallas 75235-9047, USA.
Coron Artery Dis. 1996 Jan;7(1):45-9.
This study was performed to investigate local (transmyocardial) fibrinolytic activity in patients with unstable angina.
Previous studies have reported decreased intrinsic fribrinolytic activity-increased systemic plasminogen activator inhibitor-1 (PAI-1) activity and/or decreased systemic tissue plasminogen activator (t-PA) activity-in patients with acute myocardial infarction. In contrast, the role of intrinsic fibrinolytic activity in patients with unstable angina is not well understood.
We studied 67 consecutive patients (52 men and 15 women, aged 38-82 years) undergoing cardiac catheterization for chest pain within 24 h of acute presentation: 17 with unstable angina, 33 with stable angina, and 17 with atypical chest pain with angiographically normal coronary arteries. In each, blood samples were obtained simultaneously from the aorta and coronary sinus for measurement of t-PA and PAI-1 activities.
There was no difference in coronary sinus or systemic (aortic) t-PA activity among the three groups. The coronary sinus t-PA activity was 0.092 +/- 0.054, 0.088 +/- 0.038, and 0.080 +/- 0.050 IU/ml in the control, unstable angina, and stable angina groups, respectively [not significant (NS)], and the aortic t-PA activity was 0.114 +/- 0.053, 0.099 +/- 0.057, and 0.090 +/- 0.056 IU/ml in the control unstable angina, and stable angina groups, respectively (NS). Similarly, there was no difference in coronary sinus or systemic (aortic) PAI-1 activity among the three groups: the coronary sinus PAI-1 activity was 8.2 +/- 2.0, 7.4 +/- 2.0, and 8.0 +/- 2.5 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS). The aortic PAI-1 activity was 7.8 +/- 2.1, 7.2 +/- 1.4, and 8.0 +/- 1.8 AIU/ml in the control, unstable angina, and stable angina groups, respectively (NS).
Although it has been suggested that alterations in local (transmyocardial) t-PA and PAI-1 activities may be of pathophysiologic importance in the genesis of unstable angina, our data show no difference in transmyocardial fibrinolytic activity in patients with unstable angina, stable angina, and noncardiac chest pain.
本研究旨在调查不稳定型心绞痛患者的局部（透壁心肌）纤溶活性。
既往研究报道，急性心肌梗死患者存在内源性纤溶活性降低、全身纤溶酶原激活物抑制剂-1（PAI-1）活性增加和/或全身组织纤溶酶原激活物（t-PA）活性降低的情况。相比之下，内源性纤溶活性在不稳定型心绞痛患者中的作用尚未完全明确。
我们对67例连续患者（52例男性和15例女性，年龄38 - 82岁）进行了研究，这些患者在急性发病后24小时内因胸痛接受心脏导管检查：17例为不稳定型心绞痛患者，33例为稳定型心绞痛患者，17例为冠状动脉造影正常但有非典型胸痛的患者。在每例患者中，同时从主动脉和冠状窦采集血样，以测定t-PA和PAI-1活性。
三组患者冠状窦或全身（主动脉）t-PA活性无差异。对照组、不稳定型心绞痛组和稳定型心绞痛组的冠状窦t-PA活性分别为0.092±0.054、0.088±0.038和0.080±0.050 IU/ml[无显著性差异（NS）]，主动脉t-PA活性分别为0.114±0.053、0.099±0.057和0.090±0.056 IU/ml（NS）。同样，三组患者冠状窦或全身（主动脉）PAI-1活性也无差异：对照组、不稳定型心绞痛组和稳定型心绞痛组的冠状窦PAI-1活性分别为8.2±2.0、7.4±2.0和8.0±2.5 AIU/ml（NS）。主动脉PAI-1活性在对照组、不稳定型心绞痛组和稳定型心绞痛组分别为7.8±2.1、7.2±1.4和8.0±1.8 AIU/ml（NS）。
尽管有研究提示局部（透壁心肌）t-PA和PAI-1活性改变在不稳定型心绞痛发病机制中可能具有病理生理学意义，但我们的数据显示不稳定型心绞痛、稳定型心绞痛和非心源性胸痛患者的透壁心肌纤溶活性无差异。
