Levy P J, Gonzalez M F, Hornung C A, Chang W W, Haynes J L, Rush D S
Department of Surgery, University of South Carolina, School of Medicine, Columbia 29203, USA.
J Vasc Surg. 1996 Jan;23(1):36-43, discussion 43-5. doi: 10.1016/s0741-5214(05)80033-3.
Fifty-one consecutive patients with premature lower extremity atherosclerosis were prospectively evaluated for atherogenic risk factors and primary or acquired hypercoagulability, which might contribute to early ischemia and revascularization failure.
Laboratory tests included plasma assays of (1) natural anticoagulants (NAC), lipoprotein (a) (Lp[a]), and anticardiolipin antibodies, and (2) fibrinolytic activators and inhibitors at baseline and stimulated after 20 minutes of upper extremity venous occlusion.
Forty-six (90%) of these 51 patients had laboratory abnormalities. One or more NAC deficiencies were found in 15 (30%) patients and included antithrombin III (n = 5), protein C (n = 8), protein S (n = 4), and heparin cofactor II (n = 2). Hypofibrinolysis was identified as a deficiency of stimulated tissue plasminogen activator in 22 (45%) patients and elevated plasminogen activator inhibitor-1 (PAI-1) in 29 (59%). Elevated Lp(a) was found in 43 (86%) patients. Five (10%) patients had anticardiolipin antibodies. Ten patients had combined NAC deficiency and hypofibrinolysis. Five (10%) patients had no abnormality. NAC deficiencies, especially protein C deficiency, were associated with acute ischemia (p < 0.01), prior vascular intervention (p < 0.01), an increasing number of total vascular procedures (p < 0.01), and major amputation (p < 0.01). PAI-1 was associated with a history of heart disease (p < 0.05) and prior vascular procedures (p < 0.05). Elevated Lp(a) was associated with elevated PAI-1 (p < 0.05). Retesting in 20 patients suggested that 80% of NAC deficiencies were acquired, but abnormalities persisted in 66% of patients with elevated PAI-1 and in 93% of those with elevated Lp(a).
These data strongly support the hypothesis that the convergence of atherogenic risk factors and hypercoagulability play an important role in early ischemia and poor results reported for lower extremity vascular procedures in young adults.
对51例连续性下肢过早发生动脉粥样硬化的患者进行前瞻性评估，以确定可能导致早期缺血和血管重建失败的致动脉粥样硬化危险因素及原发性或获得性高凝状态。
实验室检查包括血浆检测：（1）天然抗凝剂（NAC）、脂蛋白（a）[Lp（a）]和抗心磷脂抗体；（2）基线时以及上肢静脉闭塞20分钟后刺激状态下的纤溶激活剂和抑制剂。
这51例患者中有46例（90%）存在实验室异常。15例（30%）患者发现一种或多种NAC缺乏，包括抗凝血酶III（n = 5）、蛋白C（n = 8）、蛋白S（n = 4）和肝素辅因子II（n = 2）。22例（45%）患者纤溶功能低下表现为刺激状态下组织纤溶酶原激活物缺乏，29例（59%）患者纤溶酶原激活物抑制剂-1（PAI-1）升高。43例（86%）患者Lp（a）升高。5例（10%）患者有抗心磷脂抗体。10例患者存在NAC缺乏合并纤溶功能低下。5例（10%）患者无异常。NAC缺乏，尤其是蛋白C缺乏，与急性缺血（p < 0.01）、既往血管介入治疗（p < 0.01）、血管手术总数增加（p < 0.01）和大截肢（p < 0.01）相关。PAI-1与心脏病史（p < 0.05）和既往血管手术（p < 0.05）相关。Lp（a）升高与PAI-1升高相关（p < 0.05）。对20例患者进行复查显示，80%的NAC缺乏是获得性的，但PAI-1升高的患者中66%异常持续存在，Lp（a）升高的患者中93%异常持续存在。
这些数据有力地支持了以下假说：致动脉粥样硬化危险因素和高凝状态的共同作用在年轻成人下肢血管手术中早期缺血及不良预后方面起重要作用。
