Department of Surgical Sciences, Section of Vascular Surgery, Uppsala University, Uppsala, Sweden.
Eur J Vasc Endovasc Surg. 2013 Aug;46(2):214-22. doi: 10.1016/j.ejvs.2013.05.011. Epub 2013 Jun 13.
OBJECTIVE/BACKGROUND: Patients with peripheral arterial occlusive disease (PAOD), in particular critical limb ischaemia (CLI), carry a high risk of thrombotic events. We hypothesised that patients undergoing conservative, endovascular, or open surgical treatment for CLI have increased levels of plasminogen activator inhibitor-1 (PAI-1), leading to a prothrombotic state. The objective was to determine levels of PAI-1 in patients with acute or chronic PAOD/CLI.
Thirty-two patients with a median age of 74 (49-90) years were included. Three underwent thrombolysis for acute limb-threatening ischaemia. Twenty-six patients with chronic ischaemia received endovascular (n = 20) or open (n = 6) surgical treatment. Three were treated conservatively. Biomarkers and ankle brachial index (ABI) were measured before and up to 1 month after intervention. Patency was studied with repeated duplex ultrasound.
Ankle pressure and ABI improved after intervention (p < .001). C-reactive protein (CRP) increased from a median of 7.90 mg/L at baseline to 31.5 on day 1 (p < .001), 28.0 on day 6 (p < .001), and returned to baseline levels on day 30. PAI-1 antigen and activity decreased from day 6 and onwards post-intervention compared with baseline (p < .05). A great individual variability in PAI-1 antigen and activity was observed. Although most actively treated patients had normal PAI-1 activity, 11/29 (38%) were above that level of normality at baseline, 10/24 (42%) on day 1, 3/23 (13%) on day 6, and 5/27 (19%) on day 30 after intervention.
Endovascular and open surgical treatment resulted in improved ankle pressure and ABI. The intervention was followed by a transient increase in CRP and a sustained reduction in PAI-1 levels and activity.
目的/背景：患有外周动脉阻塞性疾病（PAOD），特别是临界肢体缺血（CLI）的患者，发生血栓事件的风险较高。我们假设，接受 CLI 保守治疗、血管内治疗或开放手术治疗的患者，其纤溶酶原激活物抑制剂-1（PAI-1）水平升高，导致血栓形成状态。目的是确定急性或慢性 PAOD/CLI 患者的 PAI-1 水平。
纳入 32 名中位年龄为 74 岁（49-90 岁）的患者。3 名患者因急性肢体威胁性缺血行溶栓治疗。26 名慢性缺血患者接受血管内（n=20）或开放（n=6）手术治疗。3 名患者接受保守治疗。干预前和干预后 1 个月测量生物标志物和踝肱指数（ABI）。通过重复双功超声检查研究通畅性。
干预后踝压和 ABI 改善（p<0.001）。C 反应蛋白（CRP）从基线中位数 7.90mg/L增加到第 1 天的 31.5（p<0.001），第 6 天的 28.0（p<0.001），并在第 30 天恢复到基线水平。与基线相比，干预后第 6 天及以后，PAI-1 抗原和活性降低（p<0.05）。观察到 PAI-1 抗原和活性的个体间变异性很大。尽管大多数积极治疗的患者 PAI-1 活性正常，但 11/29（38%）在基线时高于正常值，10/24（42%）在第 1 天，3/23（13%）在第 6 天，5/27（19%）在第 30 天。
血管内和开放手术治疗导致踝压和 ABI 改善。干预后 CRP 短暂增加，PAI-1 水平和活性持续降低。
