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纤维蛋白溶解功能受损决定经皮腔内冠状动脉成形术(PTCA)的预后。

Impaired fibrinolysis determines the outcome of percutaneus transluminal coronary angioplasty (PTCA).

作者信息

Fornitz G G, Nielsen P, Amtorp O, Kassis E, Abildgård U, Sloth C, Winther K, Ørskov H, Dalsgård J, Husted S

机构信息

Gentofte Hospital, Copenhagen, Denmark.

出版信息

Eur J Clin Invest. 2001 Jul;31(7):586-92. doi: 10.1046/j.1365-2362.2001.00855.x.

Abstract

BACKGROUND

Coronary artery stenosis lesions dilated by percutaneus transluminal coronary angioplasty (PTCA) show a disappointingly frequent recurrence of stenosis. We have investigated the possible role of fibrinolysis and various platelet-release factors - specifically in the locality of the affected vessel - by following 19 patients for 6 months after PTCA.

METHODS

PTCA was performed on 19 patients with a significant primary coronary stenosis, proven by quantitative CAAS analysis. Blood for measurement of local fibrinolysis and platelet activity was drawn from the aortic root and the coronary sinus, at three times: just before PTCA, 10 min after it, and 6 months later.

RESULTS

The incidence of restenosis at the 6 months follow-up was 37%. PTCA almost doubled the platelet-derived growth factor level (PDGF) in coronary sinus blood in all patients. The seven restenosis patients had a substantially higher tissue plasminogen activator inhibitor antigen (PAI-1ag) level in the aortic root before PTCA than the 12 who remained stenosis-free (mean 62.4 +/- 31.6 ng mL -1 compared with 33.1 + 25.3; P < 0.04) and a lower tissue plasminogen activator activity (t-PAac) level (mean 0.32 +/- 0.19 IU mL-1 compared with 0.68 +/- 0.34; P < 0.03). This was corroborated by the levels of tissue plasminogen activator inhibitor activity (PAI-1ac). At reassessment after 6 months, the restenosis patients had developed, in coronary sinus blood, a large rise of PAI-1ac (7.7 +/- 4.8 IU mL-1 rising to 15.7 +/- 13.9, P < 0.04) and a large rise of of PAI-1ag (48.8 +/- 31.3 ng mL-1 vs. 72.4 +/- 47.2; P < 0.03). But no such increase occurred in the patients who remained stenosis-free. Conclusion Our results indicate that the minor balloon injury, which is inseparable from PCTA, stimulates the local release of PDGF. We suggest that, in those patients whose fibrinolytic activity is inherently low, this rise of PDGF could be a major causative factor in restenosis. We also discuss the possibility that the preoperative level of PAI-1ac could provide a limited but useful prediction of the outcome of PTCA.

摘要

背景

经皮腔内冠状动脉成形术(PTCA)扩张的冠状动脉狭窄病变,其狭窄复发频率高得令人失望。我们通过对19例患者PTCA术后6个月的随访,研究了纤溶作用及各种血小板释放因子——特别是在病变血管局部——可能发挥的作用。

方法

对19例经定量CAAS分析证实存在明显原发性冠状动脉狭窄的患者进行PTCA。分别于PTCA术前、术后10分钟及6个月后,从主动脉根部和冠状窦采集血样,以测定局部纤溶和血小板活性。

结果

6个月随访时再狭窄发生率为37%。PTCA使所有患者冠状窦血中血小板衍生生长因子水平(PDGF)几乎翻倍。7例再狭窄患者PTCA术前主动脉根部组织纤溶酶原激活物抑制剂抗原(PAI - 1ag)水平显著高于12例无狭窄患者(平均62.4±31.6 ng/mL,对比33.1±25.3;P<0.04),而组织纤溶酶原激活物活性(t - PAac)水平较低(平均0.32±0.19 IU/mL,对比0.68±0.34;P<0.03)。组织纤溶酶原激活物抑制剂活性(PAI - 1ac)水平也证实了这一点。6个月复查时,再狭窄患者冠状窦血中PAI - 1ac大幅升高(7.7±4.8 IU/mL升至15.7±13.9,P<0.04),PAI - 1ag也大幅升高(48.8±31.3 ng/mL对比72.4±47.2;P<0.03)。但无狭窄患者未出现此类升高。结论我们的结果表明,PTCA不可避免的轻微球囊损伤会刺激局部释放PDGF。我们认为,对于纤溶活性本来就低的患者,PDGF的这种升高可能是再狭窄的主要致病因素。我们还讨论了术前PAI - 1ac水平可能对PTCA结果提供有限但有用预测的可能性。

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