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Antithrombotic efficacy of thrombin inhibitor L-374,087: Intravenous activity in a primate model of venous thrombus extension and oral activity in a canine model of primary venous and coronary artery thrombosis

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JOURNAL OF PHARMACOLOGY AND EXPERIMENTAL THERAPEUTICS 1999年第1期289卷 503-510页

作者： Cook, JJ Gardell, SJ Holahan, MA Sitko, GR Stump, GL Wallace, AA Gilberto, DB Hare, TR Krueger, JA Dyer, DL Sanderson, PEJ Vacca, JP Shafer, JA Lynch, JJ Merck Res Labs Dept Pharmacol W Point PA 19486 USA Merck Res Labs Dept Biol Chem W Point PA 19486 USA Merck Res Labs Dept Lab Anim Resources W Point PA 19486 USA Merck Res Labs Dept Med Chem W Point PA 19486 USA

The small molecule direct thrombin inhibitor L-374,087 was characterized across species in an in vitro activated partial thromboplastin clotting time (aPTT) assay and in vivo in rhesus monkey and dog thrombosis models. In vitro in rhesus, dog, and human plasma, L-374,087 concentrations eliciting 2-fold increases in aPTT were 0.25, 1.9, and 0.28 mu M, respectively. In anesthetized rhesus monkeys, 300 mu g/kg bolus plus 12 mu g/kg/ min and 300 mu g/kg bolus plus 30 mu g/kg/min L-374,087 i.v. infusions significantly reduced jugular vein thrombus extension, with both regimens limiting venous thrombus extension to 2-fold that of baseline thrombus mass compared with a 5-fold extension observed in the vehicle control group. Antithrombotic efficacy in the rhesus with the-lower-dose regimen was achieved with 2.3- to 2.4-fold increases in aPTT and prothrombin time. In a conscious instrumented dog model of electrolytic vessel injury, the oral administration of two 10 mg/kg L-374,087 doses 12 h apart significantly reduced jugular vein thrombus mass, reduced the incidence of and delayed time to occlusive coronary artery thrombosis, and significantly reduced coronary artery thrombus mass and ensuing posterolateral myocardial infarct size. Antithrombotic efficacy in the dog was achieved with 1.6- to 2.0-fold increases in aPTT at 1 to 6 h after oral dosing with L-374,087. These results indicate significant antithrombotic efficacy against both venous and coronary arterial thrombosis with L-374,087 with only moderate elevations in aPTT or prothrombin time. The oral efficacy of L-374,087 characterizes this compound as a prototype for the further development of orally active direct thrombin inhibitors.

关键词：投药口服麻醉出血时间血液凝固/药物作用冠状动脉血栓形成/血液冠状动脉血栓形成/药物疗法纤维蛋白溶解药/投药和剂量纤维蛋白溶解药/药代动力学纤维蛋白溶解药/药理学血细胞比容血红蛋白类/代谢注射静脉内颈静脉/病理学恒河猴部分促凝血酶原时间血小板计数/药物作用吡啶酮类/投药和剂量吡啶酮类/药代动力学吡啶酮类/药理学磺胺类/投药和剂量磺胺类/药代动力学磺胺类/药理学凝血酶/拮抗剂和抑制剂静脉血栓形成/血液静脉血栓形成/药物疗法动物狗女(雌)性人类男(雄)性

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Antithrombin activity during the period of percutaneous coronary revascularization - Relation to heparin use, thrombotic complications and restenosis

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第5期33卷 1248-1256页

作者： Matthai, WH Kurnik, PB Groh, WC Untereker, WJ Siegel, JE Univ Penn Sch Med Dept Med Philadelphia PA 19104 USA Univ Med & Dent New Jersey Robert Wood Johnson Med Sch Dept Med Camden NJ 08103 USA Univ Med & Dent New Jersey Robert Wood Johnson Med Sch Dept Med New Brunswick NJ 08903 USA

OBJECTIVES This study evaluated changes in antithrombin (AT) activity around the time of percutaneous transluminal coronary revascularization (PTCR) with unfractionated heparin anticoagulation and the effects these changes had on major thrombotic complications of PTCR. BACKGROUND Heparin is used during PTCR to prevent thrombosis. However, heparin, a cofactor for AT, causes AT activity to fall. AT activity <70% is associated with thrombosis. There is a prothrombotic state after heparin discontinuation that has not been well explained. METHODS Antithrombin activity was sampled at the start and end of PTCR and the next two mornings in 250 consecutive patients. We recorded occurrence of major thrombotic events, defined as 1) major thrombotic complications of PTCR;2) major in-lab thrombus formation;or 3) subacute occlusion. Discriminant analysis was employed to evaluate the relationship of AT activity to these events. Change in AT activity;and its relationship to heparin was evaluated. Evidence of restenosis at six months was obtained. RESULTS There were 14 major thrombotic events. Antithrombin activity <70%, was strongly (p = 0.006) associated with these events. The AT activity fell significantly through the morning after PTC-R when 21% of patients had AT activity < 70%;AT activity did not normalize until >20 h after heparin discontinuation. Pre-PTCR use of heparin led to lower AT activity in proportion to duration of heparin use. There was no relationship between;AT activity and restenosis. CONCLUSIONS Low AT activity may contribute to major thrombotic complications of PTCR. The way heparin is used before and after PTCR is important to development of low AT activity. (C) 1999 by the American College of Cardiology.

关键词：血管成形术气囊冠状动脉/副作用抗凝药/治疗应用抗凝血酶类/药物作用抗凝血酶类/代谢冠状血管造影术冠心病/血液冠心病/诊断显像冠心病/治疗冠状动脉血栓形成/血液冠状动脉血栓形成/病因学冠状动脉血栓形成/预防和控制随访研究肝素/治疗应用回顾性研究治疗结果女(雌)性人类男(雄)性

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Pl^A polymorphism of glycoprotein IIIa and risk of adverse events after coronary stent placement

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 2000年第1期36卷 84-89页

作者： Kastrati, A Koch, W Gawaz, M Mehilli, J Böttiger, C Schömig, K von Beckerath, N Schömig, A Deutsch Herzzentrum Munich D-80636 Munich Germany Tech Univ Munich Med Klin Rechts Isar 1 D-8000 Munich Germany

OBJECTIVE We designed this prospective study to test the hypothesis that platelet antigen (P1(A)) polymorphism of glycoprotein (GP) IIIa is associated with an increased risk for adverse events after coronary stent placement. BACKGROUND Platelets play a central role in arterial thrombosis. The P1(A) polymorphism of GP IIIa, a constituent of the fibrinogen receptor, may influence the platelet function and, thereby, the early outcome of patients after coronary stent placement. METHODS The study included 1,759 consecutive patients with stable or unstable angina and successful coronary stent placement. Platelet antigen genotypes were determined by allele-specific restriction enzyme analysis. The end point of the study was a composite of death, myocardial infarction and urgent revascularization during the first 30 days after stent placement. RESULTS The P1(A) genotype of the patients included was: 70.2% were homozygous for platelet antigen 1 (P1(A1)), 2.6% homozygous for platelet antigen 2 (P1(A2)), and 27.2% were heterozygous (p1(A1/A2)). The incidence of the composite end point was 5.5% among P1(A2) carriers and 5.4% in homozygous P1(A1) subjects (p = 0.94). It was 5.4% in p1(A1/A1) patients, 4.8% in p1(A1/A2) patients and 13.0% in P1(A2/A2) patients (P = 0.06). The combined incidence of death or myocardial infarction was 4.3% in P1(A1/A2) p1(A2/A2) patients (p = 0.02). CONCLUSION The isolated presence of the p1(A2) allele in heterozygous patients is not associated with anp detectable increase in the risk for an adverse 30-day outcome after coronary stenting. This study suggests also that an increased risk is likely to be present in homozygous carriers of the P1(A2) allele, but this should be confirmed in a much larger series of patients. (J Am Coil Cardiol 2000;36: 84-9) (C) 2000 by the American College of Cardiology.

关键词：等位基因心绞痛/外科学抗原 CD/遗传学抗原 CD/代谢抗原人血小板/血液抗原人血小板/遗传学冠状血管造影术冠状动脉血栓形成/血液冠状动脉血栓形成/并发症冠状动脉血栓形成/诊断显像冠状动脉血栓形成/遗传学 DNA/分析 DNA引物/化学表位/血液表位/遗传学遗传标记基因型整合素β3 整合素类/血液整合素类/遗传学心肌梗死/血液心肌梗死/诊断显像心肌梗死/病因学比值比血小板膜糖蛋白类/遗传学血小板膜糖蛋白类/代谢聚合酶链反应多态现象遗传预后前瞻性研究危险因素支架/副作用老年人女(雌)性人类男(雄)性中年人

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Prognostic significance of elevated hemostatic markers in patients with acute myocardial infarction

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第6期33卷 1543-1548页

作者： Li, YH Teng, JK Tsai, WC Tsai, LM Lin, LJ Guo, HR Chen, JH Natl Cheng Kung Univ Hosp Dept Internal Med Div Cardiol Tainan 70428 Taiwan

OBJECTIVES The purpose of this study was to determine whether the elevated levels of hemostatic markers in the early phase of myocardial infarction may serve as risk factors for subsequent cardiac mortality. BACKGROUND Increased plasma hemostatic markers were noted in acute myocardial infarction, indicating that the blood coagulation system is highly activated in those patients. However, there are few clinical data concerning the association between the elevated hemostatic markers and survival in patients with myocardial infarction. METHODS Blood samples were obtained from 63 patients (mean age 67 w+/- 11 years;49 male)with acute myocardial infarction within 12 h after the onset of symptoms and before the initiation of any antithrombotic treatment. We measured plasma concentrations of fibrinopeptide A (FPA), prothrombin fragment 1+2 (F1+2) and thrombin-antithrombin complex (TAT) using the enzyme-linked immunosorbent assay method, and examined the associations between the level of these markers and survival with Cox proportional hazards models. RESULTS The follow-up time was 27 +/- 17 months, and 19 patients died of cardiac causes during inr follow-up. Univariate survival analysis identified Killip class IV (hazard ratio 4.86;95% confidence interval [CI] 1.55-15.19), left ventricular ejection fraction (hazard ratio 0.94;95% CI 0.90-0.99), FPA (hazard ratio 1.54;95% CI 1.13-2.10), F1+2 (hazard ratio 2.03;95% CI 1.17-3.53) and TAT (hazard ratio 1.88;95% CI 1.27-2.79) as significant factors associated with cardiac mortality In multivariate analyses, only FPA level (hazard ratio 1.84;95% CI 1.03-3.30) and left ventricular ejection fraction (hazard ratio 0.93;95% CI 0.88-0.98) were independent predictors of cardiac mortality. CONCLUSIONS Elevated FPA in the early phase of myocardial infarction identifies patients with increased risk for subsequent cardiac death. This association appears to be independent of residual left ventricular function after infarction. (C) 1999 by

关键词：抗凝血酶Ⅲ/代谢冠状动脉血栓形成/血液冠状动脉血栓形成/诊断冠状动脉血栓形成/死亡率纤维蛋白肽A/代谢随访研究止血/生理学心肌梗死/血液心肌梗死/诊断心肌梗死/死亡率肽碎片/代谢肽水解酶类/代谢预后凝血酶原/代谢危险性评估存活率成年人老年人女(雌)性人类男(雄)性中年人

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Pravastatin therapy in hyperlipidemia: Effects on thrombus formation and the systemic hemostatic profile

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第5期33卷 1294-1304页

作者： Dangas, G Badimon, JJ Smith, DA Unger, AH Levine, D Shao, JH Meraj, P Fier, C Fallon, JT Ambrose, JA Mt Sinai Sch Med Dept Med New York NY 10029 USA Mt Sinai Sch Med Dept Pathol New York NY 10029 USA Cornell Univ Coll Med Rogosin Inst New York NY USA

OBJECTIVES The study sought to determine the effects of lipid-lowering with pravastatin on the systemic fibrinolytic profile and on thrombus formation under dynamic flow conditions. BACKGROUND Lowering cholesterol (C) decreases clinical events in coronary artery disease (CAD) patients, but an analysis of the effects of lipid-lowering on the entire hemostatic and thrombotic profile has not been conducted. METHODS We prospectively studied 93 stable patients with untreated low-density lipoprotein cholesterol (LDL-C) >145 mg/dl. The CAD patients received pravastatin, and non-CAD patients were randomized to pravastatin versus placebo (double-blind). Thrombus formation upon an injured vascular surface was assessed in a substudy of 40 patients with a previously validated ex vivo perfusion chamber system. Systemic hemostatic markers and thrombus formation were evaluated at baseline, three and six months. RESULTS Placebo produced no changes in either the lipid profile, any of the hemostatic markers, or the ex vivo thrombus formation. Both pravastatin groups (CAD and non-CAD) showed decreased LDL-C by 30% within 6 weeks (188 to 126 mg/dl, p < 0.001 vs. baseline), and decreased plasminogen activator inhibitor-1 at 3- and 6-month follow-up compared to baseline (15% to 18% decrease at 3 months and 21% to 23% at 6 months). For the tissue plasminogen activator antigen, CAD and non-CAD groups showed significant decreases at 6 months compared to baseline (10% and 13%, respectively). No significant changes were observed with treatment in d-dimer, fibrinopeptide A, prothrombin fragment F-1.2, factor Wa, von Willebrand factor, or C-reactive protein. Fibrinogen levels were significantly increased at 6 months compared to baseline, though still below the upper normal limit. In the perfusion chamber substudy, there was a decrease in thrombus area in non-CAD patients treated with pravastatin at both 3 and 6 months compared to baseline (by 21% and 34%, respectively). The CAD patients showed

关键词：阿司匹林/治疗应用血液凝固因子/代谢胆固醇 LDL/血液冠状动脉血栓形成/血液冠状动脉血栓形成/药物疗法冠状动脉血栓形成/病因学双盲法纤维蛋白溶解药/治疗应用随访研究止血/药物作用羟甲基戊二酰基CoA还原酶抑制剂/治疗应用高脂血症/血液高脂血症/并发症高脂血症/药物疗法脂蛋白(A)/血液普伐他丁/治疗应用前瞻性研究治疗结果老年人女(雌)性人类男(雄)性中年人

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Increased platelet reactivity in patients given Orbofiban after an acute coronary syndrome:: An OPUS-TIMI 16 substudy

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AMERICAN JOURNAL OF CARDIOLOGY 2000年第4期85卷 491-493页

作者： Holmes, MB Sobel, BE Cannon, CP Schneider, DJ Univ Vermont Coll Med Cardiol Unit Dept Med Burlington VT 05401 USA Brigham & Womens Hosp Cambridge MA USA Harvard Univ Sch Med Cambridge MA 02138 USA

Platelet reactivity is increased in patients with acute coronary syndromes, accounting in part for the propensity to progressive or recurrent thrombosis.1,2 Accordingly, platelet surface glycoprotein IIb-IIIa (GP IIb-IIIa) inhibitors have been used to reduce platelet aggregation and the incidence of subsequent cardiac events.3–6 The Orbofiban in Patients with Unstable coronary syndromes–Thrombolysis In Myocardial Infarction (OPUS-TIMI 16) trial was designed to determine whether orbofiban, an orally active agent of this type, was effective. Despite its promise in preliminary studies, orbofiban did not reduce the 30-day combined end point of death, myocardial infarction, or recurrent ischemia (placebo 10.7%, orbofiban 9.5%, p = NS). Furthermore, 1 of the 2 active treatment groups had an increase in death after 30 days (placebo 1.4%, orbofiban 2.3%, p <0.05).7 To clarify factors that could be responsible for the lack of efficacy, we evaluated platelet reactivity in blood samples from 15 patients enrolled in OPUS-TIMI 16.

关键词：急性病投药口服丙氨酸/投药和剂量丙氨酸/治疗应用血小板/药物作用血小板/生理学冠状动脉血栓形成/血液冠状动脉血栓形成/药物疗法纤维蛋白原/代谢血小板聚集/药物作用血小板聚集抑制剂/投药和剂量血小板聚集抑制剂/治疗应用血小板糖蛋白GPⅡb-Ⅲa复合物/拮抗剂和抑制剂吡咯烷类/投药和剂量吡咯烷类/治疗应用复发血栓溶解疗法治疗结果人类

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Evidence that high-density lipoprotein cholesterol is an independent predictor of acute platelet-dependent thrombus formation

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AMERICAN JOURNAL OF CARDIOLOGY 1999年第9期84卷 1011-1017页

作者： Naqvi, TZ Shah, PK Ivey, PA Molloy, MD Thomas, AM Panicker, S Ahmed, A Cercek, B Kaul, S Cedars Sinai Med Ctr Div Cardiol Burns & Allen Res Inst Dept Med Los Angeles CA 90048 USA Cedars Sinai Med Ctr Vasc Physiol & Thrombosis Res Lab Atherosclerosis Res Ctr Los Angeles CA 90048 USA Univ Calif Los Angeles Sch Med Los Angeles CA 90024 USA Specialty Labs Inc Santa Monica CA USA

Plasma total and low-density lipoprotein (LDL) cholesterol are established risk factors for atherosclerotic vascular disease and may also contribute to a prothrombotic risk via enhanced platelet reactivity, This study examines whether high-density lipoprotein (HDL) cholesterol, which is inversely correlated with coronary artery disease, is associated with a reduced thrombogenic potential. Platelet thrombus formation was evaluated by exposing porcine aortic media placed in Badimon perfusion chambers to flowing nonanticoagulated venous blood for 5 minutes at a shear rate of 1,000 s(-1). Forty-five subjects, 23 normal (LDL 104 +/- 31, HDL 50 + /- 15 mg/dl) and 22 hypercholesterolemic (LDL 181 +/- 45, HDL 41 + 10 mg/dl) patients without coronary artery disease were studied. Platelet aggregation and CD62 antigen expression, and assay for circulating prothrom botic factors were also performed. In univariate analysis platelet thrombus formation correlated with weight (r = 0.33, p = 0.03), diastolic blood pressure (r = 0.39, p = 0.01), HDL cholesterol (r -0.45, p = 0.003), total/HDL cholesterol (r = 0.43, p = 0.004) and LDL/HDL (r = 0.38, p = 0.01) ratios, and platelet CD62 expression (r = 0.41, p = 0.02), In multiple regression analysis only HDL cholesterol showed significant correlation with platelet thrombus formation (p = 0.03), Platelet aggregation and circulating prothrombotic factors did not correlate with platelet thrombus formation. A comparison between normal and hypercholesterolemic subjects revealed enhanced thrombus area (0.026 +/- 0.20 vs 0.045 +/- 0.039 mm(2)/mm;p = 0.04), resting CD62 expression (6 + 7% vs 15 +/- 10% positive platelets, p = 0.02), and platelet aggregation (16.7 + 5.2 vs 21.7 +/- 6.7 ohms, p = 0.04) in hypercholesterolemic subjects. Our results demonstrate that HDL cholesterol is ct significant independent predictor of ex vivo platelet thrombus formation. (C) 1999 by Excerpta Medica, Inc.

关键词：胆固醇 HDL/血液胆固醇 LDL/血液冠状动脉血栓形成/血液冠状动脉血栓形成/病理学高胆固醇血症/血液高胆固醇血症/病理学显微镜检查电子扫描模型心血管血小板聚集/生理学凝血酶原/代谢危险因素猪血管中膜/代谢血管中膜/病理学成年人动物女(雌)性人类男(雄)性中年人

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Low intracellular magnesium levels promote platelet-dependent thrombosis in patients with coronary artery disease

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AMERICAN HEART JOURNAL 2000年第2期140卷 212-218页

作者： Shechter, M Merz, CNB Rude, RK Labrador, MJP Meisel, SR Shah, PK Kaul, S Cedars Sinai Med Ctr Dept Med Div CardiolAtherosclerosis Res Ctr Cedars Sinai Burns & Allen Res Inst Los Angeles CA 90048 USA Cedars Sinai Med Ctr Dept Med Div CardiolPrevent & Rehabil Cardiac Ctr Cedars Sinai Burns & Allen Res Inst Los Angeles CA 90048 USA Univ Calif Los Angeles Sch Med Los Angeles CA USA Univ So Calif Orthoped Hosp Dept Endocrinol Los Angeles CA USA Univ So Calif Sch Med Los Angeles CA USA

Background Although reduced intracellular levels of magnesium have been described in patients with acute myocardial infarction, its significance as a regulator of thrombosis remains unknown. Methods and Results To determine whether reduced intracellular levels of magnesium enhance platelet-dependent thrombosis, we evaluated 42 patients with coronary artery disease (CAD) by exposing porcine aortic media to their Flowing unanticoagulated venous blood for 5 minutes by using an ex vivo perfusion (Badimon) chamber. Baseline analysis demonstrated significant associations between intracellular levels of magnesium, platelet-dependent thrombosis (P =.02), and platelet P-selectin (CD62P) expression (P <.05), Patients were divided into 2 groups: below (n = 22) and above (n = 20) the median intracellular levels of magnesium (1.12, mu g/mg protein). There were no significant differences in age, body mass index, serum lipids, fibrinogen, platelet count, or serum magnesium levels between the two groups. Platelet-dependent thrombosis was significantly higher in patients with intracellular levels of magnesium below compared with above median (150+/- 128 vs 45 +/- 28 mu m(2)/mm, P <.004). Neither platelet aggregation nor CD62P expression was significantly different between the two groups. Conclusions Platelet-dependent thrombosis was significantly increased in patients with stable CAD with low intracellular levels of magnesium, suggesting a potential role for magnesium supplementation in CAD.

关键词：冠心病/血液冠状动脉血栓形成/血液细胞内液/代谢镁/血液镁缺乏/血液 P选择素/血液血小板聚集/生理学危险因素猪血栓形成/血液老年人老年人 80以上动物女(雌)性人类男(雄)性中年人

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Lipoprotein(a) and coronary thrombosis and restenosis after stent placement

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JOURNAL OF THE AMERICAN COLLEGE OF CARDIOLOGY 1999年第4期33卷 1005-1012页

作者： Wehinger, A Kastrati, A Elezi, S Baum, H Braun, S Neumann, FJ Schömig, A Deutsch Herzzentrum D-80636 Munich Germany Tech Univ Munich Klinikum Rechts Isar Med Klin 1 Munich Germany Tech Univ Munich Inst Klin Chem & Pathochem Munich Germany

OBJECTIVES The objective of this prospective study was to evaluate the relation between high lipoprotein(a) levels and thrombotic and restenotic events after coronary stent implantation. BACKGROUND Lipoprotein(a) may promote atherogenesis, coronary thrombosis and restenosis after balloon angioplasty, but the clinical significance remains unclear. METHODS The study included 2,223 consecutive patients with successful coronary stent placement. According to the serum level of lipoprotein(a), patients were divided in two groups: 457 patients of the highest quintile formed the high lipoprotein(a) group, and 1,766 patients of the lower four quintiles formed the low lipoprotein(a) group. Primary end points were the incidence of angiographic restenosis at six months and the event free survival at one year. Secondary end point was the incidence of angiographic stent occlusion. RESULTS Early stent occlusion occurred in four of the 457 patients (0.9%) with high and 37 of the 1,766 patients (2.1%) with low lipoprotein(a) levels, odds ratio of 0.41 (95% confidence interval, 0.15 to 1.16). Angiographic restenosis occurred in 173 of the 523 lesions (33.2%) in the high lipoprotein(a) group and 636 of the 1,943 lesions (32.7%) in the low lipoprotein(a) group, odds ratio of 1.02 (0.83 to 1.25). The probability of event-free survival was 73.0% in the high lipoprotein(a) group and 74.8% in the low lipoprotein(a) group (p = 0.45). On the basis of the findings in the low lipoprotein(a) group, the power of this study to detect a 25% increase in the incidence of restenosis and adverse events in the group with elevated lipoprotein(a) was 90% and 75%, respectively. CONCLUSION Elevated lipoprotein(a) levels did not influence the one-year clinical and angiographic outcome after stent placement. Thrombotic events and measures of restenosis were not adversely affected by the presence of high lipoprotein(a) levels. (J Am Coil Cardiol 1999;33: 1005-12) (C) 1999 by the American College of Cardiology

关键词：血管成形术气囊冠状动脉冠状动脉血栓形成/血液冠状动脉血栓形成/诊断冠状动脉血栓形成/治疗随访研究移植物闭塞血管/血液移植物闭塞血管/诊断脂蛋白(A)/血液前瞻性研究复发敏感性与特异性支架治疗结果老年人女(雌)性人类男(雄)性中年人

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Early risk stratification of unstable angina non-Q myocardial infarction: biochemical markers of coronary thrombosis

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INTERNATIONAL JOURNAL OF CARDIOLOGY 1999年第sup1期68卷 S55-S61页

作者： Galvani, M Ferrini, D Ottani, F Eisenberg, PR Fondaz Cardiol Sacco Cardiovasc Res Unit Forli Italy GB Morgagni L Pierantoni Hosp Div Cardiol Forli Italy Civile Hosp Div Cardiol Bentivoglio Italy Washington Univ Div Cardiovasc St Louis MO USA

Coronary thrombosis is an important determinant of prognosis in patients with acute coronary syndromes (ACS), However, the identification of patients at high-risk for progression of coronary thrombosis is difficult partly because we currently lack clinically meaningful laboratory methods for its detection. The most promising approaches involve the measurement in plasma of markers of fibrin formation and degradation. Thrombin activity, as reflected by plasma or urine concentrations of fibrinopeptide A, is increased in patients with ACS and is associated with adverse outcome. However, the use of fibrinopeptide A as a marker of fibrin formation is limited by the very short half-life of the compound, by artifact due to sample acquisition, and by extremely long turnaround times. To overcome these limitations, measurement of soluble fibrin has been proposed. We have recently explored the prognostic value of a new fibrin-specific ELISA assay for soluble fibrin in patients with ACS and found that patients with the highest levels had a 2-fold increased risk of early and late cardiac events. Increases in plasma concentrations of cross-linked fibrin degradation products (XL-FDPs), which reflect increased fibrin turn-over, are a marker of risk for complications of myocardial infarction. However, until recently, assays for XL-FDPs lacked specificity, because they did not distinguish between fibrin and fibrinogen degradation products. Recently, fibrin-specific ELISAs have been described and a rapid whole blood assay for D-dimer has been developed, We recently validated the prognostic value of this whole blood agglutination assay in patients with ACS. These results suggest that: (1) The detection of significant activation of the coagulation and/or fibrinolytic system may be important for rapid risk stratification of patients with ACS;(2) patients with biochemical evidence of ongoing coronary thrombosis may particularly benefit from aggressive antithrombotic strategies;(3) sequenti

关键词：心绞痛不稳定型/血液冠状动脉血栓形成/血液纤维蛋白肽A/分析心肌梗死/血液预后凝血酶原/分析危险性评估敏感性与特异性时间因素人类

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