Decrease of Fibrinolytic Potential in the Occurence of Cerebral Ischemia

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Decrease of Fibrinolytic Potential in the Occurence of Cerebral Ischemia

One of the most present clinical manifestations of long and progressive atherothrombotic occurrences is the ischemic cerebrovascular insult, one of the leading causes of death and illness in the world. Lately, a growing number of scientists believe that disorders in the fibrinolytic mechanism function are the key to the occurrence of cerebral ischemia. The goal of this study is to investigate whether the disorder of the fibrinolytic mechanism has influence on the occurrence of ischemic cerebrovascular insult. Our study includes 90 examinees, 60 of which suffer from ischemic cerebrovascular insult and 30 are clinically healthy examinees forming the control group. The results of our investigation show that statistically a significantly larger number of patients has decreased fibrinolytic potential comparing with controls (p < 0.01). According to this, it has been noted that euglobulin lysis clot time in the patient group is significantly longer (p = 0.005). Statistically, no significant difference has been noted related to the activity of plasminogen (p = 0.085). Further on, the plasminogen activator inhibitor-1 values among the patients have been significantly higher (p = 6.20 x 10-11). Moreover, significantly higher values of tissue-type plasminogen activator antigen have been statistically noted in the patient group (p = 5.20 x 10-5). The results of this investigation impose the conclusions that the decrease in fibrinolytic potential affects the occurrence of ischemic cerebrovascular insult, that it is directly connected to the higher levels of plasminogen activator inhibitor-1 and that the growth of tissue-type plasminogen activator antigen concentration participates in the decrease of fibrinolytic potential among patients suffering from cerebral ischemia.

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  • Lučić A. Mehanizam fibrinoliznog procesa u gojaznih osoba. Doktorska disertacija. Novi Sad 1976.

  • Cesarman-Maus G Hajjar KA. Molecular mechanisms of fibrinolysis. Br J Haematol 2005; 129 (3): 307-21.

  • Baklaja R Pešić MČ Czarhecki J. Haemostasis and Haemorrhagic Disorders. Thymus Medizinischer Fachbuchverlag Bad Harzburg 2000.

  • Lijnen HR. Elements of the fibrinolytic system. Ann NY Acad Sci 2001; 902: 226-36.

  • Rijker DC Sakharov DV. Basic Principles in Thrombolysis: Regulatory Role of Plasminogen. Thromb Research 2001; 103(1): S41-9.

  • Lóopez-Lira F Rosales-León L Monroy-Martinez V Ruis Ordaz BH. The role of ß2-glycoprotein I (ß2GPI) in the activation of plasminogen. BBA 2006; 1764 (4): 815-23.

  • Bouma BN Meijers JC. New insights into factors affecting clot stability: A role for thrombin activatable fibrinolysis inhibitor (TAFI;plasma procarboxypeptidase B plasma procarboxypeptidase U procarboxypeptidase R). Semin Hematol 2004; 41 (1): 13-9.

  • Agirbasli M. Pivotal role of plasminogen-activator inhibitor 1 in vascular disease. Int J Clin Pract 2005; 59 (1): 102-6.

  • Robbie LA Dummer S Booth NA Adey GD Bennet B. Plasminogen activator inhibitor 2 and urokinase-type plasminogen activator in plasma and leukocytes in patients with severe sepsis. Br J Haematol 2000; 109: 342-8.

  • Knecht W Willemse J Stenhamre H Andersson M Berntsson P Furebring C et al. Limited mutagenesis increases the stability of human carboxypeptidase U (TAFIa) and demonstrates the importance of CPU stability over proCPU concentration in down-regulating fibrinolysis. Febs J 2006; 273 (4): 778-92.

  • Berghaus GM. Hemostasis: regulation and dysregulation. Proceedings of the ASTM residental course jointly organized with the European School of Hematology (ESH). Frankfurt (Germany) 1997;1-40.

  • Mršulja BB Kostić VS. Neurohemija u neurološkim bolestima. Medicinska knjiga. Beograd 1994.

  • Tegos TJ Kalodiki E Daskalopulou SS Nicolaides AN. Stroke: epidemiology clinical picture and risk factors. Part I of III. Angiology 2000; 51: 793-808.

  • Zhang LF et al. Proportion of different subtypes of stroke in China. Stroke 2003; 34: 2091-6.

  • Goldstein LB Adams R Becker K Furberg CD Gorelick PB Hademenos G Hill M et al. Primary prevention of ischemic stroke: A statement for health care professionals from the Stroke Council of the American Heart Association. Circulation 2001; 103: 163-82.

  • Juhan-Vague I Alessi M-C Mavri A Morange PE. Plasminogen activator inhibitor-1 inflammation obesity insulin resistance and vascular risk. J Thromb Haemost 2003; 1: 1575-9.

  • Feinberg WA Coull BM. Coagulopathies and stroke. In: Welch KMA Caplan LR Reis DJ Siesjo BK Wier B eds. Primer on Cerebrovascular Diseases. San Diego Academic Press 1997: 399-401.

  • Salomaa VV Wu KK Stinson VL Kark JD Folsom AR Liao P et al. The association of fibrinolytic activity with asymptomatic carotid atherosclerosis: The ARIC study (abstract). Circulation 1993; 687-99.

  • Glueck CJ Rovick MH Schmerler M Anthony J Feibel J Bashir M et al. Hypofibrinolytic and atherogenic risk factors for stroke. J Lab Clin Med 1995; 125: 319-25.

  • Bang C Park H Ahn M Shin H Hwang K Hong S. 4G/5G Polymorphism of the Plasminogen Activator Inhibitor-1 Gene and Insertion/Deletion Polymorphism of the Tissue-Type Plasminogen Activator Gene in Atherothrombotic Stroke. Cerebrovasc Dis 2001; 11: 294-9.

  • Kohler HP Grant PJ. Plasminogen-activator inhibitor type 1 and coronary artery disease. N Eng J Med 2000; 342: 1792-801.

  • Nilsson Ardnor S. Genetic Studies of Stroke in Northern Sweden. Medical Dissertation. Umea University 2006.

  • Macfarlane RG Pilling J. Observation on fibrinolysis. Plasminogen plasmin and antiplasmin content of human blood. Lancet 1946; 2: 562.

  • Amiral J Plassart V Grosley M Mimilla F Contant G Guyader AM. Measurement of tPA and tPA-PAI-1 complexes by ELISA using monoclonal antibodies: clinical relevance. Thromb Res 1988; 8: 99-113.

  • Smith A Patterson C Yarnell J Rumley A Ben-Shlomo Y Lowe G. Which Hemostatic Markers Add to the Predictive Value of Conventional Risk Factors for Coronary Heart Disease and Ischemic Stroke? The Caerphilly Study. Circulation 2005; 112 (20): 3080-7.

  • Anžej S Božić M Antović A Peternel P Gašperšić N Rot U. Evidence of hypercoagulability and inflammation in young patients long after acute cerebral ischaemia. Thromb Res 2007; 120 (1): 39-46.

  • Folsom AR Aleksić N Park E et al. Prospective study of fibrinolytic factors and incident coronary artery disease. The Atherosclerosis Risk in Communities (ARIC) Study. Arterioscler Thromb Vasc Biol 2001; 21: 611-7.

  • Oláh L Misz M Kappelmayer J Ajzner E Csépány T Fekete I et al. Natural Coagulation Inhibitor Proteins in Young Patients with Cerebral Ischemia. Cerebrovasc Dis 2001; 12: 291-7.

  • Lowe GD O Danesh J Lewington S Walker M Lennon L Thomson A et al. Tissue plasminogen activator antigen and coronary heart disease. Europ Heart J 2004; 25: 252-9.

  • Jood K LandenVall P Tjärnulnd-Wolf A LandenVall C Andersson M Nilsson S. Fibrinolytic Gene Polymorphism and Ischemic Stroke. Stroke 2005; 36: 2077.

  • Wang L Kittaka M Sun N et al. Chronic nicotine treatment enhances focal ischemic brain injury and depletes free pool of brain microvascular tissue plasminogen activator in rats. J Cereb Blood Flow Metab 1997; 17: 136-46.

  • Ohira T Shahar E Chambless LE Rosamond WD Mosley Jr TH Folsom AR. Risk Factors for Ischemic Stroke Subtypes. Stroke 2006; 37: 2493-8.

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