Myocardial infarction, fibrinogen

Thrombin, a serine protease, cleaves fibrinogen into fibrin to create a fibrous plug and also amplifies its own production through the activation of factor XI and cofactors V and Vlll. Thrombin also plays a crucial role in the activation of platelets through the cleavage of the protease-activated receptors on the platelet surface. Antagonists of G-protein-coupled protease-activated receptor PARi have been synthesised to study the role of thrombin PARi receptor in thrombosis and vascular injury. Thrombosis is the most common cause of death in the industrialised world and, whether through venous thromboembolism, myocardial infarction or stroke, ultimately involves the inappropriate activity of... 

Scrutton, M. C., Ross-Murphy, S. B., Bennett, G. M., Stirling, Y., and Meade, T. W. (1994). Changes in clot deformability - a possible explanation for the epidemiological association between plasma fibrinogen concentration and myocardial infarction. Bbod Coagul. Fibrinolysis 5, 719-723. 

Many mediators of inflammation have been identified— cytokines IL-6, tumor necrosis factor alpha cell adhesion molecules intracellular adhesion molecule-1 (ICAM-I), P-selectin and acute phase reactants CR.R fibrinogen, serum amyloid A, and soluble CD40 (Fig. I) (3). Myeloperoxidase is an enzyme secreted from monocytes, neutrophils, and macrophages. A single measurement taken from patient with chest pain in the emergency department predicted the early risk of myocardial infarction and the risk of major cardiac of ends in the next 30 days to six months (15). 

In the initial study described by Gold et al. (1984), recombinant t-PA was characterized for its ability to lyse 2-hour-old thrombi. Tissue plasminogen activator was infused at doses of 4.3, 10, and 25 (ig/kg/min, i.v, and resulted in reperfusion times of 40, 31, and 13 minutes, respectively. Thus, in this model of canine coronary thrombosis, t-PA exhibited dose-dependent coronary thrombolysis. Furthermore, it is possible to study the effect of different doses of t-PA on parameters of systemic fibrinolytic activation, such as fibrinogen, plasminogen, and a2-antiplasmin, as well as to assess myocardial infarct size. For example, Kopia et al. (1988) demonstrated that SK elicited dose-dependent thrombolysis in this model. 

Wilhelmsen L, Suardsudd K, Korsan-Bengsten K, Larsson B, Welvin L, Tibblin G. Fibrinogen as a risk factor for stroke and myocardial infarction. N Engl J Med 1984 311 501-505. 

Maresca G, Diblasio A, Marchioli R et al. Measuring plasma fibrinogen to predict stroke and myocardial infarction An update. Arteriosclerosis Thrombosis and Vascular Biology 1999 19 1368-1377. 

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