procedure for haemostasis ensures that following vascular damage blood remains confined

procedure for haemostasis ensures that following vascular damage blood remains confined to DHCR24 the circulatory system. components of the clot. Regardless of the site of clot the formation of a stable fibrin network is the ultimate step in thrombus formation. The conversion of fibrinogen to fibrin is brought about by cleavage of fibrinogen. This process is undertaken by thrombin which cleaves fibrinogen into two smaller peptides fibrinopeptide A and B. Fibrin monomers are formed with subsequent polymerization then. Finally the clot can be consolidated when element XIII cross-links the fibrin monomers. After the clot offers formed as well as the fibrinolytic program starts the proteolytic removal of thrombi to make sure that vessel patency can be restored. Plasminogen binds to fibrin and it is activated by cells plasminogen activator (tPA) to plasmin. Plasmin starts the dissolution of fibrin although; due to its wide specificity it causes degradation of fibrinogen aswell. Similar to the coagulation cascade the fibrinolytic program is a complicated interplay of activators and inhibitors to make sure optimal haemostasis. In disease the good stability of haemostasis is disturbed Obviously. Atherosclerosis is a multifactorial disease where vascular damage potential clients to lipid deposition and build up of platelets and fibrin. It isn’t surprising consequently that disorders of different the different parts of haemostasis can donate to the pathogenesis of atherosclerosis. The existing study compared the amount of fibrinogen and plasminogen in angiographically regular subjects and the ones with gentle/moderate and serious coronary artery disease(2). A graded relationship was discovered BMS-540215 between degrees of fibrinogen and the severe nature of coronary artery disease. Raised degrees of plasma fibrinogen have already been been shown to be an unbiased risk element for coronary artery disease(3 4 Whether that is a direct impact of hyperfibrinogenemia can be unclear even though some proof exists to claim that raised BMS-540215 fibrinogen may influence the procedure of atherogenesis by fibrin deposition within developing atherosclerotic lesions(5). Because fibrinogen in addition has been associated with other traditional cardiovascular risk factors an atherothrombotic effect mediated through a raised fibrinogen level would appear plausible. This would be indirectly supported by thrombotic association of dysfibrinogenemia(6) a condition which primarily produces a bleeding tendency but is well known to cause thrombotic events too. There are several mechanisms by which fibrinogen may increase cardiovascular risk. It binds specifically to activated platelets via glycoprotein IIb/IIIa contributing to platelet aggregation. Elevated fibrinogen levels increase plasma viscosity and promote fibrin formation. Chronic inflammatory conditions are known to result in accelerated atherosclerosis. That fibrinogen is BMS-540215 an acute-phase reactant with levels rising significantly in inflammatory states may be pathogenetically relevant. Like disorders of fibrinogen impaired fibrinolysis appears to have a role in thrombosis. Plasmin which results from the cleavage of plasminogen by plasminogen activators (PAs) predominantly mediates the intravascular clearance of fibrin. The important role of plasminogen in fibrinolysis makes it an interesting parameter to evaluate in various diseases. It is recognized that a decreased plasminogen level may affect the fibrinolytic activity and result in thrombotic tendency(7). It is therefore not surprising that plasminogen levels BMS-540215 were not found to be significantly elevated in patients with coronary artery disease. It is well known that increased levels of plasminogen activator inhibitor-1 (PAI-1) are found in myocardial infarction(8). A raised PAI-1 level would inhibit fibrinolysis by inhibiting tissue plasminogen activator and this may result in thrombotic tendency. It would have been interesting to look at PAI-1 levels as well and this aspect needs to BMS-540215 be considered in future studies. While this paper reaffirms the association of elevated fibrinogen with coronary artery disease in view of the multifaceted nature of atherosclerosis especially the emerging role of inflammation in its pathogenesis information on inflammatory markers would have been valuable(9 10 Further follow-up on the three cohorts with serial measurements of BMS-540215 different parameters would give additional insight into correlating the progression of the disease with different haemostatic and fibrinolytic parameters..

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