The Role of the Coagulation System in Heart Disease

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Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]

Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]


Overview

The fibrinolytic system dissolved intravascular clots as a result of plasmin, an enzyme that digests fibrin. Plasminogen, an inactive precursor, is converted in plasmin. Plasmin is a relatively nonspecific protease – it digests fibrin clots and other plasma proteins, including some coagulating factors. Tissue plasminogen activator (t-PA) is released from endothelial cells in response of various signals, including stasis produced by vascular occlusion.

Therapy with thrombolytic drugs tends to dissolve both pathological thrombi and fibrin deposits in sites of vascular injury.

Platelets provide the initial hemostatic plug at sites of vascular injury. They also participate in reactions that lead to atherosclerosis and pathological thrombosis. Antagonists of platelet function thus have been used in attempt to prevent thrombosis and to alter the natural progress of athrosclerotic vascular disease.

Hemostasis is the cessation of blood loss from the damaged vessel. First platelets adhere to the injured regions of blood vessel, they aggregate to form of primary hemostatic plug. Platelets stimulate local activation of plasma coagulation factors, leading to generation of fibrin clot that reinforces the platelet aggregate. Thrombosis is a pathological process in which platelets aggregate and/or fibrin clot occludes a blood vessel. Arterial thrombosis may result in ischemic necrosis of the tissue supplied by the artery. Venous thrombosis may cause tissue drained by the vein to become edematous and inflamed. Thrombosis of a deep vein may be complicated by pulmonary embolism.

Platelet aggregation and coagulation normally do not occur within an intact blood vessel. Thrombosis is prevented by several regulatory mechanisms that require a normal vascular endothelium. Prostacyclin (PGI-2), a metabolite of arachidonic acid, is synthesized by endothelial cells, and inhibits platelets aggregation and secretion. Antithrombin is a plasma protein that inhibits coagulation factors. Heparan sulfate synthesized by endothelial cells stimulate the activity of antithrombin. Protein C in combination with protein S degrade coagulating cofactors Va and VIIIa and diminishes the rates of activation of prothrombin and factor X.

A number of studies have clearly shown the association of increased plasma fibrinogen levels with cardiovascular disease. Interestingly, preliminary results from the Bezafibrate Infarction Prevention (BIP) study have pointed out that the reduction of the increased fibrinogen levels in CAD patients could decrease the incidence of cardiac death and ischemic stroke. The substantial variability of plasma fibrinogen levels owing to a number of factors including the assay used, socioeconomic and metabolic factors, etc. limit the wide application of this coagulation factor as a risk factor in every-day clinical practice. It should be mentioned that smoking cessation, weight loss, regular exercise,moderate alcohol consumption and fibrates can significantly reduce plasma fibrinogen levels.[1] [2] [3] [4] [5] [6] [7] [8] [9] [10]

Several other factors participating in blood coagulation have been associated with CVD risk,including factor VII levels, plasminogen activator inhibitor (PAI-1) and increased platelet aggregation. Compelling evidence from randomized controlled trials now exists on the beneficial effect of antiplatelet agents (mainly aspirin) in the prevention of cardiovascular events in patients with established vascular disease. However, there is no unequivocal evidence on the beneficial effect of aspirin in the primary prevention of CVD taking into account the long-term risks of therapy. It should be mentioned that in well-controlled treated hypertensive patients, as well as in men at particularly high risk, aspirin results in a significant decrease in cardiovascular events. [11] [12] [13] [14] [15] [16]

References

  1. Kannel, W. B., Wolf, P. A., Castelli, W. P. et al. (1987).Fibrinogen and risk of cardiovascular disease. JAMA,258, 1183-1186
  2. Ernst, E. and Resch, K. L. (1993). Fibrinogen as a cardiovascular risk factor: a meta-analysis and review of the literature. Ann. Intern. Med., 118, 956-963
  3. Behar, S. (1999). Lowering fibrinogen levels clinical update. BIP Study Group. Bezafibrate infarction Prevention. Blood Coagul. Fibrinolysis, 10, 41-43
  4. Barasch, E., Benderly, M., Graff, E. et al. (1995).Plasma fibrinogen levels and their correlates in 6457coronary heart disease patients. The Bezafibrate Infarction Prevention (BIP) Study. J. Clin.Epidemiol., 48, 757-765
  5. Brunner, E., Smith, G. D., Marmot, M. et al. (1996).Childhood social circumstances and psychological and behavioural factors as determinants of plasma fibrinogen. Lancet, 347, 1008-1013
  6. Muldoon, M. F., Herbert, T. B., Patterson, S. M. et al.(1995). Effects of acute psychological stress on serum lipid levels, hemo concentration, and blood viscosity.Arch. Intern. Med., 155, 615-620
  7. Meade, T. W., North, W. R., Chakrabarti, R. et al.(1977). Population-based distributions of haemostatic variables. Br. Med. Bull., 33, 283-288
  8. Ernst, E. and Resch, K. L. (1995). Therapeutic interventions to lower plasma fibrinogen concentration. Eur. Heart J., 16 (Suppl A), 47-53
  9. Mikhailidis, D. P., Ganotakis, E. S., Spyropoulos, K.A. et al. (1998). Prothrombotic and lipoprotein variables in patients attending a cardiovascular risk management clinic: response to ciprofibrate or lifestyle advice. Int. Angiol., 17, 225-233
  10. Papadakis, J. A., Ganotakis, E. S., Jagroop, I. A. et al.(1999). Effect of hypertension and its treatment on lipid, lipoprotein (a), fibrinogen, and bilirubin levels in patients referred for dyslipidemia. Am. J.Hypertens., 12, 673-681
  11. Pazzucconi, F., Mannucci, L., Mussoni, L. et al.(1992). Bezafibrate lowers plasma lipids, fibrinogen and platelet aggregability in hypertriglyceridemia.Eur. J. Clin. Pharmacol., 43, 219-223
  12. Meade, T. W. Jr (1992). Fibrinogen and other clotting factors in cardiovascular disease. In: Francis, R. B. Jr(Ed), Atherosclerotic Vascular Disease, Hemostasis, and Endothelial Function. Marcel Dekker, New York, 1-32
  13. Junker, R., Heinrich, J., Schulte, H. et al. (1997).Coagulation factor VII and the risk of coronary heart disease in healthy men. Arterioscler. Thromb. Vasc.Biol., 17, 1539-1544
  14. Elwwood, P. C., Renaud, S., Sharp, D. S. et al.(1991). Ischaemic heart disease and platelet aggregation. The Caerphilly Collaborative Heart disease Study. Circulation, 83, 38-44
  15. Hennekens, C. H. (1999). Update on aspirin in the treatment and prevention of cardiovascular disease.Am. Heart J., 137, 9-13
  16. Hansson, L., Zanchetti, A., Carruthers, S. G. et al. for the HOT Study Group (1998). Effects of intensive blood pressure lowering and low-dose aspirin inpatients with hypertension: principal results of the Hypertension Optimal Treatment (HOT) Randomized Trial. Lancet, 351, 1755-1762



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