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1999, Number 2

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Rev Mex Cardiol 1999; 10 (2)

Thrombogenic factors

Necoechea AJC

Language: Spanish
References: 47
Page: 70-84
PDF size: 1011.89 Kb.


ABSTRACT

The hemostasia of circulatory system is primarily an interaction between vascular endothelium, subendothelial constituyents, platelets and free factors in plasma. The minimal rupture of atherosclerotic plaque usually is associated with the formation of a relatively small thrombus in the vascular intima that not made protrusion in vascular lumen, without clinical ischemic events, but participate in the progression of plaque. Wherever, the endothelial dysfunction, the local and systemic thrombogenicity can give an occlusive thrombus, without rupture of plaque. The thrombogenic potential of plaque is modulated for its constitution, as the lipidic and macrophages contents, that express the tisular factor and facilitate the activation of coagulation, thrombin formation, that promote more grown of the thrombus, platelet activation, proliferation of smooth muscle and synthesis of cytokines, that contribute in inflammatory process and thrombogenicity. The acute ischemic syndromes have a wide clinical expression with common physiopathologic substrate: obstruction of circulation secondary to rupture or unstability of atherosclerotic plaque, or in less situations is due to denudation and endothelial dysfunction. Both mechanisms facilitate the formation of a thrombus rich in platelets. For this reason, one of the therapeutics goals is the recanalization and restitution of vascular flow, distal to obstruction. This work treats about the benefits and limitations of the different therapeutic options with the aim to inhibit or diminish the vascular occlusion, not only in the contest of acute coronary syndromes, but also for the prevention of futures ischemic events.


REFERENCES

  1. American Heart Association. Heart and Stroke Facts. Dallas, Texas. American Heart Association National Center, l996.

  2. Landau C, Lange RA, Hillis LD. Percutaneous transluminal coronary angioplasty. N Engl J Med 1994; 330: 981-993.

  3. Fuster V, Badimon L, Badimon JJ et al. The pathogenesis of coronary artery disease and the acute coronary syndromes. N Engl J Med 1992; 326: 310-318.

  4. Fuster V. Mechanisms leading to myocardial infarction: Insights success of vascular biology. Circulation 1994; 90: 2126-2146.

  5. Bogarty P, Hackett D, Davies G et al. Vasoreactivity of the culprit lesion in unstable angina. Circulation 1994; 90: 5-11.

  6. Hoffmeister HM, Jor M, Wendel HP et al. Alterations of coagulation and fibrinolytic and kallikrein-kinin systems in acute and postacute phases in patients with unstable angina pectoris. Circulation 1995; 91: 2520-2527.

  7. Kontny F. Reactivation of the coagulation system: Rationale for long-term antithrombotic treatment. Am J Cardiol 1997, 80 (Suppl E): 55-60.

  8. Wilhelmsen L, Svardsudd K, Korsan-Bengtsen et al. Fibrinogen as a risk factor for stroke and myocardial infarction. N Engl J Med 1984; 311: 505.

  9. Fowkes FG. Fibrinogen and cardiovascular disease in clinical practice. Eur Heart J 1995; 16 (Suppl A): 60-63.

  10. Ernst E, Resch KL. Fibrinogen as a cardiovascular risk factor. An analysis and review of the literature. Ann Inter Med 1993; 118: 956.

  11. Lam JY, Latour JG, Lesperance J et al. Platelet aggregation, coronary artery disease, progression and future coronary events. Am J Cardiol 1994; 73: 333-338.

  12. Trip MD, Manger CV, Van Capelle FJL et al. Platelet hyperactivity and prognosis in survivors of myocardial infarction. N Engl J Med 1990; 322: 15.49-1554.

  13. Merlini PA, Bauer KA, Oltrona L et al. Persistent activation of coagulation mechanisms in unstable angina and myocardial infarction. Circulation 1994; 90: 61-68.

  14. Meade TW, Ruddock V, Stirling et al. Fibrinolytic activity, clotting factors and long-term incidence of ischemic heart disease in the Northwick Park Heart Study. Lancet 1993; 342: 1076-1079.

  15. Scano AM, Lawn RM, Berg K. Lipoprotein (a) and atherosclerosis. Ann Intern Med 1991; 115: 209-218.

  16. Genest JJ, Jenner JL, McNamara JR et al. Prevalence of lipoprotein (a) excess in coronary artery disease. Am J Cardiol 1991; 67: 1039-1045.

  17. Ridker PM, Hennekens CH, Stamfer MJ. A prospective study of lipoprotein (a) and the risk of myocardial infarction. JAMA 1993; 270: 2195-2199.

  18. Schaefer EJ, Lamon-Fava S, Jenner JL et al. Lipoprotein (a) levels and risk of coronary heart disease in men. The Lipid Research Clinics Coronary Primary Prevention Trial. JAMA 1994; 271: 999-1003.

  19. Hamsten A. Coagulation factors and hyperlipidemia. Curr Opin Lipidol 1991; 2: 266-271.

  20. Daae LN, Kierulf P, Lanndaas S et al. Cardiovascular risk factors: Interactive effects of lipids, coagulation and fibrinolysis. Scand J Clin Lab Invest 1993; 7: 385-388.

  21. Patrono C, Renda G. Platelet activation and inhibition in unstable coronary syndromes. Am J Cardiol 1997; 80: 17E- 20E.

  22. Klein W, Buchwald A, Hillis S et al. Fragmin in unstable angina pectoris or in non-Q-wave acute myocardial infarction (The FRISC Study). Am J Cardiol 1997; 80: 30E-34E.

  23. Antman EM. Hirudin in acute myocardial infarction. Safety report from the thrombolysis and thrombin inhibition in myocardial infarction. (TIMI) 9ª Trial. Circulation l994; 90: 1624-1630.

  24. Topol EJ. Global use of strategies to open occluded coronary arteries (GUSTO IIb). N Engl J Med 1996; 335: 775-782).

  25. ISIS-2 (Second International Study of Infarct Survival). Collaborative Group. Randomized Trial of intravenous streptokinase, oral aspirin, both, or neither, among 17,187 cases of suspected acute myocardial infarction. ISIS-2 . Lancet 1988; 311: 349-360.

  26. The RISC Group. Risk of myocardial infarction and death during treatment with low dose aspirin and intravenous heparin in men with unstable coronary artery disease. Lancet 1990; 336: 827-830.

  27. Collaborative overview of randomized trials of antiplatelet therapy. Prevention of death, myocardial infarction and stroke by antiplatelet therapy in various categories of patients. Antiplatelet Trialist Collaboration. Br Med J 1994; 308: 81-106.

  28. Balsano F, Rizzon P, Violi F et al. Antiplatelet treatment with ticlopidine in unstable angina. A controlled multicenter clinical trial. The Studio della Ticlopidina nell’ Angina Instabile Group. Circulation 1990; 82: 17-26.

  29. Colombo A, Hall P, Nakamura S et al. Intracoronary stenting without anticoagulation accomplished with intravascular ultrasound guidance. Circulation 1995; 91: 1676-1688.

  30. Lablanche JM, McFadden EP, Bonnet JL et al. Combined antiplatelet therapy with ticlopidine and aspirin. Eur Heart J 1996; 17: 1373-1380.

  31. Leon MB, Baim DS, Gordon P et al. Clinical and angiographic results from the Stent Anticoagulation Regimen Study (STARS). Circulation 1996; 94: (Suppl I) 685.

  32. Bertrand ME, Legrand V, Boland J et al. Randomized multicenter comparison of conventional anticoagulation versus antiplatelet therapy in unplanned and elective coronary stenting. The full anticoagulation versus aspirin and ticlopidine. (FANTASTIC) study. Circulation l998; 98: 1597-1603.

  33. Breddin D, Loew D, Lechner K et al. The German-Austrian Aspirin Trial: A comparison of aspirin, placebo and phenprocouman in secondary prevention of myocardial infarction. Circulation 1980; 62: 63.

  34. The EPSIM Research Group. A controlled comparison of aspirin and oral anticoagulation in prevention of death after myocardial infarction. N Engl J Med 1982; 307: 701.

  35. Meijer A, Verheug F, Werter C. Aspirin versus coumadin in the prevention of reoclussion and recurrent ischemia after successful thrombolysis. A prospective placebo-controlled angiographic study. Results of the APRICOT study. Circulation 1993; 87: 1524.

  36. Steering Committee of the Physicians’ Health Study Research Group. Preliminary report. Findings from the aspirin components of the ongoing Physicians’ Health Study. N Engl J Med 1988; 318: 262-264.

  37. Peto R, Gray R, Collins R et al. Randomized trial of prophylactic daily aspirin in British male doctors. Br Med J 1988; 296: 313-316.

  38. Cairns JA, Lewis HD, Meade TW et al. Antithrombotic agents in coronary artery disease. Chest 1995; 108 (Suppl 4): 380-400.

  39. Schulman SP, Goldschmidt-Clemont PJ, Toplo EJ et al. Effects of integrilin, a platelet glycoprotein IIb/IIIa antagonist, in unstable angina: A randomized multicenter trial. Circulation 1996; 94: 2083-2089.

  40. The RESTORE Investigators. The effects of platelet glycoprotein IIb/IIIa blockade with tirofiban on adverse cardiac events in patients with unstable angina or acute myocardial infarction undergoing coronary angioplasty. Circulation 1997; 96: 1445-1453.

  41. Lefkovits J, Ivanhoe R, Califf R et al. Effects of platelet glycoprotein IIb/IIIa receptor blockade by chimeric monoclonal antibody (Abciximab) on acute and six months outcomes after percutaneous transluminal coronary angioplasty for acute myocardial infarction. Am J Cardiol 1996; 77: 1045-1051.

  42. The EPIC Investigators. Use of a monoclonal antibody directed against the platelet glycoprotein IIb-IIIa receptor in high-risk coronary angioplasty. N Engl J Med 1994; 330: 956-961.

  43. The CAPTURE Investigators. Randomized placebo-controlled trial of abciximab before and during intervention in refractory unstable angina. The CAPTURE study. Lancet 1997; 349: 1429-1435.

  44. The EPILOG Investigators. Platelet glycoprotein IIB-IIIa receptor blockade and low dose heparin during percutaneous coronary revascularization. N Engl J Med 1997; 336: 1689-1696.

  45. Tcheng JE. Impact of eptifibatide on early ischemic events in acute ischemic coronary syndromes: A review of the IMPACT II Trial. Am J Cardiol 1997; 80: 218-228.

  46. Cannon CP, McCabe CH, Borzak S et al. Randomized trial of an oral platelet glycoprotein IIb/IIIa antagonist, sibrafiban, in patients after an acute coronary syndrome. Results of the TIMI 12 trial. Circulation 1998; 97: 340-349.

  47. Kereiakes DJ, Kleiman NS, Ferguson JJ et al. Pharmacodynamic efficacy, clinical safety, and outcomes after prolonged platelet glycoprotein IIb/IIIa receptor blockade with oral xemilofiban. Results of a multicenter, placebo controlled, randomized trial. Circulation 1998; 98: 1268-1278.




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