medigraphic.com
ISSN 0188-2198 (Impreso)

1999, Número 2

<< Anterior Siguiente >>

Rev Mex Cardiol 1999; 10 (2)


Factores trombogénicos

Necoechea AJC

Idioma: Español
Referencias bibliográficas: 47
Paginas: 70-84
Archivo PDF: 1011.89 Kb.


RESUMEN

La hemostasia del sistema circulatorio es primariamente una función de interacción entre endotelio vascular, constituyentes subendoteliales, plaquetas y factores solubles en el plasma. La ruptura mínima de la placa aterosclerosa se asocia usualmente con la formación de un trombo plaquetario relativamente pequeño en la íntima vascular, que no se extiende hacia la luz vascular y no induce eventos isquémicos clínicamente evidentes, pero contribuyen a mayor progresión de la placa. Sin embargo, la disfunción endotelial, la trombogenicidad local y sistémica aumentadas pueden dar lugar a trombo oclusivo, aún en ausencia de ruptura franca de la placa. El potencial trombogénico de la placa es modulado por su estructura constitutiva donde el contenido de lípidos y macrófagos que expresan factor tisular inducen activación del sistema de coagulación, que resulta en generación de trombina que promueve el crecimiento del trombo, activa factores de coagulación, induce activación plaquetaria, estimula la proliferación de músculo liso vascular y síntesis de citocinas inflamatorias que contribuyen al proceso inflamatorio y trombogenicidad. Los síndromes isquémicos agudos representan una gama amplia de expresión clínica, con un sustrato fisiopatológico común, la oclusión u obstrucción de la circulación por ruptura e inestabilidad de la placa aterosclerosa, o en un menor número de casos por denudación y disfunción endotelial. Ambos mecanismos que favorecen la formación de un trombo obstructivo rico en plaquetas. De ahí que uno de los objetivos terapéuticos sea la recanalización y restitución del flujo vascular distal a la obstrucción. El presente artículo analiza los beneficios y limitaciones de los diferentes enfoques terapéuticos para inhibir o disminuir la oclusión trombótica vascular, no sólo en el contexto de los síndromes isquémicos agudos, sino también su papel en prevenir eventos isquémicos futuros.


REFERENCIAS (EN ESTE ARTÍCULO)

  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.




2020     |     www.medigraphic.com