Heparina no fraccionada en el manejo del síndrome coronario agudo.
Non fractioned heparina in acute coronary syndrome management
Palabras clave:
heparina, antitrombina III, glicosaminoglicanos, isquemia miocárdica. (es)heparin, antithrombin III, glycosaminoglycans, myocardial ischemia (en)
La formación de trombos es un proceso normal que tiene como objetivo prevenir sangrados importantes ante la presencia de una noxa que altere la integridad vascular. Sin embargo en algunas patologías estos fenómenos trombóticos se desencadenan espontáneamente o son exagerados con respecto al daño vascular y llevan a la producción de diferentes cuadros clínicos; en estos casos el uso de la anticoagulación juega un papel fundamental. El primer medicamento usado para este fin fue la heparina, la cual ha resistido el paso del tiempo y continua vigente en muchos contextos clínicos, como se evidencia en diferentes guías de consenso sobre el tema.
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Hirsh J, Raschke R. Heparin and Low-Molecular-Weight-Heparin. The Seventh ACCP Conference on Antithrombotic and Trombolytic Therapy. CHEST. 2004; 126: 188-203.
Baglin T, Barrowcliffe T, Cohen A. Guidelines on the use and monitoring of heparin. Bjh. 2006; 133:19-34.
Mehta R, Johnson M. Uptdate on anticoagulant medications for the interventional Radiologist. J Vasc Interv Radiol. 2006; 17: 597-612.
Owen CA. A history of blood coagulation. Rochester MN: Mayo Foundation for medical education and research, 2001.
Jorpes E. The chemistry of heparin. Biochem F. 1935; 29: 1817-30.
Crafoord C. Preliminary report on postoperative treatment with heparin as a preventive of thrombosis. Acta Chir Scand. 1937;79:407-26.
Brinkhous KM, Smith HP, Warner ED, et al. The inhibition of blood clotting: an unidentified substance which acts in conjuction with heparin to prevent the conversion of prothrombin into thrombin. Am J Physiol 1939; 125: 683-687.
Abildgaard U. Highly purified antithrombin III with heparin cofactor activity prepared by disc electrophoresis. Scand J Clin Lab Invest. 1968; 21:89-91
Walker C, Royston D. Thrombin generation and its inhibition: a review of the scientific basic and mechanism of action of anticoagulant therapies. Br J Anaesth. 2002; 88: 848-63.
Bick R, Frenkel E, Walenga J, et al. Unfractionated heparin, low molecular weight heparins, and pentasaccharide: Basic mechanism of action, pharmacology, and clinical use. Hematol Oncol Clin N Am 2005; 19: 1-51.
Olsom ST, Bjork L. Predominant contribution of surface approximation to the mechanism of heparin acceleration of the antitrombin-trombin reaction. Elucidation from salt concentration effect. J Biol Chem. 1991; 266: 6353-64.
Olsom ST, Bjork L, Sheffer R, et al. Role of the antithrombic binding pentasaccharide in heparin acceleration antithrombin proteinase reactions. J Biol Chem. 1992; 267: 12528-38.
Alban S. From Heparins to factor Xa inhibitors and beyond. Eur J Clin Invest. 2005; 35 (suppl.1):12-20.
Fareed J, Walenga JM, Hoppensteadt D, Racanelli A, Coyne E. Chemical and biochemical heterogeneity in low molecular weight heparins: implications for clinical use and standardization. Semin Thromb Hemost. 1989;15:440- 63.
Hirsh J. Heparin. N Eng J Med. 1991;324: 1565-1574.
Bjornsson TO, Wolfram BS, Kitchell BB. Heparin Kinetics determined by three assay methods. Clin Pharmacol Ther 1982; 31: 104-113.
de Swart CA, Nijmeyer B, Roelofs JM, Sixma JJ. Kinetics of intravenously administered heparin in normal humans. Blood 1982; 60: 1251-8.
Buller H, Agnelli G, Hull RD, Hyers T. Antithrombotic Therapy for Venous Thromboembolic Disease. The Seventh ACCP Conference on Antithrombotic and Trombolytic Therapy. CHEST 2004;126: 401-428.
Hull RD, Raskob GE, Rosenbloom D, et al. Optimal therapeutic level of heparin therapy in patients with venous thrombosis. Arch Intern Med. 1992; 152: 1589-1595.
Braunwald E, Antman EM, Beasley JW et al. ACC/AHA guidelines for the management of patients with unstable angina and non-ST-segment elevation myocardial infarction. A report of the American College of Cardiology/American. Heart Association Task Force on Practice Guidelines (Committee on the Management of Patients With Unstable Angina). J Am Coll Cardiol. 2000; 36: 970-1062.
de Werf F, Ardissino D, Betriu A, et al. Management of acute myocardial infarction in patients presenting with ST- segment elevation. The Task Force on the Management of Acute Myocardial Infarction of the European Society of Cardiology. Eur Heart J. 2003; 24: 28-66.
Ayala T, Schulman S. Pathogenesis and Early Management of Non-ST-segment Elevation Acute Coronary Syndromes. Cardiol Clin. 2006; 24: 19-35.
Braunwald E. Unstable angina: an etiologic approach to management. Circulation. 1998; 98: 2219-22.
Davies M. The pathophysiology of acute coronary syndromes. Heart. 2000; 83: 361-66.
Stary HC, Chandler AB, Glagov S, et al. A definition of initial, fatty streak, and intermediate lesions of atherosclerosis. Circulation. 1994; 89 :2462-78.
Glagov S, Weisenberg E, Zarins CK, et al. Compensatory enlargement of human atherosclerotic coronary arteries. N Eng J Med. 1987;316: 1371-1375.
Davies M. Stability and instability: two faces of coronary atherosclerosis. The Paul Dudley White Lecture 1995. Circulation. 1996; 94: 2013-20.
Kolodgie FD, Virmani R, Burke AP, et al. Pathologic assessment of the vulnerable human coronary plaque. Heart. 2004; 90:1385-91.
Davies MJ, Thomas A. Thrombosis and acute coronary artery lesions in sudden cardiac ischemic death. N Engl J Med. 1984; 310: 1137-40.
Galis ZS, Sukhova GK, Lark MW, et al. Increased expression of matrix metalloproteinases and matrix degrading activity in vulnerable regions of human atherosclerotic plaques. J Clin Invest. 1994; 94: 2493-503.
Sukhova GK, Shi GP, Simon DI, et al. Expression of the elastolytic cathepsins S and K in human atheroma and regulation of their production in smooth muscle cells. J Clin Invest. 1998;102: 576-83.
Rioufol G, Finet G, Ginon I, et al. Multiple atherosclerotic plaque rupture in acute coronary syndrome: a three-vessel intravascular ultrasound study. Circulation. 2002; 106: 804-8.
Lee RT, Schoen FJ, Loree HM, et al. Circumferential stress and matrix metalloproteinase 1 in human coronary atherosclerosis. Implications for plaque rupture. Arterioscler Thromb Vasc Biol. 1996; 16:1070-3.
Richardson PD, Davies MJ, Born GV. Influence of plaque configuration and stress distribution on fissuring of coronary atherosclerotic plaques. Lancet. 1989; 2: 941-4.
Arbustini E, Dal Bello P, Morbini P, et al. Plaque erosion is a major substrate for coronary thrombosis in acute myocardial infarction. Heart. 1999; 82:269-72.
Fuster V, Fayad Z, Badimon J. Acute coronary syndromes: biology. Lancet. 1999; 353: 5-9.
Kroll MH, Hellums JD, McIntyre LV, et al. Platelets and shear stress. Blood. 1996; 88:1525-41.
Zimarino M, De Caterina R. Glycoprotein IIb-IIIa Antagonists in Non-ST Elevation Acute Coronary Syndromes and Percutaneous Interventions: from Pharmacology to Individual Patient´s Therapy Part 1: The Evidence of Benefit. J Cardiovasc Pharmacol. 2004; 43: 325-332.
Mallat Z, Hugel B, Ohan J, et al. Shed membrane microparticles with procoagulant potential in human atherosclerotic plaques: a role for apoptosis in plaque thrombogenicity. Circulation. 1999; 99:348-53.
Nemerson Y. Tissue factor and hemostasis. Blood. 1988; 71:1-8.
Osende JI, Badimon JJ, Fuster V, et al. Thrombogenicity in type 2 diabetes mellitus patients is associated with glycemic control. J Am Coll Cardiol. 2001; 38:1307-12.
Narkiewicz K, van de Borne PJ, Hausber M, et al. Cigarette smoking increases sympathetic outflow in humans. Circulation. 1998; 98:528-34.
Cortes D, O´Rourke RA. Current approaches to patients with acute coronary syndromes. Curr Probl Cardiol. 2002; 27:145-184.
Bertrand M, Maarten L, Keith A, Lars C. Management of acute coronary syndromes in patients presenting without persistent ST-segment elevation. The Task Force on the Management of Acute Coronary Syndromes of the European Society of Cardiology. Eur Heart J. 2002; 23: 1809-1840
Oler A, Whooley MA, Oler J, Grady D. Adding heparin to aspirin reduces the incidence of myocardial infarction and death in patients with unstable angina. A meta-analysis. JAMA. 1996; 276: 811-15.
Telford AM, Wilson C. Trial of heparin versus atenolol in prevention of myocardial infarction in intermediate coronary syndrome. Lancet. 1981;1(8232):1225-8.
Theroux P; Ouimet H; McCans J; Latour JG; et al. Aspirin, heparin, or both to treat acute unstable angina. N Engl J Med. 1988; 319:1105-11.
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: 827-30.
Neri Serneri GG; Gensini GF; Poggesi L, et al. Effect of heparin, aspirin, or alteplase in reduction of myocardial ischaemia in refractory unstable angina. Lancet. 1990;335: 615-8.
Becker RC; Cannon CP; Tracy RP, et al. Relation between systemic anticoagulation as determined by activated partial thromboplastin time and heparin measurements and in-hospital clinical events in unstable angina and non-Q wave myocardiaL infarction. Thrombolysis in Myocardial Ischemia III B Investigators. Am Heart J. 1996;131:421-33.
Bijsterveld NR; Moons AH; Meijers JC. Rebound thrombin generation after heparin therapy in unstable angina. A randomized comparison between unfractionated and low-molecular-weight heparin. J Am Coll Cardiol. 2002; 39:811-7.
Harrington R, Becker R, Ezekowitz M, et al. Antithrombotic Therapy for Coronary Artery Disease. The Seventh ACCP Conference on Antithrombotic and Trombolytic Therapy. CHEST. 2004;126: 513-548.
Eisenberg PR. Role of heparin in coronary thrombolysis. CHEST. 1992;1 (suppl):131-139.
Mitchell, JRA. Anticoagulation in coronary artery disease: Retrospect and prospect. Lancet. 1981; 1:257.
Second International Study of Infarct Survival Collaborative Group. Randomised trial of intravenous streptokinase, oral aspirin, both, or neither among 17,187 cases of suspected acute myocardial infarction: ISIS-2. Lancet. 1988; 2:349-60.
Krumholz HM; Hennen J; Ridker PM, et al. Use and effectiveness of intravenous heparin therapy for treatment of acute myocardial infarction in the elderly. J Am Coll Cardiol. 1998;31:973-9.
The GUSTO Angiographic Investigators. The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. N Engl J Med. 1993; 329:1615-22.
O´Connor CM, Meese R, Carney R, Smith J, et al. A randomized trial of intravenous heparin in conjunction with anistreplase (anisoylated plasminogen streptokinase activator complex) in acute myocardial infarction: the Duke University Clinical Cardiology Study (DUCCS) 1. J Am Coll Cardiol. 1994; 23:11-8
Gruppo Italiano per lo Studio della Sopravvivenza nell´Infarto Miocardico.GISSI-2: a factorial randomised trial of alteplase versus streptokinase and heparin versus no heparin among 12,490 patients with acute myocardial infarction. Lancet. 1990; 336: 65-71.
Third International Study of Infarct Survival Collaborative Group.ISIS-3: a randomised comparison of streptokinase vs tissue plasminogen activator vs anistreplase and of aspirin plus heparin vs aspirin alone among 41,299 cases of suspected acute myocardial infarction. Lancet. 1992; 339:753-70.
de Bono DP, Simoons ML, Tijssen J, et al. Effect of early intravenous heparin on coronary patency, infarct size, and bleeding complications after alteplase thrombolysis: results of a randomised double blind European Cooperative Study Group trial. Br Heart J. 1992; 67:122-8.
Menon V, Harrington R, Hochman J, et al. Thrombolysis and Adjunctive Therapy in Acute Myocardial Infarction. The Seventh ACCP Conference on Antithrombotic and Trombolytic Therapy. CHEST. 2004;126: 549-575.
The Global Use of Strategies to Open Occluded Coronary Arteries (GUSTO) IIa Investigators. Randomized trial of intravenous heparin versus recombinant hirudin for acute coronary syndromes. Circulation. 1994; 90:1631-7.
Antman EM. Hirudin in acute myocardial infarction. Safety report from the Thrombolysis and Thrombin Inhibition in Myocardial Infarction (TIMI) 9A Trial. Circulation. 1994; 90:1624-30.
Bowers J, Ferguson J. The use of activated clotting times to monitor heparin therapy during and after interventional procedures. Clin Cardiol. 1994. 17: 357-361.
Narins CR, Hillegass WB, Nelson CL, et al. Relation Between Activated Clotting Time During Angioplasty and Abrupt Closure. Circulation 1996; 93: 667 - 671.
Popma JJ, Berger P, Ohman EM, et al. Antithrombotic therapy During Percutaneous Coronary Intervention. The Seventh ACCP Conference on Antithrombotic and Trombolytic Therapy. CHEST. 2004;126: 576-599
Ellis S, Roubin G, Wilentz J, et al. Effect of 18- to 24- hour heparin administration for prevention of restenosis after uncomplicated coronary angioplasty. Am Heart J. 1989; 117: 777-782
Turpie AGG, Robinson JG, Doyle DJ, et al. Comparison of high-dose with low-dose subcutaneous heparin to prevent left ventricular mural thrombosis in patients with acute transmural anterior myocardial infarction. N Engl J Med. 1989; 320:352-357
Kroon C, ten Hove WR, de Boer A, et al. Highly variable anticoagulant response after subcutaneous administration of high-dose (12,500 IU) heparin in patients with myocardial infarction and healthy volunteers. Circulation. 1992; 86:1370-5
Violaris AG, Trudgill NJ, Rowlands L, et al. Variable and circadian response to a fixed high-dose (12 500 IU twice daily) subcutaneous heparin regimen after thrombolytic therapy for acute myocardial infarction. Coron Artery Dis. 1994; 5:257-65.
Goldhaber S. Conjunctive Heparin Therapy Limitations of Subcutaneous Administration. Circulation. 1992; 86: 1639-41.
The SCATI (Studio sulla Calciparina nell´Angina e nella Trombosi Ventricolare nell´Infarto) Group: Randomised controlled trial of subcutaneous calcium-heparin in acute myocardial infarction. Lancet. 1989; 2: 182-186.
Prandoni P, Bagatella P, Bernardi E, et al. Use of an Algorithm for administering subcutaneous heparin in the treatment of deep venous thrombosis. Ann Intern Med. 1998; 129: 299-302
Prandoni P, Carnovali M, Marchiori A. Subcutaneous Adjusted-Dose unfractionated heparin vs Fixed-Dose low -molecular -weight heparin in the initial treatment of venous thromboembolism. Arch Intern Med. 2004; 164: 1077-1083.
Anand S, Ginsberg JS, Kearon C, et al. The relation between the activated partial thromboplastin time response and recurrence in patients with venous thrombosis treated with continuous intravenous heparin. Arch Intern Med. 1996; 156: 1677-1681.
Anand S, Bates S, Ginsberg JS, et al. Recurrent venous thrombosis and heparin therapy. An evaluation of the importance of early activated partial thromboplastin times. Arch Intern Med.1999; 159: 2029-2032.
Klearon C, Johnston M, Moffat K, et al. Effect of warfarin on activated partial thromboplastin time in patients receiving heparin. Arch Intern Med. 1998; 158: 1140-3.
Klearon C, Ginsberg JS, Julian J, et al. Comparison of fixed-dose weight-adjusted unfractionated heparin and low-molecular-weight heparin for acute treatment of venous thromboembolism. JAMA. 2006; 296: 935-942
Carson J. Subcutaneous unfractionated heparin vs low - molecular - weight heparin for acute thromboembolic disease. Issues of efficacy and cost. JAMA. 2006; 296: 991-3
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