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• W2013333586 abstract "During the years (1955–1968) that I spent in the intramural program of the National Heart, Lung and Blood Institute (NHLBI), one of my major research goals was to elucidate the physiological determinants of myocardial oxygen consumption [1Braunwald E. 13th Bowditch Lecture. The determinants of myocardial oxygen consumption.Physiologist. 1969; 12: 65-93PubMed Google Scholar, 2Braunwald E. Covell J.W. Maroko P.R. Ross J, J.r. Effect of drugs and of counterpulsation on myocardial oxygen consumption.Circulation. 1969; 40: 220-8Crossref Google Scholar]. This work led naturally to thinking about how an understanding of these determinants could be used to improve the imbalance between myocardial oxygen supply and demand in myocardial ischemia; this imbalance is most extreme in acute myocardial infarction (AMI). Since the survival of patients with this condition is greatly dependent on the size of the infarct [2Braunwald E. Covell J.W. Maroko P.R. Ross J, J.r. Effect of drugs and of counterpulsation on myocardial oxygen consumption.Circulation. 1969; 40: 220-8Crossref Google Scholar], my colleagues and I wondered whether clinical outcome might be improved if the imbalance between myocardial oxygen supply and demand in evolving AMI were corrected before there was widespread, irreversible ischemic damage. In 1968, together with a talented research fellow, the late Peter Maroko, and the NHLBI team (John Ross, Burton Sobel, and James Covell), now transplanted to the University of California, San Diego, we began experiments in anesthetized dogs that showed that ischemic damage could indeed be modified [2Braunwald E. Covell J.W. Maroko P.R. Ross J, J.r. Effect of drugs and of counterpulsation on myocardial oxygen consumption.Circulation. 1969; 40: 220-8Crossref Google Scholar, 3Maroko P.R. Kjekshus J.K. Sobel B.E. Watanabe T. Covell J.W. Ross J, J.r. Braunwald E. Factors influencing infarct size following coronary artery occlusion.Circulation. 1971; 43: 67-82Crossref PubMed Google Scholar]. Interventions that we had shown previously to reduce myocardial oxygen demand, such as beta adrenergic blockade and lowering of ventricular afterload, reduced myocardial ischemic damage while interventions that increase oxygen demand, such as beta adrenergic stimulation or tachycardia or those that reduce collateral blood flow, expanded this damage [3Maroko P.R. Kjekshus J.K. Sobel B.E. Watanabe T. Covell J.W. Ross J, J.r. Braunwald E. Factors influencing infarct size following coronary artery occlusion.Circulation. 1971; 43: 67-82Crossref PubMed Google Scholar]. The most potent salutary intervention was early reperfusion [4Ginks W.R. Sybers P.R. Maroko P.R. Covell J.W. Sobel B.E. Ross Jr, J. Coronary artery reperfusion. II. Reduction of myocardial infarct size at one week after the coronary occlusion.J Clin Invest. 1972; 51: 2717-23Crossref PubMed Google Scholar, 5Maroko P.R. Braunwald E. Modification of myocardial infarct size after coronary occlusion.Ann Intern Med. 1973; 79: 720-33Crossref PubMed Google Scholar]. Actually, three decades earlier, Blumgart et al. [6Blumgart H.L. Gilligan D.R. Schlesinger M.J. Experimental studies on the effect of temporary occlusion of coronary arteries.Am Heart J. 1941; 22: 374-89Crossref Google Scholar] had shown in the dog that short (<20 min) occlusions of a coronary artery did not lead to myocardial infarction (MI). In 1933, Tillet and Garner [7Tillet W. Garner R. The fibrinolytic activity of hemolytic streptococci.J Exp Med. 1933; 58: 485-502Crossref PubMed Google Scholar, 8Maroo A. Topol E.J. The early history and development of thrombolysis in acute myocardial infarction.J Thromb Haemost. 2004; 2: 1867-70Abstract Full Text Full Text PDF PubMed Scopus (12) Google Scholar] isolated a fibrinolytic substance from the beta hemolytic streptococcus; it was later named streptokinase. In 1950, when I was a student at New York University School of Medicine and Bellevue Hospital, Tillet was chairman of medicine and I first learned about streptokinase from him. I observed Tillet and his co‐worker, Sherry, administer streptokinase for the lysis of fibrinous pleural adhesions in patients with empyema [9Tillet W. Sherry S. Read C. The use of streptokinase‐streptodornase in the treatment of chronic empyema.J Thorac Surg. 1951; 21: 325-41Abstract Full Text PDF PubMed Google Scholar]. After further purification of streptokinase, it seemed logical to study this agent in patients with AMI, and Sherry et al. [10Sherry S. Fletcher A. Alkjaersigm N. Smyrniotis F. An approach to intravascular fibrinolysis in man.Trans Assoc Am Physicians. 1957; 70: 288-96PubMed Google Scholar] subsequently infused streptokinase intravenously into patients with this condition. In the late 1970s, Chazov [11Chazov E.I. Matveeva L.S. Mazaev A.V. Sargin K.E. Sadovskaia G.V. Ruda M.I. Intracoronary administration of fibrinolysin in acute infarction [in Russian].Terapeuticheskii Arkhiv. 1976; 8: 48Google Scholar] and Rentrop and their associates [12Rentrop P. Blanke H. Karsch K.R. Kaiser H. Kostering H. Leitz K. Selective intracoronary thrombolysis in acute myocardial infarction and unstable angina pectoris.Circulation. 1981; 63: 307-17Crossref PubMed Google Scholar] used coronary angiography to show that the intracoronary administration of streptokinase caused lysis of coronary thrombi in patients with AMI. Thus, two important concepts, the use of a plasminogen activator to lyse coronary thrombi and the desirability of limiting the extent of infarction, came together. My colleagues and I, now working at Harvard Medical School, showed in 1981 that intracoronary streptokinase indeed salvaged ischemic myocardium in patients with evolving MI [13Markis J.E. Malagold M. Parker J.A. Silverman K.J. Barry W.H. Als A.V. Paulin S. Grossman W. Braunwald E. Myocardial salvage after intracoronary thrombolysis with streptokinase in acute myocardial infarction: assessment of intracoronary thallium‐201.N Engl J Med. 1981; 305: 777-82Crossref PubMed Google Scholar]. The GISSI investigators then conducted the first megatrial of fibrinolytic therapy and in 1986 established clearly that the intravenous administration of streptokinase early in the course of AMI reduced the mortality [14Gruppo Italiano per lo Studio della Steptochinasi nell'Infarto Miocardico (GISSI)Effectiveness of intravenous thrombolytic treatment in acute myocardial infarction.Lancet. 1986; 1: 397-402PubMed Google Scholar], thereby establishing lytic therapy as a cornerstone of clinical management. The TIMI (Thrombolysis in Myocardial Infarction) Study Group was born in 1984, and, in the first trial conducted by this group, demonstrated the superiority of the direct plasminogen activator, tPA, over the indirect activator, streptokinase, in restoring patency of occluded coronary arteries. [15The TIMI Study GroupThe thrombolysis in myocardial infarction (TIMI) trial. Phase I findings.N Engl J Med. 1985; 312: 932-6Crossref PubMed Google Scholar] This observation led to the ‘open artery hypothesis,’ which posits that an open infarct‐related artery is beneficial post‐AMI, irrespective of how opening is achieved [16Braunwald E. Myocardial reperfusion, limitation of infarct size, reduction of left ventricular dysfunction, and improved survival. Should the paradigm be expanded.Circulation. 1989; 79: 441-4Crossref PubMed Scopus (0) Google Scholar, 17Kim C.B. Braunwald E. Potential benefits of late reperfusion of infarcted myocardium: the open artery hypothesis.Circulation. 1993; 88: 2426-36Crossref PubMed Google Scholar, 18Lamas G.A. Flaker G.C. Mitchell G. Smith S.C. Gersh B.J. Wun C.‐.C. Moye Rouleau J.L. Rutherford J.D. Pfeffer M.A. Braunwald E. for the Survival and Ventricular Enlargement InvestigatorsEffect of infarct artery patency on prognosis after acute myocardial infarction.Circulation. 1995; 92: 1101-9Crossref PubMed Google Scholar]. Subsequently, the GUSTO 1 megatrial demonstrated that this improved coronary patency translated into a further reduction of mortality from that achieved by streptokinase [19The GUSTO investigatorsAn international randomized trial comparing four thrombolytic strategies for acute myocardial infarction.N Engl J Med. 1993; 329: 673-82Crossref PubMed Scopus (3658) Google Scholar]. Subsequent TIMI trials, conducted with Carolyn McCabe, my collaborator for 22 years, and the Harvard‐Brigham team, which includes Elliott Antman and Christopher Cannon, defined the pharmacologic properties of the bolus fibrinolytic agent tenecteplase in patients with AMI [20Cannon C.P. Gibson C.M. McCabe C.H. Adgey J. Schweiger M.J. Sequeira R.F. Grollier G. Giugliano R.P. Frey M. Mueller H.S. Stengart R.M. Weaver W.D. Van de Werf F. Braunwald E. for the TIMI 10B investigatorsTNK‐tissue plasminogen activator compared with front‐loaded alteplase in acute myocardial infarction: results of the TIMI 10B trial.Circulation. 1998; 98: 205-14Crossref Scopus (327) Google Scholar]; tenecteplase is now the most widely used fibrin‐specific lytic. The TIMI group also showed that the administration of another bolus plasminogen activator, retavase, to patients with AMI while in the ambulance resulted in earlier myocardial reperfusion than when administered after arrival in the hospital [21Morrow D.A. Antman E.M. Sayah A. Schuhwerk K.C. Giugliano R.P. De Lemos J.A. Waller M. Cohen S.A. Rosenberg D.G. Cutler S.S. McCabe C.H. Walls R.M. Braunwald E. on behalf of the Early Retavase‐Thrombolysis in Myocardial Infarction (ER‐TIMI) 19 InvestigatorsEvaluation of the time saved by prehospital initiation of reteplase for ST‐elevation MI: results of the Early Retevase (ER)‐TIMI 19 trial.J Am Coll Cardiol. 2002; 40: 71-7Crossref PubMed Scopus (0) Google Scholar] supporting of the concept that in patients with evolving MI ‘time is muscle’. More recently, the TIMI group has demonstrated that the addition of the thienopyridine clopidogrel to aspirin improves coronary patency and clinical outcome in AMI patients treated with both direct and indirect plasminogen activators [22Sabatine M.S. Cannon C.P. Gibson C.M. Lopez‐Sendon J.L. Montalescot G. Theroux P. Lewis B.S. Murphy S.A. McCabe C.H. Braunwald E. Effect of clopidogrel pretreatment before percutaneous coronary intervention in patients with ST‐elevation myocardial infarction treated with fibrinolysis: the PCI‐CLARITY study.JAMA. 2005; 294: 1224-32Crossref PubMed Scopus (0) Google Scholar]. Also, we have obtained evidence that the low‐molecular‐weight heparin, enoxaparin, with its balanced anti‐Xa and ‐IIa activities, is superior to unfractionated heparin in maintaining coronary patency following the fibrinolysis [23Antman E.M. Louwerenburg H.W. Baars H.F. Wesdorp J.C.L. Hamer B. Bassand J.P. Bigonzi F. Pisapia G. Gibson C.M. Heidbuchel H. Braunwald E. Van de Werf F. Enoxaparin as adjunctive antithrombin therapy for ST‐elevation myocardial infarction: results of the ENTIRE‐TIMI 23 trial.Circulation. 2002; 105: 1642-9Crossref PubMed Scopus (0) Google Scholar]. We shall soon learn from the EXTRACT‐TIMI 25 trial, involving more than 25 000 patients, whether use of this agent translates into further clinical benefit [24Antman E.M. Morrow D.A. McCabe C.H. Jiang F. White H.D. Fox K.A.A. Sharma D. Chew P. Braunwald E. Enoxaparin versus unfractionated heparin as antithrombin therapy in patients receiving fibrinolysis for ST‐elevation myocardial infarction: design and rationale for the enoxaparin and thrombolysis reperfusion for acute myocardial infarction treatment – thrombolysis in myocardial infarction study 25 (ExTRACT‐TIMI 25).Am Heart J. 2005; 149: 217-26Crossref PubMed Scopus (0) Google Scholar]. It has been, and continues to be, an exhilarating experience to participate in efforts to use fibrinolytic, antiplatelet, and antithrombin agents to limit infarct size and thereby improve the outcome of patients with an AMI, which remains the most common cause of death in the Western world." @default.
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• W2013333586 title "Personal reflections on fibrinolytic therapy of acute myocardial infarction" @default.
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