title: Intracoronary thrombolysis in acute myocardial infarction: experimental background and clinical experience.
abstract: Occlusive intracoronary (IC) thrombosis was produced experimentally in dogs by placement of a copper coil. The thrombus was consistently lysed by application of Thrombolysin (streptokinase and plasminogen) at the site of occlusion, 1 to 6 hours after thrombosis. Thrombolysin has no toxic effect on the coronary artery wall or the myocardium. Reperfusion after 30 to 60 minutes of occlusion frequently resulted in ventricular fibrillation, but gradual reperfusion reduced the probability of ventricular fibrillation. Intramyocardial bleeding was noted after reperfusion in areas of advanced necrosis and was shown to be the consequence, rather than the cause, of necrosis. The reperfused myocardium remained hypocontractile, but in contrast to the occlusion period, its mechanical function could be enhanced by inotropic stimulation. After experimental studies confirmed the feasibility and safety of IC thrombolysis, the technique was applied within 3 hours of onset of pain in 29 patients with evolving acute myocardial infarction (AMI) and showing ST elevations without pathologic Q waves. Nitroglycerin (NTG), 0.1 mg, was injected into the occluded coronary artery to rule out spasm; NTG failed to open the occluded artery. A special, very flexible, radiopaque No. 2 French catheter was advanced through the angiography catheter to the site of occlusion. Thrombolysin was infused at a rate of 4000 to 6000 IU/min until patency was achieved, followed by 2000 IU/min for 60 minutes. Lysis of clot was achieved in 27 of 29 patients. The single death (unrelated to the procedure) occurred subsequently in a patient in whom the artery was not reopened. After successful thrombolysis, 12 patients underwent elective coronary bypass surgery because of multiple stenoses. The need for early reperfusion is emphasized for effective IC thrombolysis therapy in evolving AMI.
mesh_terms: D000818:Animals; D001145:Arrhythmias, Cardiac / Q000209:etiology; D003402:Creatine Kinase / Q000378:metabolism; D004285:Dogs; D004562:Electrocardiography; D009203:Myocardial Infarction / Q000188:drug therapy / Q000503:physiopathology*; D009204:Myocardial Revascularization; D009336:Necrosis / Q000378:metabolism; D010958:Plasminogen / Q000627:therapeutic use*; D013300:Streptokinase / Q000627:therapeutic use*; D013997:Time Factors
chemical_list: D010958:Plasminogen; D003402:Creatine Kinase; D013300:Streptokinase