(Circulation. 1999;99:2714-2716.)
© 1999 American Heart Association, Inc.
Editorial |
From the Cardiology Division, University of Washington and Veterans Affairs Medical Center, Seattle, Wash.
Correspondence to J. Ward Kennedy, MD, Cardiology Division (111C), VA Medical Center, 1660 S Columbian Way, Seattle, WA 98108.
Key Words: Editorials angioplasty thrombolysis myocardial infarction
The management of acute myocardial infarction (AMI) was altered dramatically with the introduction of intracoronary thrombolytic therapy in the late l970s by Rentrop and others.1 The visualization of coronary artery occlusion by angiography performed during the first few hours of AMI and the removal of some of these thrombi at the time of emergent coronary artery bypass surgery convinced the medical community that AMI was, as was thought years earlier, due to "coronary thrombosis." After the publication of a number of randomized clinical trials (RCTs) of intracoronary and intravenous lytic therapy, reperfusion of acutely occluded coronary artery beds with thrombolytic therapy became a standard treatment of AMI by the mid-1980s.2
While thrombolytic therapy was gaining early
acceptance as a means to achieve reperfusion, a parallel
pathway for achieving reperfusion was developing with catheter-based
techniques. Reports of PTCA for the management of AMI appeared in
1983.3 Soon a vigorous competition developed between
pharmacological and mechanical methods of reperfusion. Important
differences between these 2 competing approaches were apparent.
Thrombolytic therapy could be initiated rapidly once the
diagnosis was made, with treatment instituted in the emergency
department or even before hospitalization,4 and it did not
require the technical skills of a proceduralist for its implementation.
However, because reperfusion did not occur until 60 to 90
minutes after the onset of treatment, the occurrence of successful
reperfusion (or its failure) could not be ascertained with certainty by
use of clinical markers, and there was an obligatory risk of
intracranial hemorrhage (ICH) of 0.5% to
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