Abstract
The influence of tissue plasminogen activator (tPA) and heparin versus heparin alone on anatomic characteristics of patent infarct-related coronary arteries and the development of these angiographic descriptors in coronary arteries that remain patent during the hospital course was examined in 108 patients who participated in a placebo-controlled trial of recombinant tissue-type plasminogen activator in acute myocardial infarc tion. Coronary angiography was performed 18 ± 6 hours after treatment in 47 patients (group A) and at 10 days in 61 patients (group B). Quantitative coronary angiography of the infarct-related lesion was performed, and luminal irregularity was quantitated with an ulceration index. Of the 47 patients in group A, 7 (29%) treated with placebo had Thrombolysis in Myocardial Infarction grade 2 or 3 perfusion, whereas 18 (78%) treated with t-PA had grade 2 or 3 (p <0.001); there was no difference between patients who had grade 2 or 3 perfusion in group B (placebo 59% vs t-PA 75%). In group A, at 10 days, the luminal area of the infarct artery had increased from 0.59 ± 0.11 to 0.9 ± 0.24 mm2 and from 0.75 ± 0.16 to 1.31 ± 0.39 mm2 for placebo- and t-PA-treated patients, respectively (p <0.04). There was no change in the ulcerative index over time in either placebo- or t-PA-treated patients. It is concluded that early after infarction, t-PA produces marked and rapid improvement in overall patency as compared with heparin, although this difference was attenuated at 10 days because of spontaneous recanalization in the placebo group. Future studies of thrombolytic agents should consider the substantial improvement in luminal area of patients receiving heparin alone.
Original language | English (US) |
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Pages (from-to) | 379-383 |
Number of pages | 5 |
Journal | The American Journal of Cardiology |
Volume | 72 |
Issue number | 5 |
DOIs | |
State | Published - Aug 15 1993 |
Bibliographical note
Funding Information:From St. Michael’s Hospital; the Western and General Divisions, The Toronto Hospital; Sunnybrook Health Science Centre; and University of Toronto, Toronto, Ontario, Canada; the Cardiovascular Division, Department of Medicine, University of Minnesota, Minneapolis, Minnesota; and the Department of Clinical Epidemiology and Biostatistics, Faculty of Health Sciences, McMaster University, Hamilton, Ontario, Canada. This study was supported by Burroughs Wellcome Co., Research Triangle Park, North Carolina. Manuscript received January 19, 1993; revised manuscript received March 17, 1993, and accepted March 18.