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Frequency of low-grade residual coronary stenosis after thrombolysis during acute myocardial infarction

  • James C. Marshall
    Correspondence
    Address for reprints: James C. Marshall, DO, Presbyterian Medical Center, Philadelphia Heart Institute, 39th and Market Streets, Philadelphia, Pennsylvania 19104.
    Affiliations
    From the Division of Cardiology, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA

    From the Robert Wood Johnson Medical School, Camden, New Jersey, USA
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  • Harvey L. Waxman
    Affiliations
    From the Division of Cardiology, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA

    From the Robert Wood Johnson Medical School, Camden, New Jersey, USA
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  • Anthony Sauerwein
    Affiliations
    From the Division of Cardiology, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA

    From the Robert Wood Johnson Medical School, Camden, New Jersey, USA
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  • Ian Gilchrist
    Affiliations
    From the Division of Cardiology, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA

    From the Robert Wood Johnson Medical School, Camden, New Jersey, USA
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  • Peter B. Kurnik
    Affiliations
    From the Division of Cardiology, Cooper Hospital/University Medical Center, University of Medicine and Dentistry of New Jersey, Camden, New Jersey, USA

    From the Robert Wood Johnson Medical School, Camden, New Jersey, USA
    Search for articles by this author
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      Abstract

      The clinical, angiographic and demographic characteristics of 42 patients with low-grade (<50%) residual stenosis at the infarct lesion after thrombolysis for acute myocardial infarction (MI) were assessed. The study group (group I) represented 21% of 198 consecutive patients receiving thrombolytic therapy over a 59-month period. Data on the 156 remaining patients were pooled for comparison (group II). Group I patients were predominantly men (86%) who were cigarette smokers (81%). Group II patients were predominantly men (75%, p > 0.10) but were significantly older (52 ± 12 vs 56 ± 10 years, p = 0.02). Prior acute MI or angina was unusual in group I. Sixty percent had no significant (>50%) residual coronary artery disease while 25% had residual single artery disease. Average significant (>50% diameter stenosis) residual vessel disease was 0.6 ± 1.0 for group I and 1.9 ± 0.9 for group II (p < 0.001). In group I, average residual infarct lesion diameter stenosis was 36 ± 7% in the right anterior oblique and 34 ± 8% in the left anterior oblique views. Thirty-nine group I patients were discharged with medical therapy and 100% follow-up was obtained over a mean interval of 18 ± 17 months. Fifteen patients experienced chest pain after acute MI accounting for 17 discrete events. Fifty-nine percent of group I had a benign course on follow-up. Eight events were classified as unstable angina, 4 as acute MI and 5 as atypical angina. Documented coronary vasospasm occurred in 3. The infarct narrowing accounted for 58% of documented ischemia and 41% of symptomatic events. Antiplatelet agents, warfarin and residual lesion morphology did not clearly influence frequency of events, whereas data regarding cigarette smoking were suggestive (p = 0.06). Events clearly associated with the infarct narrowing occurred earlier (4 ± 4 months) than events not related to (23 ± 15 months, p < 0.01). Ischemic events unrelated to the infarct lesion were often related to progressive stenosis or occlusion at the site of previously nonsignificant disease.
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