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Sabol MB, Luippold RS, Hebert J, et al. Association Between Serial Measures of Systemic Blood Pressure and Early Coronary Arterial Perfusion Status Following Intravenous Thrombolytic Therapy. J Thromb Thrombolysis. 1994;1(1):79-84doi: 10.1007/BF01062000.
Sabol, M. B., Luippold, R. S., Hebert, J., Ball, S. P., Corrao, J. M., & Becker, R. C. (1994). Association Between Serial Measures of Systemic Blood Pressure and Early Coronary Arterial Perfusion Status Following Intravenous Thrombolytic Therapy. Journal of thrombosis and thrombolysis, 1(1), 79-84. https://doi.org/10.1007/BF01062000
Sabol, et al. "Association Between Serial Measures of Systemic Blood Pressure and Early Coronary Arterial Perfusion Status Following Intravenous Thrombolytic Therapy." Journal of thrombosis and thrombolysis vol. 1,1 (1994): 79-84. doi: https://doi.org/10.1007/BF01062000
Sabol MB, Luippold RS, Hebert J, Ball SP, Corrao JM, Becker RC. Association Between Serial Measures of Systemic Blood Pressure and Early Coronary Arterial Perfusion Status Following Intravenous Thrombolytic Therapy. J Thromb Thrombolysis. 1994;1(1):79-84. doi: 10.1007/BF01062000. PMID: 10603516.
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J Thromb Thrombolysis. 1994;1(1):79-84. doi: 10.1007/BF01062000.

Association Between Serial Measures of Systemic Blood Pressure and Early Coronary Arterial Perfusion Status Following Intravenous Thrombolytic Therapy.

Journal of thrombosis and thrombolysis

Sabol, Luippold, Hebert, Ball, Corrao, Becker

Affiliations

  1. Department of Internal Medicine, University of Massachusetts Medical School, Worcester, Massachusetts.

PMID: 10603516 DOI: 10.1007/BF01062000

Abstract

Background: Systemic hypotension, at times transient while in other instances more prolonged, is common among patients with myocardial infarction (MI). It also is a characteristic feature for patients experiencing either advanced congestive heart failure or cardiogenic shock. In this group of patients, thrombolytic therapy has failed to exert. favorable impact on their high in-hospital mortality. Although it has been postulated that the success of thrombolytic therapy is directly linked to systemic blood pressure' there is little information available in human subjects. Methods and Results: In a University of Massachusetts Thrombolysis Data Bank Study, 127 patients with MI who were given intravenous thrombolytic therapy (tPA or streptokinase) within 6 hours from symptom onset (4.2 +/- 1.5 hours) had serial systemic blood pressure measurements (at the time of hospital arrival, treatment initiation, and every 30 minutes during the thrombolytic infusion) and underwent coronary angiography within 120 minutes of treatment initiation. All patients received intravenous heparin and oral aspirin. By univariate analysis, disastolic blood pressure below 80 mmHg at the time of treatment initiation was associated with a reduced angiographic coronary perfusion grade [Thrombolysis in Myocardial Infarction (TIMI) flow grade; p + 0.02]. A correlation analysis of tPA-treated patients indicated that a greater maximum change in diastolic blood pressure during treatment correlated inversely with coronary perfusion (r +.24, p < 0.05). By multivariate regression analysis, however, only shorter time to treatment (p + 0.001) and thrombolysis with tPA (p + 0.02) were independent predictors of coronary arterial perfusion grade. Conclusion: Systemic blood pressure (and presumably proximal coronary arterial perfusion pressure) in the ranges investigated in this study is not an independent predictor of coronary reperfusion following intravenous thrombolytic therapy with either tPA or streptokinase. It seems likely, therefore, that properties intrinsic to the ruptured plaque and occlusive thrombus, and potentially the local metabolic environment, either alone or acting synergistically with perfusion pressure, are determinants of thrombolytic success. Further investigation of factors influencing the efficacy of thrombolysis should be undertaken.

References

  1. Am J Cardiol. 1967 Oct;20(4):457-64 - PubMed
  2. Chest. 1991 Mar;99(3):708-14 - PubMed
  3. Circulation. 1981 Mar;63(3):489-97 - PubMed
  4. Lancet. 1990 Jul 14;336(8707):71-5 - PubMed
  5. J Am Coll Cardiol. 1986 Apr;7(4):717-28 - PubMed
  6. Circulation. 1988 Oct;78(4):906-19 - PubMed
  7. J Am Coll Cardiol. 1992 Mar 1;19(3):639-46 - PubMed
  8. Circulation. 1990 Sep;82(3):781-91 - PubMed
  9. Circulation. 1980 Jun;61(6):1105-12 - PubMed
  10. Lancet. 1986 Feb 22;1(8478):397-402 - PubMed
  11. J Am Coll Cardiol. 1989 Jul;14(1):40-6; discussion 47-8 - PubMed
  12. Jpn Circ J. 1984 Jul;48(7):678-89 - PubMed
  13. Nihon Juigaku Zasshi. 1984 Feb;46(1):11-9 - PubMed
  14. Mol Cell Biochem. 1978 Aug 16;20(3):149-57 - PubMed
  15. Jpn Circ J. 1984 Jul;48(7):650-8 - PubMed
  16. J Am Coll Cardiol. 1992 May;19(6):1129-35 - PubMed
  17. Circulation. 1973 Sep;48(3):588-96 - PubMed
  18. J Am Coll Cardiol. 1991 Oct;18(4):1077-84 - PubMed
  19. J Am Coll Cardiol. 1992 Dec;20(7):1482-9 - PubMed
  20. Am J Cardiol. 1988 Sep 1;62(7):347-51 - PubMed
  21. Thromb Haemost. 1993 Jan 11;69(1):45-9 - PubMed
  22. Am J Med. 1955 Apr;18(4):622-32 - PubMed
  23. Am Heart J. 1977 Mar;93(3):280-8 - PubMed
  24. Am J Cardiol. 1993 May 1;71(12):1021-4 - PubMed
  25. Thromb Haemost. 1991 May 6;65(5):549-52 - PubMed
  26. J Am Coll Cardiol. 1992 Mar 1;19(3):647-53 - PubMed
  27. Am Heart J. 1967 Oct;74(4):578-81 - PubMed
  28. J Am Coll Cardiol. 1992 Dec;20(7):1626-33 - PubMed
  29. Johns Hopkins Med J. 1979 Mar;144(3):73-80 - PubMed
  30. Circulation. 1988 Dec;78(6):1345-51 - PubMed
  31. J Biol Chem. 1980 Mar 10;255(5):2005-13 - PubMed
  32. Am J Cardiol. 1985 Apr 1;55(8):871-7 - PubMed
  33. N Engl J Med. 1991 Oct 17;325(16):1117-22 - PubMed
  34. N Engl J Med. 1993 Sep 2;329(10 ):673-82 - PubMed
  35. Thromb Haemost. 1991 May 6;65(5):553-9 - PubMed
  36. Am Heart J. 1988 Nov;116(5 Pt 1):1212-7 - PubMed
  37. J Am Coll Cardiol. 1990 Jul;16(1):223-31 - PubMed

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