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. 2004 Mar;27(3):144-50.
doi: 10.1002/clc.4960270309.

Myoglobin--a marker of reperfusion and a prognostic indicator in patients with acute myocardial infarction

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Myoglobin--a marker of reperfusion and a prognostic indicator in patients with acute myocardial infarction

M Perwaiz Iqbal et al. Clin Cardiol. 2004 Mar.

Abstract

Background: Early noninvasive identification of patients with occluded infarct-related arteries after thrombolysis has important prognostic and therapeutic implications. Recent reports indicate that plasma kinetics of cardiac marker proteins could be very useful in diagnosis of myocardial reperfusion. Although angiographic assessment remains the ideal procedure for determining patency, it is expensive, invasive, not within the reach of most patients in developing countries, and the long-term follow-up data are still sparse.

Hypothesis: The present study was undertaken to investigate whether plasma kinetics of myoglobin in conjunction with clinical markers and another biochemical marker, creatine kinase, could be used to predict myocardial reperfusion more accurately and to investigate the correlation between myoglobin release after thrombolysis and mortality in patients with acute myocardial infarction (AMI) over a follow-up period of 18 months.

Methods: Eighty-three consecutive patients with AMI receiving streptokinase treatment were studied for plasma kinetics of myoglobin in conjunction with clinical markers and creatine kinase to predict reperfusion and were followed for a period of 18 months.

Results: Increased baseline mean +/- standard deviation levels of myoglobin were observed among "nonresponders" to streptokinase treatment compared with "responders" (469 +/- 386 microg/l vs. 270 +/- 211 microg/l). There was significantly more release of myoglobin following thrombolytic treatment among the responders than among the nonresponders (mean ratio of myoglobin levels at 90 min to 0 min 6.01 +/- 9.2 vs. 1.03 +/- 0.64). In a follow-up of 61 patients over a period of 18 months, 31% mortality was observed in the nonresponder group compared with 11.7% in the responder group. In responders, the mean ratio of myoglobin levels at 90 and 0 min was significantly less among those who died (p = 0.019) than among those who survived.

Conclusion: A myoglobin release profile in combination with other clinical markers offers inexpensive, noninvasive, and a reasonably reliable way of assessing coronary artery patency after thrombolytic treatment.

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