Vol 19, No 2 (2012)
Original articles
Published online: 2012-03-30

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Thrombolytic effect of streptokinase infusion assessed by ST-segment resolution between diabetic and non-diabetic myocardial infarction patients

Mohammad Masoomi, Sadra Samadi, Mehrdad Sheikhvatan
Cardiol J 2012;19(2):168-173.


Background: Recently, it has been hypothesized that type 2 diabetes might interfere with acute intravenous thrombolysis effectiveness as estimated by angiographic or electrocardiographic criteria. In our study, we compared the thrombolytic effect of streptokinase infusion between diabetic and non-diabetic myocardial infarction (MI) patients.
Methods: In a prospective interventional study, 240 consecutive patients who were admitted to the emergency ward and diagnosed with ST-elevation MI (STEMI) were enroled and classified into diabetics (n = 85) and non-diabetics (n = 155). Streptokinase was given to each patient at a dose of 1.5 million units in 1 h. Twelve-lead ECG was recorded immediately before the start of thrombolytic therapy and at 180 min afterwards for the patients with STEMI. The ST-segment elevation resolution was calculated and stratified as complete resolution (> 70% ST-resolution), partial resolution (30–70% ST-resolution), or failed resolution (< 30% ST-resolution).
Results: Complete ST-resolution occurred in 31.6% of diabetic and 51.0% of non-diabetic patients, respectively (p < 0.001). The incidence of partial ST-resolution in diabetic and non- -diabetic patients was 40.5% and 40.0%, whereas 27.8% of patients in the diabetic group and 9.0% of patients in the non-diabetic group showed failed ST resolution. ST-resolution was independent of the location of MI. Multivariate analysis showed that diabetes mellitus, as well as higher Killip class and lower ejection fraction, could effectively predict ST-resolution failure.
Conclusions: Failure of ST-segment resolution 180 min after streptokinase infusion is notably higher in diabetic vs non-diabetic patients. This failure rate is correlated with higher Killip class and lower ejection fraction. (Cardiol J 2012; 19, 2: 168–173)

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