STREPTOKINASE-INDUCED TRANSIENT AGGRAVATION OF MYOCARDIAL INJURY

We examined the relationship between streptokinase infusion, intensity of myocardial injury and systemic hypotension in patients receiving s treptokinase for treatment of evolving acute myocardial infarction. Tw enty consecutive patients treated with streptokinase for evolving acut e myocardial infarction received continuous blood pressure and S-T seg ment monitoring of the 12 lead electrocardiogram (ECG) for at least 5 h, commencing prior to commencement of the streptokinase infusion. Agg ravation of injury, manifested both by episodic increases in S-T segme nt elevation on the electrocardiogram (ECG) (P < 0.001), and in mean S -T segment elevation (P < 0.05) occurred within the first 20 min after initiation of streptokinase infusion. Hypotension also occurred trans iently in most patients, with a mean minimum systolic blood pressure o f 92 +/- 22 (S.D.) mmHg occurring 16 +/- 5 min after commencement of s treptokinase. There was no correlation between the extent of aggravati on of injury and that of hypotension. All patients showed ECG evidence of reperfusion, with a reduction of S-T elevation in the reference le ad to 50% of maximal value, after a median of 62 min (range 9-174 min) . It is concluded that streptokinase aggravates injury prior to reperf usion, although probably not via the induction of hypotension. It is p ossible that this effect contributes to the 'early hazard' of thrombol ytic therapy.