Impact of different reperfusion modalities on ventricular function after acute myocardial infarction.
Single-plane contrast ventriculography was performed on admission and before hospital discharge in more than 200 patients with acute myocardial infarction participating in a series of prospective clinical trials including intracoronary streptokinase, percutaneous transluminal coronary angioplasty (PTCA), intravenous tissue plasminogen activator (rt-PA) and thrombolysis (intravenous rt-PA or streptokinase) followed by PTCA. Both global ejection fraction (EF) and regional wall motion of the infarct zone were measured to assess serial changes. Patients treated with intracoronary streptokinase 3.6 +/- 1.8 hours after symptom onset had no increase in EF (mean change 1 +/- 6%, difference not significant [NS]), but patients treated with primary PTCA at 3.0 +/- 1.2 hours did (mean improvement 8 +/- 7%, p less than 0.001). Patients treated with sequential intravenous streptokinase and PTCA 2.6 +/- 1.3 hours after symptom onset showed similar improvement in EF (mean change 6 +/- 12%, p less than 0.002). Patients treated with rt-PA had no change in EF whether treated with rt-PA alone or rt-PA followed by immediate angioplasty (mean change -2 +/- 8% and 0.5 +/- 8%, p = NS, respectively). When angioplasty was used in patients with persistent occlusion after thrombolytic therapy, EF improved in those who had received intravenous streptokinase (mean change 10 +/- 7%, p less than 0.002), but not those who had received rt-PA (+0.5%, p = NS). However, infarct zone regional wall motion improved in patients treated with intracoronary streptokinase (+0.59 +/- 0.79 standard deviation/chord, p less than 0.05), primary PTCA (+1.32 +/- 1.32, p less than 0.001).(ABSTRACT TRUNCATED AT 250 WORDS)
O'Neill
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Department of Internal Medicine, William Beaumont Hospital, Royal Oak, Michigan 48072.
D000800:Angioplasty, Balloon; D002986:Clinical Trials as Topic; D003131:Combined Modality Therapy; D003326:Coronary Circulation; D003331:Coronary Vessels; D006321:Heart / Q000503:physiopathology*; D006801:Humans; D009200:Myocardial Contraction; D009203:Myocardial Infarction / Q000503:physiopathology / Q000628:therapy*; D010477:Perfusion; D013300:Streptokinase / Q000627:therapeutic use*; D013318:Stroke Volume; D013997:Time Factors; D010959:Tissue Plasminogen Activator / Q000627:therapeutic use*
D013300:Streptokinase; D010959:Tissue Plasminogen Activator