Long-term effect of thrombolytic therapy on left ventricular ejection fraction after acute myocardial infarction.

To assess the long-term effect of thrombolytic therapy on left ventricular (LV) systolic function, 222 patients with acute myocardial infarction treated with intravenous tissue plasminogen activator within 4 hours of symptom onset underwent assessment of LV ejection fraction (EF) by radionuclide equilibrium angiography at hospital discharge and 1 year later. Mean EF at hospital discharge (46 +/- 12) was similar to that at 1 year (45 +/- 13). Stepwise multivariate linear regression analysis identified EF at discharge and patency of the infarct-related artery before discharge as independent predictors of EF change at 1 year (p = 0.0002 and 0.003, respectively). Random assignments to invasive versus conservative treatment strategies or to early versus delayed beta-blocker therapy did not affect EF change during follow-up. No significant deterioration of EF was observed in patients with larger infarcts. However, EF decreased from 45 +/- 10 at hospital discharge to 39 +/- 12 (p = 0.005) at 1-year follow-up in a subgroup of patients with history of prior infarction. Thus, patients with acute myocardial infarction, treated with intravenous tissue plasminogen activator early after onset of symptoms, appear to have stable LV function between hospital discharge and 1 year follow-up. The change in EF between hospital discharge and 1 year can be predicted from the EF value at discharge, patency of the infarct-related artery before discharge and history of previous myocardial infarction.

Early tPA treatment and aeromedical transport of patients with acute myocardial infarction.

Over a 2-year period 192 patients with acute myocardial infarction (AMI) were transported by helicopter and treated with recombinant tissue-plasminogen activator (tPA). All patients were entered into the Thrombolysis in Myocardial Infarction-Phase II (TIMI II) trial. Eighty-two of these patients were treated with tPA after aeromedical transport to a tertiary care center. One hundred ten patients had tPA treatment initiated by the flight crew prior to transport. The flight crews initiated therapy 28 +/- 11 minutes after arrival at the sending hospital. The post-flight treated patients received the tPA bolus 82 +/- 20 minutes after arrival at the sending hospital (P less than .0001), and 41 +/- 18 minutes after arrival at the receiving hospital (P less than .0001). Based on enzyme and electrocardiographic changes, all patients in the study had a confirmed diagnosis of AMI before discharge. Patients with inferior myocardial infarction (MI) treated with tPA in-flight were more likely to suffer from bradycardia and hypotension requiring atropine injection during transport than the post-flight treated patients or in-flight treated patients with anterior MI. There was no in-flight mortality in either group. Our experience indicates that patients with AMI can be transported safely during tPA therapy. Also, a trained team whose sole responsibility is the early evaluation and initiation of therapy in a patient with AMI can function as accurately and significantly more rapidly than tertiary care emergency department and ICU personnel following identical protocols.