Thrombolysis with recombinant tissue-type plasminogen activator (rt-PA) and anisoylated plasminogen streptokinase activator (APSAC) in myocardial infarction has been proved to reduce mortality. A new front-loaded infusion regimen of 100 mg of rt-PA with an initial bolus dose of 15 mg followed by an infusion of 50 mg over 30 min and 35 mg over 60 min has been reported to yield higher patency rates than those achieved with standard regimens of thrombolytic treatment. The effects of this front-loaded administration of rt-PA versus those obtained with APSAC on early patency and reocclusion of infarct-related coronary arteries were investigated in a randomized multicenter trial in 421 patients with acute myocardial infarction. Coronary angiography 90 min after the start of treatment revealed a patent infarct-related artery (Thrombolysis in Myocardial Infarction [TIMI] grade 2 or 3) in 84.4% of 199 patients given rt-PA versus 70.3% of 202 patients given APSAC (p = 0.0007). Early reocclusion within 24 to 48 h was documented in 10.3% of 174 patients given rt-PA versus 2.5% of 163 patients given APSAC. Late reocclusion within 21 days was observed in 2.6% of 152 patients given rt-PA versus 6.3% of 159 patients given APSAC. There were 5 in-hospital deaths (2.4%) in the rt-PA group and 17 deaths (8.1%) in the APSAC group (p = 0.0095). The reinfarction rate was 3.8% and 4.8%, respectively. Peak serum creatine kinase and left ventricular ejection fraction at follow-up angiography were essentially identical in both treatment groups. There were more bleeding complications after APSAC (45% vs. 31%, p = 0.0019).(ABSTRACT TRUNCATED AT 250 WORDS)

No abstract

SUMMARY Percutaneous transluminal coronary angioplasty (PTCA) was performed in 21 patients with acute myocardial infarction (AMI) treated by intracoronary infusion of streptokinase within 8 hours after the onset of symptoms. Streptolysis therapy began a mean of 3.6 1.2 hours (±+ SD) after the onset of symptoms. The vessel was occluded in 14 patients and highly stenosed in seven. After the infusion of 67,300 + 63,200 IU of streptokinase over 26.1 21.5 minutes, patency of the occluded vessels was reached.PTCA as performed 20-60 minutes after the end of streptokinase treatment in 19 patients and 24 and 31 hours after treatment in two patients. The dilation was successful in 17 patients (81%). The degree of vessel obstruction was reduced from 90.2 + 7.3% to 58.6 19.5% (area method) and from 71.4 + 12.4% to 39.2 + 19.7% (diameter method). The improvement was 31.5 18.4% and 32.2 ± 19.3%, respectively. No reocclusion was induced by PTCA. Twenty patients were discharged. One died during hospitalization; at autopsy, the treated vessel was still patent. During the follow-up period, two reinfarctions and one asymptomatic reocclusion occurred.The clinical findings during the hospital course and the follow-up period were compared with those of a control group of 18 patients with AMI and comparable coronary stenoses who were treated only with streptokinase infusion. Four of these patients had a reinfarction during the hospital course, and three died during the follow-up period.PTCA can be performed safely and successfully immediately after intracoronary infusion of streptokinase in patients with AMI. By reducing the subtotal stenosis, this treatment contributes to the reperfusion of the ischemic myocardium, diminishes the risk of a reocclusion and seems to improve the prognosis.

No abstract

No abstract

No abstract

No abstract

SUMMARY The spontaneous course of ST-segment elevation (2ZST) in 24 patients with acute anterior myocardial infarction (AMI) was studied by precordial ST-segment mapping, which was recorded at 2-hour intervals during the first 48 hours after admission. Change of 2ST between two registrations was expressed as mV/hr, and was compared with clinical and hemodynamic parameters, course of MB-CK curve, calculated infarct mass and arrhythmias. After an initial rapid increase, there was a decrease of ZST, which reaches a plateau-like curve approximately 12 hours after the onset of chest pain. A second new increase of ZST exceeding a value of 0.6 mV/hr correlates well with extension of necrosis, verified by re-elevation of MB-CK. During the first 2 days, extension of necrosis could be detected in 50% of our patients.As new ischemic episodes and extension of necrosis in AMI occur frequently and are promptly indicated by an increase of ZST, the physician should, while monitoring therapeutic interventions, concentrate on such a second increase rather than on a decrease of ZST (which may occur spontaneously), as has been suggested in most previous reports.MANY REPORTS HAVE EVALUATED therapeutic interventions in patients with acute myocardial infarction by precordial ST-segment mapping,"'' but only a few have been concerned with the spontaneous course of ST-segment elevation (2ST) during myocardial infarction by daily ST-segment mapping;12-17 there are none with multiple measurements within the first hours after onset of chest pain, when therapeutic interventions are expected to have the best effect on minimizing final infarct size. Therefore, it is necessary to know the spontaneous course of ZST during this period for accurate interpretation of therapeutic intervention.After improving the technique of precordial mapping so that accurate measurements within a relatively short period were possible without interfering greatly with the normal activity of the coronary care unit (CCU), we followed the spontaneous course of IST closely and redefined its diagnostic value. Materials and MethodsTwenty-four patients (19 male, five female), ages 26-81 years (mean age 59.5 years), were studied. All were admitted to the CCU within 24 hours (mean 4.8 hours) after the onset of acute chest pain. All had an ECG compatible with the diagnosis of acute transmural anterior myocardial infarction. Patients with initial signs of pericarditis (pericardial friction rub) or complete bundle branch block were excluded.Precordial mapping was performed with a flexible synthetic plate (32 X 24 cm) containing 48 silveroxydized copper electrodes. Contact diameter of elec-