Principal Findings:

Patency of the infarct-related artery (TIMI Perfusion grade 2 or 3 flow) at 60 min after the start of thrombolysis was significantly higher in rt-PA-treated patients (77.8% vs. 59.5% for APSAC-treated patients and 59.3% for combination-treated patients [rt-PA vs. APSAC, p = 0.02; rt-PA vs. combination, p = 0.03]).

At 90 min, the incidence of both infarct-related artery patency and TIMI grade 3 flow was significantly higher in rt-PA-treated patients (60.2% had TIMI Perfusion grade 3 flow vs. 42.9% and 44.8% of APSAC- and combination-treated patients, respectively [rt-PA vs. APSAC, p < 0.01; rt-PA vs. combination, p = 0.02]).

The incidence of unsatisfactory outcome was 41.3% for rt-PA compared with 49% for APSAC and 53.6% for the combination (rt-PA vs. APSAC, p = 0.19; rt-PA vs. combination, p = 0.06).

The mortality rate at 6 weeks was lowest in the rt-PA-treated patients (2.2% vs. 8.8% for APSAC and 7.2% for combination thrombolytic therapy [rt-PA vs. APSAC, p = 0.02; rt-PA vs. combination, p = 0.06]).

Use of a standardized heparin nomogram to achieve therapeutic anticoagulation after thrombolysis:
Subtherapeutic activated partial thromboplastin time values were noted in 4%, 14%, 29%, 46%, 37%, and 34% of patients 8, 12, 24, 48, 72, and 96 hours, respectively, after heparin treatment was begun.
Patients with subtherapeutic values at 24 hours were younger (mean ±SD, 55.2 ±10.6 vs. 59.6 ±10.6 years, P = .02) and weighed more (86.4 ±13.5 vs. 78.9 ±15.7 kg, P = .007) than patients with therapeutic values.
Centers that used the nomogram had significantly fewer subtherapeutic values at 48 and 96 hours. In addition, heparin therapy was interrupted less frequently at centers that used the nomogram (38.1% vs. 68.7%, P <. 001).
Major spontaneous hemorrhage, reinfarction, and reocclusion rates were low and were about the same in the two groups.

Reocclusion was observed more frequently in arteries with TIMI 2 vs. TIMI 3 flow (10.4% vs. 2.2%, p = 0.003), in ulcerated lesions (10.7% vs. 3.0%, p = 0.009) and in the presence of collateral vessels (18.2% vs. 5.6%, p = 0.03). Similar trends were observed for eccentric (7.3% vs. 2.3%, p = 0.06) and thrombotic (8.4% vs. 3.3%, p = 0.06) lesions. Reocclusion was associated with more severe mean percent stenosis (77.9% vs. 73.9%, p = 0.04). Lesion length, reference segment diameter and Fourier measures of lesion irregularity were not associated with reocclusion.

Patients with any previous history of angina were less likely than with those without angina to experience in-hospital death (3% vs. 8%) (P = .03), severe congestive heart failure (CHF) or shock (1% vs. 7%, P = .006), or the combined end point of in-hospital death, severe CHF, or shock (4% vs. 12%, P = .004). Moreover, patients with any history of angina were more likely to have a smaller creatine kinase (CK)-determined infarct size (119 vs. 154 CK integrated units; P = .01) and were less likely to have Q waves on their ECG (57% vs. 69%; P = .01).

In the subset of patients who experienced angina within the 48 hours before infarction (compared with those who did not), there was a trend toward less likely in-hospital death (3% vs. 6%; P = .09), a lower incidence of severe CHF or shock (1% vs. 6% P = .008), a lower combined end point of death, CHF, or shock (3% vs. 10%; P = .006), smaller infarct size assessed by CK (115 vs. 151 CK units; P = .03), and a trend toward fewer Q-wave infarcts.

However, patients with a history of previous angina did have a trend toward more recurrent ischemic pain. Of importance is that the beneficial in-hospital effects of previous angina were not dependent on angiographically visible coronary collaterals.