This study was designed to investigate the possible role of pre- and posttreatment plasma D-dimer concentration as a reflection of coronary artery thrombolysis. Blood was collected from 206 patients with angiographically documented acute coronary occlusion presenting within 6 hours of symptom onset who were enrolled in a prospective study comparing intravenous APSAC (30 U) (IV-APSAC) with intracoronary streptokinase (160,000 U) (IC-SK). D-dimer concentrations in 104 patients after IV-APSAC therapy were higher than in 90 patients after IC-SK (mean ± standard error, 1,009 ± 60 vs 603 ± 45, p <0.001), but there was no difference in patients with and without reperfusion (1,096 ± 88 vs 875 ± 67, p = 0.1 for IV-APSAC, and 587 ± 48 vs 634 ± 95, p = 0.6 for IC-SK). The median concentrations before treatment were similar in the IV-APSAC and IC-SK groups (93 and 90 ng/ml, respectively). These were higher than the value in 25 ambulatory control subjects (72 ng/ml) but lower than in 29 post-AMI (6 to 30 hours) patients and in preoperative orthopedic patients (140 ng/ml each). There was no difference in D-dimer concentrations in patients with grade 0 or grade 1 coronary artery occlusion (median 85 vs 90 ng/ml) or in patients with or without ultimate successful reperfusion (median 85 vs 93 ng/ml). After incubation of pretreatment plasma (obtained from 30 patients with AMI) with t-PA, the D-dimer reactivity increased from (mean ± standard error) 82 ± 6.7 to 968 ± 128 ng/ml, a concentration no different from the same patients after thrombolytic treatment (937 ± 109 ng/ml). These findings support the concept that coronary artery thrombi contribute a relatively small amount of D-dimer to the blood before and after thrombolytic treatment and that the major source of plasminogen activator-derived D-dimer in AMI patients is the blood itself, most likely from soluble crosslinked fibrin polymers.
ASJC Scopus subject areas
- Cardiology and Cardiovascular Medicine