Relation of plasma D-dimer concentrations to coronary artery reperfusion before and after thrombolytic treatment in patients with acute myocardial infarction

Benjamin Brenner, Charles W. Francis, Patricia G. Fitzpatrick, Robert L. Rothbard, Christopher Cox, Rosemary A. Hackworthy, Jeffrey L. Anderson, Sherman G. Sorensen, Victor J. Marder

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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.

Original languageEnglish (US)
Pages (from-to)1179-1184
Number of pages6
JournalThe American Journal of Cardiology
Issue number17
Publication statusPublished - May 15 1989
Externally publishedYes


ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine

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