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Thromb Haemost 1998; 80(06): 881-886
DOI: 10.1055/s-0037-1615382
Letters to the Editor
Schattauer GmbH

Augmented Platelet Aggregation as Predictor of Reocclusion after Thrombolysis in Acute Myocardial Infarction

Thomas K. Nordt
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Martin Moser
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Benedikt Kohler
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Johannes Ruef
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Karlheinz Peter
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Wolfgang Kübler
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
,
Christoph Bode
1   From the Abteilung Kardiologie, Medizinische Klinik und Poliklinik, Ruprecht-Karls-Universität Heidelberg, Germany
› Author Affiliations
Further Information

Publication History

Received 05 February 1998

Accepted after resubmission 21 August 1998

Publication Date:
07 December 2017 (online)

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Summary

Rationale. Reocclusion after thrombolysis diminishes the benefits of early reperfusion after acute myocardial infarction (AMI). No clinical or laboratory variables have been identified as predictors for reocclusion yet. Methods and results. To evaluate hemostatic variables as potential risk determinants platelet aggregation (PA, representing platelet activity), thrombin/antithrombin complexes (TAT, representing thrombin generation), and plasminogen activator inhibitor type 1 (PAI-1, representing endogenous fibrinolysis) were determined in 31 patients with AMI at 0, 1, 2, and 12 h after the start of thrombolysis as well as at hospital discharge. Reocclusion (defined as reinfarction or angiographically confirmed, clinically silent coronary reocclusion) occurred in 5 patients within 5-14 days and in 8 patients within 1 year. TAT plasma concentrations were lower in patients with reocclusion than in those without (9.9 ± 5.7 vs. 22.9 ± 22.2 ng/ml at 2 h, 6.5 ± 3.1 vs. 11.2 ± 6.4 ng/ml at 12 h, means ± SD, p <0.05 each). Neither concentration nor activity of PAI-1 in plasma differed between both patient groups. However, both slope and maximum of PA (induced by 2 μmol/l ADP) were augmented in patients with reocclusion (slope: 39.4 ± 1.7 vs. 32.5 ± 7.4 at 2 h, p <0.001; 42.6 ± 2.6 vs. 36.6 ± 8.9 at 12 h, p <0.01). Results were independent of the thrombolytic agent used (alteplase or reteplase). A PA slope at 2 h higher than the average slope before thrombolysis (37.2 ± 5.7) could be identified as best predictor for early (within 5-14 d, p = 0.017, sensitivity 1.00, specificity 0.69) and late reocclusion (within 1 y, p=0.009, 0.88 and 0.74, respectively). Conclusions. Increased PA following coronary thrombolysis appears to be associated with early and late reocclusion. This marker could be useful in identifying patients who may benefit from more aggressive anti-platelet (such as GP IIb/IIIa receptor antagonists), interventional, or both strategies.

 

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