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Arteriosclerosis, Thrombosis, and Vascular Biology
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Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2258-2265
Published online before print August 2, 2007, doi: 10.1161/ATVBAHA.107.149633
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(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:2258.)
© 2007 American Heart Association, Inc.


Thrombosis

No-Reflow Phenomenon After Acute Myocardial Infarction Is Associated With Reduced Clot Permeability and Susceptibility to Lysis

Jaroslaw Zalewski; Anetta Undas; Jacek Godlewski; Ewa Stepien; Krzysztof Zmudka

From the Institute of Cardiology (J.Z., A.U., J.G., K.Z.), Jagiellonian University School of Medicine, and John Paul II Hospital (J.Z., J.G., E.S.), Cracow, Poland.

Correspondence to Jaroslaw Zalewski, Institute of Cardiology, Jagiellonian University School of Medicine, John Paul II Hospital, 80 Pradnicka Street, 31-202 Cracow, Poland. E-mail jzalewski{at}szpitaljp2.krakow.pl

Objective— We assessed the relationship between fibrin clot properties and the no-reflow phenomenon after primary coronary intervention (PCI).

Methods and Results— Epicardial blood flow was assessed by TIMI scale and corrected TIMI frame count (cTFC), and perfusion by TIMI Myocardial Perfusion Grade (TMPG) after PCI during ST-segment elevation myocardial infarction (STEMI). Fibrin clot permeability (Ks) and susceptibility to lysis in assays using exogenous thrombin (t50%) and without thrombin (tTF) were determined in 30 no-reflow patients (TIMI ≤2) and in 31 controls (TIMI-3) after uneventful 6 to 14 months from PCI. Patients with TIMI ≤2 had lower Ks by 18% (P<0.0001) and prolonged fibrinolysis by 33% for t50% (P<0.0001) and by 45% for tTF (P<0.0001). cTFC was correlated with Ks (r=–0.56, P<0.0001), t50% (r=0.49, P<0.001), and tTF (r=0.54, P<0.001). Ks increased in a stepwise fashion with TIMI flow (P<0.0001) and TMPG (P<0.0001), whereas both fibrinolysis times decreased with TIMI flow (P<0.0001 for both) and TMPG (P<0.01 for both). Multiple regression models showed that only Ks and fibrinogen were independent predictors of cTFC (P<0.05 for both), TIMI ≤2 flow (P<0.05 for both) and TMPG-0/1 (P<0.05 for both).

Conclusions— Survivors of myocardial infarction with a history of the no-reflow after PCI are characterized with more compact fibrin network and its resistance to lysis.

Fibrin clot properties were assessed in patients after primary coronary angioplasty in acute myocardial infarction. The clots composed of a more compact fibrin network with attenuated fibrinolysis were detected in patients with impaired reperfusion. Reduced clot permeability and fibrinolysis may be a novel prothrombotic mechanism, which might contribute to the pathogenesis of the no-reflow phenomenon.


Key Words: myocardial infarction • primary coronary angioplasty • no-reflow phenomenon • fibrin clot • fibrinolysis