CC-BY 4.0 · TH Open 2018; 02(02): e173-e181
DOI: 10.1055/s-0038-1645876
Original Article
Georg Thieme Verlag KG Stuttgart · New York

Prediction of Ischemic Events after Percutaneous Coronary Intervention: Thrombelastography Profiles and Factor XIIIa Activity

Rolf P. Kreutz
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
2  Department of Clinical Pharmacology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Glen Schmeisser
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Andrea Schaffter
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Sri Kanuri
2  Department of Clinical Pharmacology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Janelle Owens
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
2  Department of Clinical Pharmacology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Benjamin Maatman
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Anjan Sinha
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Elisabeth von der Lohe
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
,
Jeffrey A. Breall
1  Krannert Institute of Cardiology, Indiana University School of Medicine, Indianapolis, Indiana, United States
› Author Affiliations
Funding This study was supported, in part, by the Indiana Clinical and Translational Sciences Institute, funded, in part, by grant number U54-RR025761 (Anantha Shekhar, PI) from the National Institutes of Health, National Center for Research Resources, Clinical and Translational Sciences Award, as well as the Indiana University Health Values Grant, the Indiana University Health – Indiana University School of Medicine Strategic Research Initiative, and internal funding from the Department of Medicine, Indiana University School of Medicine, Indianapolis. Sample processing and storage was performed in part by the Specimen Storage Facility (SSF) of the Indiana Clinical and Translational Sciences Institute (CTSI) which is supported, in part, by a Clinical and Translational Sciences Award (grant no. UL1TR001108; Anantha Shekhar, PI) and CTSI SSF facility construction was funded in part by grant CO6-RR020128–01 (R.S. Fife, PI; K. Cornetta, Co-I).
Further Information

Publication History

06 December 2017

14 March 2018

Publication Date:
07 May 2018 (online)

Abstract

Background High plasma fibrin clot strength (MA) measured by thrombelastography (TEG) is associated with increased risk of cardiac events after percutaneous coronary interventions (PCIs). Factor XIIIa (FXIIIa) cross-links soluble fibrin, shortens clot formation time (TEG-K), and increases final clot strength (MA).

Methods We analyzed platelet-poor plasma from patients with previous PCI. Kaolin-activated TEG (R, K, MA) in citrate platelet-poor plasma and FXIIIa were measured (n = 257). Combined primary endpoint was defined as recurrent myocardial infarction (MI) or cardiovascular death (CVD). Relationship of FXIIIa and TEG measurements on cardiac risk was explored.

Results FXIIIa correlated with TEG-MA (p = 0.002) and inversely with TEG-K (p < 0.001). High MA (≥35.35 mm; p = 0.001), low K (<1.15 min; p = 0.038), and elevated FXIIIa (≥83.51%; p = 0.011) were associated with increased risk of CVD or MI. Inclusion of FXIIIa activity and low TEG-K in risk scores did not improve risk prediction as compared with high TEG-MA alone.

Conclusion FXIIIa is associated with higher plasma TEG-MA and low TEG-K. High FXIIIa activity is associated with a modest increase in cardiovascular risk after PCI, but is less sensitive and specific than TEG-MA. Addition of FXIIIa does not provide additional risk stratification beyond risk associated with high fibrin clot strength phenotype measured by TEG.