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Coronary Progenitor Cells and Soluble Biomarkers in Cardiovascular Prognosis after Coronary Angioplasty
Published on: January 28, 2020
C-reactive protein and fibrin clot strength measured by thrombelastography after coronary stenting
Rolf P Kreutz1, Janelle Owens, Jeffrey A Breall
1Krannert Institute of Cardiology, Indiana University School of Medicine, 1800 N. Capitol Avenue, Indianapolis, IN 46202, USA. rkreutz@iupui.edu
Insights
Elevated C-reactive protein (CRP) after coronary stenting is linked to stronger blood clots, independent of fibrinogen levels. This finding suggests a connection between inflammation, clot strength, and thrombotic risk in patients with coronary artery disease.
Area of Science:
- Cardiovascular Medicine
- Clinical Chemistry
- Hematology
Background:
- Inflammation plays a key role in coronary artery disease (CAD) progression.
- C-reactive protein (CRP) is a marker of inflammation associated with increased risk of ischemic events and hypercoagulability after coronary stenting.
- Heightened blood clot strength, measured by thrombelastography (TEG), is also linked to adverse outcomes post-stenting.
Purpose of the Study:
- To investigate the relationship between C-reactive protein (CRP) levels and plasma fibrin clot strength in patients following coronary stenting.
- To determine if CRP influences clot strength independently of fibrinogen concentration.
Main Methods:
- Plasma fibrin clot strength was measured using thrombelastography (TEG) in 54 patients 16-24 hours after elective percutaneous coronary intervention (PCI).
- Coagulation was initiated in citrated plasma with kaolin and CaCl2.
- Plasma levels of CRP and fibrinogen were quantified using enzyme-linked immunoassay.
Main Results:
- Increasing quartiles of CRP were significantly associated with increased maximal plasma fibrin clot strength (P < 0.001) and body mass index (BMI) (P = 0.04).
- Patients in the highest CRP quartile exhibited significantly greater maximal fibrin clot strength compared to those in the lowest quartile (G: 3438 ± 623 vs. 2184 ± 576 dyn/cm, P < 0.0001).
- Fibrinogen concentration did not differ significantly across CRP quartiles (P = 0.97).
Conclusions:
- Patients with coronary artery disease undergoing stenting and elevated CRP levels post-PCI demonstrate increased maximal plasma fibrin clot strength.
- The prothrombotic risk associated with elevated CRP may be mediated by procoagulant changes and enhanced fibrin clot tensile strength, irrespective of fibrinogen levels.
Abstract:
Inflammation is implicated in the progression of coronary artery disease and the molecular processes of inflammation and thrombosis are closely intertwined. Elevated levels of C-reactive protein (CRP) have been associated with an elevated risk of adverse ischaemic events after coronary stenting and hypercoagulability. Heightened whole blood clot strength measured by thrombelastography (TEG) has been associated with adverse ischaemic events after stenting. We intended to examine the relationship of CRP to plasma fibrin clot strength in patients after coronary stenting. Plasma fibrin clot strength was measured by TEG in 54 patients 16-24 h after undergoing elective percutaneous coronary intervention (PCI). Coagulation was induced in citrated plasma by addition of kaolin and CaCl2. Plasma levels of CRP and fibrinogen were measured by enzyme-linked immunoassay. Increasing quartiles of CRP were associated with increasing levels of maximal plasma fibrin clot strength measured by TEG (P < 0.001) and increasing BMI (P = 0.04). Patients in the highest quartile of CRP had significantly higher maximal fibrin clot strength (G) than the patients in the lowest quartile (G: 3438 ± 623 vs. 2184 ± 576 dyn/cm, P < 0.0001). Fibrinogen concentration was not significantly different across quartiles of CRP (P = 0.97). Patients with established coronary artery disease undergoing coronary stenting who have elevated CRP after PCI exhibit heightened maximal plasma fibrin clot strength as compared with those with low CRP. Thrombotic risk associated with elevated CRP may be linked to procoagulant changes and high tensile fibrin clot strength independent of fibrinogen concentration.
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