Elevated NT-proBNP is associated with unfavorably altered plasma fibrin clot properties in atrial fibrillation

Matusik, Paweł T.; Matusik, Patrycja S; Kornacewicz-Jach, Zdzisława; Małecka, Barbara; Ząbek, Andrzej; Undas, Anetta

doi:10.1016/j.ijcard.2017.05.060

Cited by 26 publications

(39 citation statements)

References 41 publications

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“…We investigated 65 patients with AF free of myocardial infarction or venous thromboembolism within the previous three months, with creatinine clearance ≥ 15 mL/min, and without liver cirrhosis, known cancer, or acute infection. Detailed methodology of the study was presented previously [3]. Vitamin K antagonists and low-molecular-weight heparin (the last dose ≥ 12 h) were discontinued before the blood draw.…”

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confidence: 99%

Association of cardiac troponin I with prothrombotic alterations in atrial fibrillation

et al. 2018

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confidence: 99%

Association of cardiac troponin I with prothrombotic alterations in atrial fibrillation

et al. 2018

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“…51 The prothrombotic fibrin clot phenotype, including K s reduced by 7.5% and lysis time prolonged by 13.8%, characterized patients with prior ischemic stroke. 52 Reduced K s observed within the first 24 hours since the onset of stroke symptoms in nonthrombolysed patients remained unaltered after 60 days from the event, suggesting that the prothrombotic clot phenotype is a persistent feature of patients suffering from ischemic stroke. 53 The worse prognosis is observed in patients with atrial fibrillation (AF) who experienced acute cerebrovascular episode.…”

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confidence: 98%

Plasma fibrin clot structure and thromboembolism: clinical implications

Ząbczyk¹,

Undas²

2017

Polish Archives of Internal Medicine

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A and-much slower-B from the N -termini of the Aα and Bβ chains, respectively, resulting in the formation of fibrin monomer with exposed binding sites in the E domain. Fibrin monomers polymerize via noncovalent interactions between the D and E domains with subsequent lateral aggregation promoted mainly by intermolecular cross -linking of α chains and probably by interactions between α and γ chains.3,4 A half -staggered fibrin structure forms a protofibril.Fibrin resistance to plasmin degradation is determined largely by covalent cross -linking mediated by activated factor XIII (FXIII), a transglutaminase enzyme whose formation from zymogen FXIII is catalyzed by thrombin. Active FXIII catalyzes the formation of covalent bonds between γ -γ, γ -α, and α -α chains of contiguous fibrin polypeptide chains.5 FXIII also links α 2 -antiplasmin and plasminogen activator inhibitors to fibrin to ensure clot resistance to enzymatic degradation. 5Fibrinogen and fibrin specifically bind a variety Fibrin formation and structure Fibrin is the main protein component of a blood clot and intravascular thrombi in all locations. Efficient fibrin formation and its normal functions are essential for hemostasis.1 Fibrinogen, the soluble fibrin precursor synthesized in the liver, is a 340 -kDa glycoprotein composed of 3 paired polypeptide chains (AαBβγ) 2 that are cross -linked together by 29 disulfide bonds. Fibrinogen contains 3 main structural regions connected by α -helical coils: a central E domain composed of the N -termini of all 6 polypeptide chains and 2 outer D domains with C -termini of the Bβ and γ chains. The C -terminal of the Aα chain is a globular structure located near the central E domain. Approximately 10% of total plasma fibrinogen molecules contain γ' chain, whose presence may contribute to cardiovascular disease. [1][2][3] Fibrin formation is initiated by thrombin cleavage of the Aα and Bβ chains of fibrinogen. AbsTRACTFibrin formed as a result of fibrinogen polymerization is the main protein component of a clot in a test tube and intravascular thrombi in vivo. Fibrin clot structure characterized by fiber diameter and pore size differs between healthy persons and those with thromboembolic diseases, in part due to the quality and quantity of fibrinogen and the magnitude of thrombin generation. A key measure of plasma clot structure is its permeability, reflected by the Darcy constant (K s ). Reduced K s is a typical feature of the prothrombotic fibrin clot phenotype, which is associated with faster formation of denser fibrin mesh, relatively resistant to lysis. Low K s has been reported in patients with prior or acute myocardial infarction (MI), stroke, or venous thromboembolism (encompassing deep vein thrombosis [DVT] and pulmonary embolism [PE]), as well as in those with prothrombotic conditions (eg, in several thrombophilic states) and in the presence of cardiovascular risk factors (eg, obesity). Antithrombotic and anticoagulant agents, along with statins, have been shown to increase K s . Growing evidence indic...

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“…We observed that the highest ORBIT bleeding score was associated with impaired kidney function and use of aspirin or clopidogrel that have been reported to unfavorably alter fibrin structure and function and also predispose to bleeding. 4,9 The exact mechanisms underlying these observations remain to be established. Our study supports the concept of a complex clinical and biomarker -based approach in the bleeding risk assessment in patients with AF regarding moderate prediction using schemas based only on age and comorbidities.…”

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“…Calibrated automated thrombography (Thrombinoscope BV, Maastricht, the Netherlands) was used to measure endogenous thrombin potential as described. 9 Fibrin clot permeability was measured using a pressure -driven system as described previously. 9 A permeation coefficient (Ks), which indicates the pore size in the fiber network (higher values indicate looser fibrin structure), was calculated.…”

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The ORBIT bleeding score is associated with lysis and permeability of fibrin clots

2019

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associated with plasma fibrin clot properties and thrombin generation in patients with AF. Methods We studied 100 patients with documented nonvalvular AF, derived from the cohort described in detail elsewhere. 9 Briefly, the exclusion criteria were: current anticoagulation, myocardial infarction or venous thromboembolism within the preceding 3 months, malignancy, acute infection, kidney failure requiring dialysis, and liver cirrhosis. ORBIT (hypertension, abnormal renal / liver function, stroke, bleeding history or predisposition, labile international normalized ratio, elderly [>65 years], drugs / alcohol concomitantly), 10 HEMORR 2 HAGES (hepatic or renal disease, ethanol abuse, malignancy, older [aged >75], reduced platelet count, rebleeding risk, hypertension [uncontrolled], anemia, genetic CYP 2C9 polymorphisms, excessive fall risk, stroke / TIA history), 11 HAS-BLED, 12 and modified HAS-BLED 13 scores were used to evaluate bleeding risk. The study protocol was approved by the University Ethics Committee. Standard assay techniques were used in routine laboratory investigations. N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels were measured using an immunoassay

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Elevated NT-proBNP is associated with unfavorably altered plasma fibrin clot properties in atrial fibrillation

Cited by 26 publications

References 41 publications

Association of cardiac troponin I with prothrombotic alterations in atrial fibrillation

Association of cardiac troponin I with prothrombotic alterations in atrial fibrillation

Plasma fibrin clot structure and thromboembolism: clinical implications

The ORBIT bleeding score is associated with lysis and permeability of fibrin clots

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