C-reactive protein and fibrin clot strength measured by thrombelastography after coronary stenting

Kreutz, Rolf P.; Owens, Janelle; Breall, Jeffrey A.; Lu, Dongsi; Lohe, Elisabeth von der; Bolad, Islam; Sinha, Anjan; Flockhart, David A.

doi:10.1097/mbc.0b013e32835cc193

Cited by 17 publications

(19 citation statements)

References 30 publications

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“…As previously shown in subjects with stable coronary artery disease undergoing PCI, CRP levels also correlated with plasma fibrin clot strength in patients with NSTEMI in our study (9). …”

Section: Discussionsupporting

confidence: 89%

“…Both plasma fibrinogen and C-reactive protein were measured by commercially available ELISA as previously described (9). …”

Section: Methodsmentioning

confidence: 99%

“…However, inhibition of platelet activation by clopidogrel may affect plasma fibrin clot strength in addition to platelet inhibition. We have previously demonstrated that inflammation measured by C-reactive protein in patients with stable coronary artery disease is associated with heightened plasma fibrin clot strength (9). We hypothesized that in patients with acute coronary syndromes high fibrin clot strength was predominant contributor to thrombin induced whole blood clot strength, a measure previously shown to be associated with increased rate of adverse ischemic events.…”

Section: Introductionmentioning

confidence: 99%

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Plasma and Whole Blood Clot Strength Measured by Thrombelastography in Patients Treated with Clopidogrel during Acute Coronary Syndromes

Owens

Kreutz

2013

Thrombosis Research

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Introduction Treatment with clopidogrel, a selective platelet P2Y12 receptor antagonist, reduces risk of recurrent ischemic events in patients with acute coronary syndrome (ACS), by limiting platelet aggregation and activation. Stable whole blood clot formation requires activation of platelets, generation of fibrin and final fibrin crosslinks. In this study we intended to compare plasma and whole blood thrombelastography (TEG) measurements in patients during ACS. Materials and Methods Whole blood and plasma samples from 32 patients with nonST segment elevation myocardial infarction (NSTEMI) were collected after administration of clopidogrel. Whole blood and plasma fibrin clot strength (MA) were determined by TEG. Platelet aggregation was determined by light transmittance aggregometry (LTA) using adenosine 5′-diphosphate (ADP), thrombin receptor activation peptide (TRAP), or collagen as agonists. Fibrinogen and C-reactive protein (CRP) concentrations were measured by ELISA. Results Heightened plasma fibrin clot strength was associated with increased platelet reactivity stimulated by ADP (ρ=0.536; p=0.002), TRAP (ρ=0.481; p=0.007), and collagen (ρ=0.538; p=0.01). In contrast to plasma fibrin MA, whole blood MA did not correlate with platelet aggregation. Platelet count was the primary contributor to the difference in thrombin induced whole blood MA and plasma fibrin MA. Increasing levels of CRP were associated with increased plasma fibrin clot strength and platelet reactivity. Conclusions Our data suggest that inflammation is associated with increased plasma fibrin clot strength and lower platelet inhibition by clopidogrel during ACS. Platelet count is main contributor to additional contractile force of whole blood TEG as compared to plasma TEG during treatment with clopidogrel.

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“…As previously shown in subjects with stable coronary artery disease undergoing PCI, CRP levels also correlated with plasma fibrin clot strength in patients with NSTEMI in our study (9). …”

Section: Discussionsupporting

confidence: 89%

“…Both plasma fibrinogen and C-reactive protein were measured by commercially available ELISA as previously described (9). …”

Section: Methodsmentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Plasma and Whole Blood Clot Strength Measured by Thrombelastography in Patients Treated with Clopidogrel during Acute Coronary Syndromes

Owens

Kreutz

2013

Thrombosis Research

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“…Also, platelets have relevant functions in inflammation and it has been shown that thrombosis and inflammation share several key molecular mechanisms and linked processes [23]. Similarly, MPV has been investigated in connection with both thrombosis and inflammation [24] and elevated CRP may be linked to procoagulant changes and high tensile fibrin clot strength independent of fibrinogen concentration [25]. This may favor the deleterious process of plaque vulnerability and thrombus formation [26] which may explain also the higher incidence of thrombosis complications seen in hypoxemic CHD patients.…”

Section: Discussionmentioning

confidence: 98%

Thrombocytopenia in congenital heart disease patients

Martínez‐Quintana

Rodríguez‐González

2014

Platelets

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Thrombocytopenia has been identified as a mechanism of the increased incidence of thromboembolism and death in hypoxemic congenital heart disease (CHD) patients. About 387 CHD patients (344 non-hypoxemic and 43 hypoxemic) were followed-up during a median of 34.3 (24.5; 49.9) months. Demographic, clinical, analytical parameters, and survival curves between CHD with platelet levels above and below 150,000/μl were determined. On one hand, in the subgroup of non-hypoxemic CHD patients, 8 out of 344 (2.3%) patients showed some type of bleeding and 8 (2.3%) patients showed some type of thrombosis. On the other hand, in the hypoxemic subgroup, 6 out of 43 (13.9%) patients had some type of bleeding and 5 (11.6%) patients showed some type of thrombosis. The binary logistic regression multivariate analysis being under oral anticoagulation/antiplatelet therapy (OR, 4.192 (1.207-14.550), p = 0.024) and having hypoxemia (OR, 4.041 (1.087-15.029); p = 0.037) favored the occurrence of bleeding. Meanwhile, the only factor which favored thrombosis was being hypoxemic (OR, 5.703 (1.334-24.387); p = 0.019). Also, being hypoxemic (OR, 0.217 (0.070-0.670), p = 0.008) and having a high MPV (OR, 0.534 (0.383-0.744); p = 0.001) favored a low platelet count (< 150 × 10(3)/µl). Kaplan-Meier survival analysis showed significant differences between CHD patients with a platelet count lower and higher than 150 × 10(3)/μl (p = 0.009). Bleeding and thrombotic complications are more frequent in hypoxemic CHD patients irrespective of platelet counts. Larger platelets, as reflected by an increased mean platelet volume, and the higher CRP concentration seen in hypoxemic CHD patients may explain to some extent the higher incidence of thrombotic events in hypoxemic patients.

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“…During acute coronary syndromes (ACS), activation of coagulation and thrombin generation is a central step preceding coronary thrombosis and treatment with heparin or low molecular weight heparin is standard of care in the initial in-hospital management of ACS [4]. Risk associated with continued prothrombotic changes related to vascular inflammation may be an important mediator of long term recurrent risk of ischemic events in patients with coronary stenting [5–10]. While large scale efforts have been directed at identifying genetic variants causally linked to the development of coronary artery disease, fewer efforts have been directed specifically at identifying single nucleotide polymorphisms (SNPs) associated with recurrent ischemic risk in patients with established coronary artery disease [11].…”

Section: Introductionmentioning

confidence: 99%

Factor XIII Val34Leu polymorphism and recurrent myocardial infarction in patients with coronary artery disease

Kreutz

Bitar

Owens

et al. 2014

J Thromb Thrombolysis

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Factor XIII (FXIII) is necessary for cross linking of fibrin strands and generation of stable fibrin clot. FXIII Val34Leu is a common genetic single nucleotide polymorphism that has been associated with accelerated fibrin stabilization and reduced rate of fibrinolysis. The contribution of Val34Leu to long term risk of recurrent myocardial infarction (MI) in patients with coronary stenting has not been conclusively established. The objective of the study was to examine the effects of Val34Leu on fibrin generation, platelet aggregation, and long term clinical outcomes in patients with coronary artery disease treated with dual antiplatelet therapy. Patients with angiographically documented coronary artery disease who were treated with aspirin and clopidogrel were enrolled (n = 211). Light transmittance aggregometry and plasma fibrin clot formation using thrombelastography (TEG) were determined. Genotyping of Val34Leu was performed using Taqman assay. Clinical events during follow up were recorded. Homozygous carriers of 34Leu variant had significantly shorter fibrin clot formation time as compared to wild type individuals (TEG K: 1.27 ± 0.3 vs. 1.68 ± 1.1 min, p = 0.011). The Val34Leu variant was associated with gene dose dependent increased risk of MI (log rank, p = 0.002) or occurrence of composite of MI and CV death (log rank, p = 0.005) with highest event rates observed in homozygous carriers of 34Leu. In summary, FXIII Val34Leu polymorphism was associated with increased rate of fibrin stabilization in homozygous carriers of the variant and may increase risk of recurrent MI and death in patients with angiographically established coronary artery disease treated with dual antiplatelet therapy.

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C-reactive protein and fibrin clot strength measured by thrombelastography after coronary stenting

Cited by 17 publications

References 30 publications

Plasma and Whole Blood Clot Strength Measured by Thrombelastography in Patients Treated with Clopidogrel during Acute Coronary Syndromes

Plasma and Whole Blood Clot Strength Measured by Thrombelastography in Patients Treated with Clopidogrel during Acute Coronary Syndromes

Thrombocytopenia in congenital heart disease patients

Factor XIII Val34Leu polymorphism and recurrent myocardial infarction in patients with coronary artery disease

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