Reduced clot permeability and susceptibility to lysis in patients with acute coronary syndrome: Effects of inflammation and oxidative stress

Undas, Anetta; Szułdrzyński, Konstanty; Stępień, Ewa; Zalewski, J; Godlewski, Jacek; Tracz, Wiesława; Pasowicz, Mieczysław; Żmudka, Krzysztof

doi:10.1016/j.atherosclerosis.2007.05.028

Cited by 176 publications

(197 citation statements)

References 23 publications

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“…Glycation of the fibrinogen molecules is largely responsible for altered fibrin clot features found at elevated glucose levels (10,11). We extended previous observations by showing a potent impact of diabetes on fibrin properties, easily detectable also in myocardial infarction patients despite the fact that acute myocardial ischemia itself is associated with deleterious clot alterations similar to those described in diabetic patients (12). A short-term increase in glucose levels does not modify fibrin structure, which explains the similar permeability observed in the HG and NG groups.…”

Section: Short-term Outcomessupporting

confidence: 72%

“…Moreover, hyperglycemia, both in diabetic patients and under in vitro conditions, is linked to unfavorably altered fibrin clot properties and reduced fibrinolysis compared with the results at normoglycemia (10,11). Recently, we have showed that in patients with acute myocardial infarction, a history of type 2 diabetes is associated with impaired plasma clot permeability and fibrinolysis (12). The effect of hyperglycemia on clot properties in acute myocardial infarction patients with no history of diabetes has not been investigated yet.…”

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confidence: 99%

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Hyperglycemia Is Associated With Enhanced Thrombin Formation, Platelet Activation, and Fibrin Clot Resistance to Lysis in Patients With Acute Coronary Syndrome

et al. 2008

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OBJECTIVE -Acute hyperglycemia on admission for acute coronary syndrome worsens the prognosis in patients with and without known diabetes. Postulated mechanisms of this observation include prothrombotic effects. The aim of this study was to evaluate the effect of elevated glucose levels on blood clotting in acute coronary syndrome patients.RESEARCH DESIGN AND METHODS -We studied 60 acute coronary syndrome patients within the first 12 h after pain onset, including 20 subjects with type 2 diabetes, 20 subjects with no diagnosed diabetes but with glucose levels Ͼ7.0 mmol/l, and 20 subjects with glucose levels Ͻ7.0 mmol/l. We determined generation of thrombin-antithrombin complexes (TATs) and soluble CD40 ligand (sCD40L), a platelet activation marker, at the site of microvascular injury, together with ex vivo plasma fibrin clot permeability and lysis time.RESULTS -The acute coronary syndrome patients with no prior diabetes but elevated glucose levels had increased maximum rates of formation and total production of TATs (by 42.9%, P Ͻ 0.0001, and by 25%, P Ͻ 0.0001, respectively) as well as sCD40L release (by 16.2%, P ϭ 0.0011, and by 16.3%, P Ͻ 0.0001, respectively) compared with those with normoglycemia, whereas diabetic patients had the highest values of TATs and sCD40L variables (P Ͻ 0.0001 for all comparisons). Patients with hyperglycemia, with no previously diagnosed diabetes, had longer clot lysis time (by ϳ18%, P Ͻ 0.0001) similar to that in diabetic subjects, but not lower clot permeability compared with that in normoglycemic subjects.CONCLUSIONS -Hyperglycemia in acute coronary syndrome is associated with enhanced local thrombin generation and platelet activation, as well as unfavorably altered clot features in patients with and without a previous history of diabetes.

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Section: Short-term Outcomessupporting

confidence: 72%

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confidence: 99%

Hyperglycemia Is Associated With Enhanced Thrombin Formation, Platelet Activation, and Fibrin Clot Resistance to Lysis in Patients With Acute Coronary Syndrome

et al. 2008

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“…All specimens were analysed under a Zeiss SEM (FEI, USA) at a magnification of 10,000 ×, which could detect an individual fiber. Fiber structural parameters (thickness and density) were further measured using the Image J software (version 1.43) according to a modified method of Undas et al (Undas et al, 2008). For quantitative analysis of the pore sizes in fibrin clots, the thresholding algorithm (0, 60) was run to highlight the black areas (no fibers).…”

Section: Scanning Electron Microscopy (Sem)mentioning

confidence: 99%

“…The specimens were then mounted on aluminium stubs and coated with gold-palladium, and micrographs captured by SEM (FEI, USA). Representative images were captured at 5,000× magnification and the images analysed using a method described previously (Neergaard-Petersen et al, 2013;Undas et al, 2008). Fiber thickness and density were assessed from SEM images using image analysis software package Image J (version 1.43).…”

Section: Scanning Electron Microscopymentioning

confidence: 99%

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Manipulating fibrin structure of hematomas enhances large bone defects healing

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Patients with paroxysmal nocturnal hemoglobinuria demonstrate a prothrombotic clotting phenotype which is improved by complement inhibition with eculizumab

et al. 2020

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Paroxysmal nocturnal hemoglobinuria (PNH) is a rare hematological disorder, characterized by complement‐mediated intravascular hemolysis and thrombosis. The increased incidence of PNH‐driven thrombosis is still poorly understood, but unlike other thrombotic disorders, is thought to largely occur through complement‐mediated mechanisms. Treatment with a C5 inhibitor, eculizumab, has been shown to significantly reduce the number of thromboembolic events in these patients. Based on previously described links between changes in fibrin clot structure and thrombosis in other disorders, our aim was to investigate clot structure as a possible mechanism of thrombosis in patients with PNH and the anti‐thrombotic effects of eculizumab treatment on clot structure. Clot structure, fibrinogen levels and thrombin generation were examined in plasma samples from 82 patients from the National PNH Service in Leeds, UK. Untreated PNH patients were found to have increased levels of fibrinogen and thrombin generation, with subsequent prothrombotic changes in clot structure. No link was found between increasing disease severity and fibrinogen levels, thrombin generation, clot formation or structure. However, eculizumab treated patients showed decreased fibrinogen levels, thrombin generation and clot density, with increasing time spent on treatment augmenting these antithrombotic effects. These data suggest that PNH patients have a prothrombotic clot phenotype due to increased fibrinogen levels and thrombin generation, and that the antithrombotic effects of eculizumab are, in‐part, due to reductions in fibrinogen and thrombin generation with downstream effects on clot structure.

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Reduced clot permeability and susceptibility to lysis in patients with acute coronary syndrome: Effects of inflammation and oxidative stress

Cited by 176 publications

References 23 publications

Hyperglycemia Is Associated With Enhanced Thrombin Formation, Platelet Activation, and Fibrin Clot Resistance to Lysis in Patients With Acute Coronary Syndrome

Hyperglycemia Is Associated With Enhanced Thrombin Formation, Platelet Activation, and Fibrin Clot Resistance to Lysis in Patients With Acute Coronary Syndrome

Manipulating fibrin structure of hematomas enhances large bone defects healing

Patients with paroxysmal nocturnal hemoglobinuria demonstrate a prothrombotic clotting phenotype which is improved by complement inhibition with eculizumab

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