Platelet hyperactivity and fibrin clot structure in transient ischemic attack individuals in the presence of metabolic syndrome: a microscopy and thromboelastography study

Strokes are commonly preceded by transient ischemic attacks (TIAs). TIA is often associated with metabolic syndrome (causing chronic inflammation), resulting in a proinflammatory- and procoagulant-environment. The aim of this study was to determine whether platelet- and fibrin network-morphology or...

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Veröffentlicht in:Cardiovascular Diabetology 2015-07, Vol.14 (1), p.86-86, Article 86
Hauptverfasser: van Rooy, Mia-Jeanne, Duim, Wiebren, Ehlers, Rene, Buys, Antoinette V, Pretorius, Etheresia
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container_start_page 86
container_title Cardiovascular Diabetology
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creator van Rooy, Mia-Jeanne
Duim, Wiebren
Ehlers, Rene
Buys, Antoinette V
Pretorius, Etheresia
description Strokes are commonly preceded by transient ischemic attacks (TIAs). TIA is often associated with metabolic syndrome (causing chronic inflammation), resulting in a proinflammatory- and procoagulant-environment. The aim of this study was to determine whether platelet- and fibrin network-morphology or coagulation profiles of individuals that suffered a TIA in the presence of metabolic syndrome was altered when compared to healthy individuals. The study consisted of 40 voluntary participants. Twenty individuals that suffered a TIA in the previous 48 h with at least two metabolic syndrome risk factors present and twenty healthy age-matched controls. Scanning electron- and atomic force microscopy was used to study platelet- and fibrin-morphology, atomic force microscopy was used to study platelet- and fibrin fiber-elasticity and thromboelastography for the study of coagulation profiles. Statistical analysis was performed to compare the two groups. In all cases a p-value of less than 0.05 was considered statistically significant. Platelets of the control group appeared spherical with few pseudopodia present while the platelets of the TIA individuals presented with numerous pseudopodia and spreading, indicating activation. Platelet aggregation was also present. The fibrin networks of the healthy individuals consist of thick and thin fibers that form an organized network of fibers. The fibrin networks of the TIA individuals appeared less organized with less taut fibers. Fibrin fiber thickness was found to be significantly increased in the TIA group (p-value  0.05) from the healthy controls, indicating a normal functioning coagulation cascade. The findings indicate that pathological clot formation is not caused by alterations in the coagulation cascade but rather by the premature activation of platelets (as a result of chronic inflammation) that in turn causes altered fibrin formation.
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TIA is often associated with metabolic syndrome (causing chronic inflammation), resulting in a proinflammatory- and procoagulant-environment. The aim of this study was to determine whether platelet- and fibrin network-morphology or coagulation profiles of individuals that suffered a TIA in the presence of metabolic syndrome was altered when compared to healthy individuals. The study consisted of 40 voluntary participants. Twenty individuals that suffered a TIA in the previous 48 h with at least two metabolic syndrome risk factors present and twenty healthy age-matched controls. Scanning electron- and atomic force microscopy was used to study platelet- and fibrin-morphology, atomic force microscopy was used to study platelet- and fibrin fiber-elasticity and thromboelastography for the study of coagulation profiles. Statistical analysis was performed to compare the two groups. In all cases a p-value of less than 0.05 was considered statistically significant. Platelets of the control group appeared spherical with few pseudopodia present while the platelets of the TIA individuals presented with numerous pseudopodia and spreading, indicating activation. Platelet aggregation was also present. The fibrin networks of the healthy individuals consist of thick and thin fibers that form an organized network of fibers. The fibrin networks of the TIA individuals appeared less organized with less taut fibers. Fibrin fiber thickness was found to be significantly increased in the TIA group (p-value &lt;0.001) when compared to healthy controls. The thicker fibers formed irregular networks with thick masses of fibrin fibers. Platelet and fibrin fiber elasticity was found to be significantly lower in the experimental group (p-value 0.0042 and p-value 0.0007 respectively). The hemostatic profiles of the diseased individuals did not differ significantly (p-value &gt; 0.05) from the healthy controls, indicating a normal functioning coagulation cascade. The findings indicate that pathological clot formation is not caused by alterations in the coagulation cascade but rather by the premature activation of platelets (as a result of chronic inflammation) that in turn causes altered fibrin formation.</abstract><cop>England</cop><pub>BioMed Central Ltd</pub><pmid>26140921</pmid><doi>10.1186/s12933-015-0249-5</doi><tpages>1</tpages><orcidid>https://orcid.org/0000-0002-9108-2384</orcidid><oa>free_for_read</oa></addata></record>
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subjects Adult
Aged
Atomic force microscopy
Blood Coagulation
Blood Platelets - metabolism
Blood Platelets - ultrastructure
Care and treatment
Case-Control Studies
Cerebral ischemia
Comparative analysis
Complications and side effects
Elasticity
Female
Fibrin - metabolism
Fibrin - ultrastructure
Fibrinolysis
Humans
Ischemic Attack, Transient - blood
Ischemic Attack, Transient - complications
Ischemic Attack, Transient - diagnosis
Male
Metabolic Syndrome - blood
Metabolic Syndrome - complications
Metabolic Syndrome - diagnosis
Microscopy, Atomic Force
Microscopy, Electron, Scanning
Middle Aged
Original Investigation
Platelet Activation
Platelet Aggregation
Predictive Value of Tests
Risk Factors
Thrombelastography
title Platelet hyperactivity and fibrin clot structure in transient ischemic attack individuals in the presence of metabolic syndrome: a microscopy and thromboelastography study
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