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Thromboelastography on plasma reveals delayed clot formation and accelerated clot lyses in HIV-1 infected persons compared with healthy controls.

Rönsholt FF, Gerstoft J, Ullum H, Johansson PI, Katzenstein TL, Ostrowski SR - BMC Infect. Dis. (2015)

Bottom Line: In 67 successfully long-term treated HIV+ and 15 CON we analyzed stored plasma samples by TEG, with or without addition of tissue-type plasminogen activator (tPA), and measured levels of C-reactive protein, thrombomodulin, syndecan-1, sVE-cadherin, soluble CD40 ligand (sCD40L), adrenaline and noradrenaline.Compared to CON, HIV+ had delayed clot formation (reaction (R)-time 14.2 min. vs. 11.2 min., p = 0.0004) and reduced clot formation rapidity (angle 22.6° vs. 48.6°, p = <0.0001).Plasma from long-term treated HIV infected persons displays a hypocoagulable profile with reduced fibrinolytic resistance as compared to healthy controls.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases 8632, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, 2100, Copenhagen Ø, Denmark. frederikkefr@gmail.com.

ABSTRACT

Background: Thromboembolic events among HIV infected persons are a recognized clinical problem but the underlying mechanisms are poorly understood. To assess whether coagulation and fibrinolysis differ between long-term treated HIV infected individuals (HIV+) and healthy controls (CON), we investigated functional plasma coagulation by thrombelastography (TEG) and plasma markers of endothelial and platelet activation.

Methods: In 67 successfully long-term treated HIV+ and 15 CON we analyzed stored plasma samples by TEG, with or without addition of tissue-type plasminogen activator (tPA), and measured levels of C-reactive protein, thrombomodulin, syndecan-1, sVE-cadherin, soluble CD40 ligand (sCD40L), adrenaline and noradrenaline.

Results: Compared to CON, HIV+ had delayed clot formation (reaction (R)-time 14.2 min. vs. 11.2 min., p = 0.0004) and reduced clot formation rapidity (angle 22.6° vs. 48.6°, p = <0.0001). Clot lyses induced by tPA was accelerated in HIV+ displaying enhanced clot degradation after 30 and 60 min (53.9% vs. 24.2%, p < 0.0001 and 77.4% vs. 59.9%, p < 0.0001, respectively). sCD40L and TEG R-time correlated negatively in both HIV+ and CON (Rho =-0.502, p < 0.001 and rho =-0.651, p = 0.012).

Discussion: No previous studies have examined plasma coagulation by TEG in HIV, however, we have previously demonstrated that HIV+ display hypocoagulability in whole blood by TEG in accordance with the results of this study. Others have reported of HIV associated changes in the hemostatic system in a pro-coagulant direction based on measurements of isolated components of the coagulation pahways. In disease conditions, the flowing blood may change from "normal" to hyper- or hypocoagulant or to hyper- or hypofibrinolytic. A balance may exist in the flowing blood, i.e. between blood cells and the plasma phase, so that pro-coagulant blood cells are balanced by a hypocoagulable plasma phase; thus alterations that may promote thromboembolic events in the patient may at the same time appear as a hypocoagulable profile when evaluated in vitro.

Conclusion: Plasma from long-term treated HIV infected persons displays a hypocoagulable profile with reduced fibrinolytic resistance as compared to healthy controls.

No MeSH data available.


Related in: MedlinePlus

Plasma concentrations of soluble markers of endothelial function, sympathoadrenal activation, and platelet activation. Please note different ranges, scales, and units on Y axes
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Fig3: Plasma concentrations of soluble markers of endothelial function, sympathoadrenal activation, and platelet activation. Please note different ranges, scales, and units on Y axes

Mentions: HIV+ and controls had comparable levels of HS CRP, syndecan-1, thrombomodulin, sVE-Cadherin, sCD40L, adrenaline, and noradrenaline (Fig. 3) and these markers were similar in HIV+ stratified by history of smoking (ever vs. never), current HIV RNA levels, and current CD4-count (data not shown).Fig. 3


Thromboelastography on plasma reveals delayed clot formation and accelerated clot lyses in HIV-1 infected persons compared with healthy controls.

Rönsholt FF, Gerstoft J, Ullum H, Johansson PI, Katzenstein TL, Ostrowski SR - BMC Infect. Dis. (2015)

Plasma concentrations of soluble markers of endothelial function, sympathoadrenal activation, and platelet activation. Please note different ranges, scales, and units on Y axes
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

License 1 - License 2
Show All Figures
getmorefigures.php?uid=PMC4581408&req=5

Fig3: Plasma concentrations of soluble markers of endothelial function, sympathoadrenal activation, and platelet activation. Please note different ranges, scales, and units on Y axes
Mentions: HIV+ and controls had comparable levels of HS CRP, syndecan-1, thrombomodulin, sVE-Cadherin, sCD40L, adrenaline, and noradrenaline (Fig. 3) and these markers were similar in HIV+ stratified by history of smoking (ever vs. never), current HIV RNA levels, and current CD4-count (data not shown).Fig. 3

Bottom Line: In 67 successfully long-term treated HIV+ and 15 CON we analyzed stored plasma samples by TEG, with or without addition of tissue-type plasminogen activator (tPA), and measured levels of C-reactive protein, thrombomodulin, syndecan-1, sVE-cadherin, soluble CD40 ligand (sCD40L), adrenaline and noradrenaline.Compared to CON, HIV+ had delayed clot formation (reaction (R)-time 14.2 min. vs. 11.2 min., p = 0.0004) and reduced clot formation rapidity (angle 22.6° vs. 48.6°, p = <0.0001).Plasma from long-term treated HIV infected persons displays a hypocoagulable profile with reduced fibrinolytic resistance as compared to healthy controls.

View Article: PubMed Central - PubMed

Affiliation: Department of Infectious Diseases 8632, Copenhagen University Hospital Rigshospitalet, Blegdamsvej 9, 2100, Copenhagen Ø, Denmark. frederikkefr@gmail.com.

ABSTRACT

Background: Thromboembolic events among HIV infected persons are a recognized clinical problem but the underlying mechanisms are poorly understood. To assess whether coagulation and fibrinolysis differ between long-term treated HIV infected individuals (HIV+) and healthy controls (CON), we investigated functional plasma coagulation by thrombelastography (TEG) and plasma markers of endothelial and platelet activation.

Methods: In 67 successfully long-term treated HIV+ and 15 CON we analyzed stored plasma samples by TEG, with or without addition of tissue-type plasminogen activator (tPA), and measured levels of C-reactive protein, thrombomodulin, syndecan-1, sVE-cadherin, soluble CD40 ligand (sCD40L), adrenaline and noradrenaline.

Results: Compared to CON, HIV+ had delayed clot formation (reaction (R)-time 14.2 min. vs. 11.2 min., p = 0.0004) and reduced clot formation rapidity (angle 22.6° vs. 48.6°, p = <0.0001). Clot lyses induced by tPA was accelerated in HIV+ displaying enhanced clot degradation after 30 and 60 min (53.9% vs. 24.2%, p < 0.0001 and 77.4% vs. 59.9%, p < 0.0001, respectively). sCD40L and TEG R-time correlated negatively in both HIV+ and CON (Rho =-0.502, p < 0.001 and rho =-0.651, p = 0.012).

Discussion: No previous studies have examined plasma coagulation by TEG in HIV, however, we have previously demonstrated that HIV+ display hypocoagulability in whole blood by TEG in accordance with the results of this study. Others have reported of HIV associated changes in the hemostatic system in a pro-coagulant direction based on measurements of isolated components of the coagulation pahways. In disease conditions, the flowing blood may change from "normal" to hyper- or hypocoagulant or to hyper- or hypofibrinolytic. A balance may exist in the flowing blood, i.e. between blood cells and the plasma phase, so that pro-coagulant blood cells are balanced by a hypocoagulable plasma phase; thus alterations that may promote thromboembolic events in the patient may at the same time appear as a hypocoagulable profile when evaluated in vitro.

Conclusion: Plasma from long-term treated HIV infected persons displays a hypocoagulable profile with reduced fibrinolytic resistance as compared to healthy controls.

No MeSH data available.


Related in: MedlinePlus