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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

The thromboelastography tracing curve; as the clot forms the curve expands and when the clot lyses the curve collapses. R = reaction time, α = angle, MA = maximal amplitude, TMA = time to maximal amplitude, LY = percentage amplitude reduction, CLT = clot lysis time
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Fig1: The thromboelastography tracing curve; as the clot forms the curve expands and when the clot lyses the curve collapses. R = reaction time, α = angle, MA = maximal amplitude, TMA = time to maximal amplitude, LY = percentage amplitude reduction, CLT = clot lysis time

Mentions: The parameters recorded were: reaction time (R, time till initial fibrin clot formation), angle (rapidity of fibrin clot formation), maximal amplitude (MA, strength of the fibrin clot), time to maximal amplitude (TMA), lysis after 30 and 60 min (LY30 and LY60, percentage amplitude reduction 30 and 60 min after MA, respectively), and clot lysis time (CLT, time between MA and 2 mm amplitude) (Fig. 1).Fig. 1


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)

The thromboelastography tracing curve; as the clot forms the curve expands and when the clot lyses the curve collapses. R = reaction time, α = angle, MA = maximal amplitude, TMA = time to maximal amplitude, LY = percentage amplitude reduction, CLT = clot lysis time
© Copyright Policy - OpenAccess
Related In: Results  -  Collection

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

Fig1: The thromboelastography tracing curve; as the clot forms the curve expands and when the clot lyses the curve collapses. R = reaction time, α = angle, MA = maximal amplitude, TMA = time to maximal amplitude, LY = percentage amplitude reduction, CLT = clot lysis time
Mentions: The parameters recorded were: reaction time (R, time till initial fibrin clot formation), angle (rapidity of fibrin clot formation), maximal amplitude (MA, strength of the fibrin clot), time to maximal amplitude (TMA), lysis after 30 and 60 min (LY30 and LY60, percentage amplitude reduction 30 and 60 min after MA, respectively), and clot lysis time (CLT, time between MA and 2 mm amplitude) (Fig. 1).Fig. 1

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