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Coagulation changes during presyncope and recovery.

Gerhard Cvirn¹, Axel Schlagenhauf, Bettina Leschnik

¹Institute of Physiological Chemistry, Medical University of Graz, Graz, Austria.

|August 10, 2012

Summary

This summary is machine-generated.

Orthostatic stress causes significant changes in blood coagulation, leading to increased coagulability during recovery from presyncope. This sustained hypercoagulability may pose a risk for thromboembolic events in susceptible individuals.

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Area of Science:

Physiology
Cardiovascular Science
Hematology

Background:

Orthostatic stress activates the coagulation system, but the extent of activation during presyncope is not fully understood.
Presyncope, a near-fainting state, is induced by orthostatic challenges like head-up tilt and lower body negative pressure.

Purpose of the Study:

To investigate coagulation system activation during presyncope induced by combined head-up tilt (HUT) and lower body negative pressure (LBNP).
To assess coagulation changes during orthostatic stress and recovery, and their relationship to hemoconcentration.

Main Methods:

Healthy males underwent HUT and LBNP to induce presyncope, with measurements taken before, during, and after stress.
Coagulation parameters assessed included thrombelastometry, platelet aggregation, endogenous thrombin potential, endothelial activation markers, and thrombin generation markers.
Blood cell counts and plasma mass density were measured to account for volume changes.

Main Results:

Presyncope resulted in a 25% plasma volume loss and increased blood cell counts, prothrombin, and thrombin levels, consistent with hemoconcentration.
Markers of endothelial activation and thrombin generation (F1+2, TAT) increased significantly beyond the hemoconcentration effect.
While endothelial markers normalized during recovery, F1+2 and TAT remained elevated, indicating persistent hypercoagulability.

Conclusions:

Presyncope induces significant coagulation activation and sustained hypercoagulability during recovery, exceeding changes due to hemoconcentration alone.
This post-presyncope hypercoagulability could be a risk factor for thromboembolic events, especially in individuals with pre-existing cardiovascular conditions.