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Homocysteine activates platelets in vitro.

Irwin V Mohan¹, I Anita Jagroop, Dimitri P Mikhailidis

¹Academic Surgical Unit, Imperial College at St Mary's, London, UK. irwin.mohan@doctors.org.uk

Clinical and Applied Thrombosis/Hemostasis : Official Journal of the International Academy of Clinical and Applied Thrombosis/Hemostasis

|December 28, 2007

Summary

Elevated homocysteine activates platelets and increases blood clotting, particularly in critical limb ischemia patients. This occurs indirectly at homocysteine levels around 50 micromol/L.

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Area of Science:

Cardiovascular Science
Hematology
Biochemistry

Background:

Hyperhomocysteinemia is linked to thrombogenicity, but the exact mechanism is debated.
Understanding homocysteine's impact on platelet function and coagulation is crucial for managing vascular disease.

Purpose of the Study:

To investigate the association between elevated plasma homocysteine levels and platelet activation.
To examine the effect of homocysteine on blood coagulation and red blood cell integrity.

Main Methods:

Blood samples from healthy subjects and critical limb ischemia patients were analyzed.
Platelet aggregation, P-selectin, and Glycoprotein IIb/IIIa expression were assessed via flow cytometry.
Thromboelastography and lactate dehydrogenase measurements were performed to evaluate coagulation and red blood cell integrity.

Main Results:

Homocysteine exposure induced platelet activation and hypercoagulability in vitro.
These prothrombotic effects were more pronounced in patients with critical limb ischemia.
The observed changes in platelet function occurred indirectly at homocysteine concentrations around 50 micromol/L.

Conclusions:

Elevated homocysteine levels contribute to a prothrombotic state through platelet activation and enhanced coagulation.
Critical limb ischemia patients exhibit heightened sensitivity to homocysteine's thrombotic effects.
Homocysteine's prothrombotic action on platelets appears to be indirect.