Platelet function in mitochondriopathy with stroke and stroke-like episodes

Nicole Kotzailias; Josef Finsterer; Maria Zellner; Claudia Marsik; Tanja Dukic; Bernd Jilma

doi:10.1160/TH03-03-0156

Thrombosis and Haemostasis, Table of Contents

Thromb Haemost 2004; 91(03): 544-552
DOI: 10.1160/TH03-03-0156

Platelets and Blood Cells

Schattauer GmbH

Platelet function in mitochondriopathy with stroke and stroke-like episodes

Authors

Nicole Kotzailias

¹Department of Clinical Pharmacology, Vienna University, Vienna, Austria

⁴Department of Neurology, Neurological Rehabilitation, Vienna University, Vienna, Austria Trial Center: Department of Clinical Pharmacology, University of Vienna, Austria
Josef Finsterer

²Department of Neurology, Neurological Hospital Rudolfstiftung, Vienna, Austria
Maria Zellner

³Department of Surgical Research, Vienna University, Austria
Claudia Marsik

¹Department of Clinical Pharmacology, Vienna University, Vienna, Austria
Tanja Dukic

¹Department of Clinical Pharmacology, Vienna University, Vienna, Austria
Bernd Jilma

¹Department of Clinical Pharmacology, Vienna University, Vienna, Austria

Abstract

Summary

Stroke and stroke-like episodes are frequent complications in mitochondriopathy, particulary in MELAS syndrome (mitochondrial myopathy, encephalopathy, lactic acidosis and stroke like episodes) which is a disorder of the mitochondrial oxidative metabolism in diverse cell types. To clarify a possible pathological aspect of stroke in these patients, we investigated platelet function before and after physical exercise. Ten patients with mitochondriopathy and stroke and ten healthy sex and age matched controls were investigated in an analyst blinded, prospective cross-sectional trial. Exercise decreased intraplatelet adenosine triphosphate (ATP) concentrations by -22% from baseline in patients with mitochondriopathy (p<0.01 between groups) while exercise increased ATP-levels by 28% healthy controls (p=0.01 vs baseline). Thrombin receptor activating peptide (TRAP) stimulated P-selectin expression increased up to 50% (p<0.05) in healthy subjects following exercise compared to 39% (p>0.05) in patients with mitochondriopathy. Exercise trendwise decreased platelet plug formation under shear stress by 24% in patients as measured by the platelet function analyzer PFA-100®. Tromboelastography showed firm thrombus formation and delayed lysis in patients following exercise. In conclusion, this trial has shown that ATP depletion during and after exercise probably accounts for a defective oxidative metabolism in platelets of patients with mitochondriopathy and stroke. This might induce decreased platelet function in these patients but fails to explain the increased stroke rate. Therefore other mechanisms seem to be etiologically involved in the pathogenesis of stroke in patients with mitochondriopathy.

Keywords

Platelet function - ATP - exercise - mitochondriopathy - stroke

Full Text

References

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