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Platelet function in mitochondriopathy with stroke and stroke-like episodes
Nicole Kotzailias1, Josef Finsterer, Maria Zellner
1Department of Clinical Pharmacology-TARGET, Vienna University School of Medicine, Währinger Gürtel 18-20, A-1090, Vienna, Austria. nicole.hergovich@univie.ac.at
Thrombosis and Haemostasis
|February 26, 2004
Summary
Exercise depletes adenosine triphosphate (ATP) in platelets of patients with mitochondriopathy, impacting platelet function. However, this ATP depletion does not fully explain the increased stroke risk in these individuals.
Area of Science:
- Mitochondrial Medicine
- Neurology
- Hematology
Background:
- Mitochondriopathy, including MELAS syndrome, frequently causes stroke-like episodes due to impaired mitochondrial oxidative metabolism.
- The precise pathological mechanisms linking mitochondriopathy to stroke remain unclear.
Purpose of the Study:
- To investigate platelet function alterations in patients with mitochondriopathy and stroke before and after physical exercise.
- To explore the role of adenosine triphosphate (ATP) levels and platelet activation in exercise-induced stroke pathogenesis.
Main Methods:
- A prospective, cross-sectional trial involving 10 patients with mitochondriopathy and stroke and 10 healthy controls.
- Measurement of intraplatelet ATP concentrations, P-selectin expression (platelet activation), platelet plug formation (PFA-100), and thrombus formation/lysis (thromboelastography) before and after exercise.
Main Results:
- Exercise significantly decreased intraplatelet ATP levels in patients (-22%) but increased them in controls (+28%).
- Platelet activation (P-selectin) showed a trend towards a blunted response in patients post-exercise.
- Exercise led to decreased platelet plug formation and increased thrombus formation/lysis in patients, suggesting altered platelet function.
Conclusions:
- Exercise-induced ATP depletion in platelets likely contributes to defective oxidative metabolism in mitochondriopathy patients.
- While altered platelet function is observed, it does not fully account for the elevated stroke incidence in these patients.
- Additional, yet unidentified, mechanisms are likely involved in the pathogenesis of stroke in mitochondriopathy.