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Succinate links atrial dysfunction and cardioembolic stroke.

Sarah E Nelson1, Zsuzsanna Ament1, Zoe Wolcott1

  • 1From the Departments of Neurology and Anesthesiology/Critical Care Medicine (S.E.N.), Johns Hopkins Hospital, Baltimore, MD; Center for Genomic Medicine (Z.A., Z.W., W.T.K.) and Division of Neurocritical Care and Emergency Neurology, Department of Neurology (Z.A., Z.W., W.T.K.), Massachusetts General Hospital, Harvard Medical School; and Division of Cardiovascular Medicine (R.E.G.), Beth Israel Deaconess Hospital, Boston, MA.

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Summary
This summary is machine-generated.

Altered levels of succinate, α-ketoglutarate, and malate are linked to cardioembolic (CE) stroke and atrial dysfunction. These metabolic changes may indicate an underlying connection between energy metabolism and CE stroke risk.

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Area of Science:

  • Biochemistry
  • Cardiology
  • Neurology

Background:

  • Cardioembolic (CE) stroke is a significant cause of morbidity and mortality.
  • Atrial dysfunction is a known risk factor for CE stroke.
  • The underlying mechanisms linking atrial dysfunction to CE stroke remain incompletely understood.

Purpose of the Study:

  • To investigate whether altered metabolic profiles mediate the relationship between atrial dysfunction and CE stroke.
  • To explore the association between specific metabolites, atrial dysfunction markers, and stroke recurrence risk.

Main Methods:

  • Plasma samples from 367 acute stroke patients were analyzed for 144 metabolites using liquid chromatography-tandem mass spectrometry.
  • Patients were categorized into CE stroke and non-CE stroke groups.
  • Associations between metabolites, atrial dysfunction (including P-wave terminal force, left atrial enlargement, and atrial fibrillation), and stroke recurrence scores (CHADS2, CHA2DS2-VASc) were assessed using logistic regression.

Main Results:

  • Three tricarboxylic acid cycle metabolites—succinate, α-ketoglutarate, and malate—were significantly associated with CE stroke.
  • These metabolites were also linked to markers of subclinical atrial dysfunction, including left atrial enlargement.
  • Succinate levels were particularly associated with increased stroke recurrence risk, as indicated by CHADS2 and CHA2DS2-VASc scores.

Conclusions:

  • Metabolite profiling revealed significant alterations in succinate, α-ketoglutarate, and malate in patients with CE stroke and atrial dysfunction.
  • These findings suggest a potential link between impaired energy metabolism and the pathogenesis of CE stroke.
  • Succinate may serve as a potential biomarker for CE stroke risk and recurrence.