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Platelet sialic acid as a potential pathogenic factor in coronary heart disease

Robert Mandic1, Claus Opper, Jürgen Krappe

  • 1Department of Otorhinolaryngology, Head and Neck Surgery, Philipps University Marburg, Deutschhausstrasse 3, D-35037 Marburg, Germany. mandic@mailer.uni-marburg.de

Thrombosis Research
|August 17, 2002
PubMed

Insights

Patients with coronary heart disease (CHD) have fewer negatively charged sialic acids on their platelets, leading to increased platelet aggregation and a higher risk of heart disease.

Area of Science:

  • Biochemistry
  • Hematology
  • Cardiovascular Science

Background:

  • Patients with coronary heart disease (CHD) show increased platelet aggregation.
  • The underlying reasons for this heightened aggregation in CHD patients were previously unknown.
  • Platelet surface charge, influenced by sialic acid, may play a role in cell interactions.

Purpose of the Study:

  • To investigate if reduced platelet sialic acid content is a pathogenic factor in coronary heart disease (CHD).
  • To determine the relationship between sialic acid levels and platelet aggregation in CHD patients.

Main Methods:

  • Platelets were isolated from patients with CHD and healthy controls.
  • The proportion of low-density platelets was quantified.
  • Sialic acid content on platelet surfaces was measured.
  • Neuraminidase susceptibility was assessed to determine sialic acid localization.

Main Results:

  • A higher proportion of low-density platelets was observed in CHD patients compared to controls.
  • Platelets from CHD patients exhibited significantly lower sialic acid content.
  • Sialic acid was predominantly located on the outer surface of platelets, as indicated by neuraminidase sensitivity.

Conclusions:

  • Lower sialic acid content on platelets may contribute to increased platelet aggregation in CHD patients.
  • Reduced negative surface charge due to lower sialic acid levels could diminish platelet repulsion, facilitating aggregation.
  • This finding suggests a potential mechanism linking platelet surface chemistry to cardiovascular disease pathogenesis.

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