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A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium
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A Model of Disturbed Flow-Induced Atherosclerosis in Mouse Carotid Artery by Partial Ligation and a Simple Method of RNA Isolation from Carotid Endothelium

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[Lipoprotein (a) in patients with carotid atherosclerosis]

T V Baidina1, M A Danilova1, V Yu Mishlanov1

  • 1Vagner Perm State Medical University, Perm, Russia.

Zhurnal Nevrologii I Psikhiatrii Imeni S.S. Korsakova
|September 26, 2018
PubMed

Insights

Serum lipoprotein (a) correlates with endothelial dysfunction and precerebral artery atherosclerosis severity. This suggests lipoprotein (a) contributes to atherogenesis and stroke risk through prothrombotic effects on hemostasis.

Area of Science:

  • Cardiovascular Medicine
  • Neurology
  • Biochemistry

Background:

  • Lipoprotein (a) [Lp(a)] is an emerging risk factor for atherosclerotic cardiovascular disease.
  • Endothelial dysfunction plays a critical role in the pathogenesis of atherosclerosis and stroke.
  • The precise mechanisms linking Lp(a) to cerebrovascular events require further elucidation.

Purpose of the Study:

  • To investigate the association between serum Lp(a) levels and the presence and severity of atherosclerotic lesions in precerebral arteries.
  • To explore the relationship between Lp(a) and endothelial function in patients with carotid artery atherosclerosis.
  • To determine the potential role of Lp(a) in stroke development.

Main Methods:

  • Cross-sectional study involving 38 patients with established carotid artery atherosclerosis (28 post-stroke, 10 asymptomatic).
  • Duplex scanning was used to assess atherosclerotic lesions in precerebral arteries.
  • Serum Lp(a) levels were measured using immunosorbent assay; neutrophil-cultured Lp(a) was also analyzed.

Main Results:

  • A significant correlation was observed between serum Lp(a) levels and endothelium-dependent vasodilation of the brachial artery.
  • Culture supernatant Lp(a) levels showed a relationship with the severity of atherosclerotic lesions in precerebral arteries.
  • Elevated Lp(a) was associated with prolonged prothrombin time, indicating an impact on hemostasis.

Conclusions:

  • Lipoprotein (a) may contribute to atherogenesis by promoting endothelial dysfunction.
  • The prothrombotic effects of Lp(a) on hemostasis are implicated in the mechanism of stroke development.
  • These findings highlight Lp(a) as a potential therapeutic target for preventing cerebrovascular disease.
Abstract

Keywords:
carotid atherosclerosislipoprotein (a)stroke

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