Scientific Reports (Jun 2024)

Amyloid beta is associated with carotid wall echolucency and atherosclerotic plaque composition

  • Dimitrios Delialis,
  • Georgios Georgiopoulos,
  • Simon Tual-Chalot,
  • Lasthenis Angelidakis,
  • Evmorfia Aivalioti,
  • Georgios Mavraganis,
  • Kateryna Sopova,
  • Antonios Argyris,
  • Peggy Kostakou,
  • Christina Konstantaki,
  • Maria Papaioannou,
  • Diamantis Tsilimigras,
  • Konstantinos Chatoupis,
  • Achilleas A. Zacharoulis,
  • George Galyfos,
  • Fragiska Sigala,
  • Konstantinos Stellos,
  • Kimon Stamatelopoulos

DOI
https://doi.org/10.1038/s41598-024-64906-8
Journal volume & issue
Vol. 14, no. 1
pp. 1 – 11

Abstract

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Abstract Circulating amyloid-beta 1–40 (Αb40) has pro-atherogenic properties and could serve as a biomarker in atherosclerotic cardiovascular disease (ASCVD). However, the association of Ab40 levels with morphological characteristics reflecting atherosclerotic plaque echolucency and composition is not available. Carotid atherosclerosis was assessed in consecutively recruited individuals without ASCVD (n = 342) by ultrasonography. The primary endpoint was grey scale median (GSM) of intima-media complex (IMC) and plaques, analysed using dedicated software. Vascular markers were assessed at two time-points (median follow-up 35.5 months). In n = 56 patients undergoing carotid endarterectomy, histological plaque features were analysed. Plasma Αb40 levels were measured at baseline. Ab40 was associated with lower IMC GSM and plaque GSM and higher plaque area at baseline after multivariable adjustment. Increased Ab40 levels were also longitudinally associated with decreasing or persistently low IMC and plaque GSM after multivariable adjustment (p < 0.05). In the histological analysis, Ab40 levels were associated with lower incidence of calcified plaques and plaques without high-risk features. Ab40 levels are associated with ultrasonographic and histological markers of carotid wall composition both in the non-stenotic arterial wall and in severely stenotic plaques. These findings support experimental evidence linking Ab40 with plaque vulnerability, possibly mediating its established association with major adverse cardiovascular events.