Arterial stiffness and atherosclerosis: mechanistic and pathophysiologic interactions

Research output: Chapter in Book/Report/Conference proceedingChapterpeer-review

Abstract

There are significant mechanistic and pathophysiologic interactions between arterial stiffness, atherosclerosis, and hemodynamic stress. Atherosclerosis is triggered by endothelial cell dysfunction. Subsequent lipid accumulation and increased inflammation facilitate the formation of pathological vulnerable plaques. This results in the development of atherosclerotic cardiovascular disease. In contrast, arterial stiffness results from elastin breakdown, wall calcification, fibrosis, collagen, and elastin cross-linking, increased vascular smooth muscle cell tone, and endothelial cell dysfunction. Both these types of vascular failure share pathophysiological mechanisms, involving aging, inflammation, and metabolic and hemodynamic risk factors. In addition, both are important contributors to cardiovascular risk. The systemic hemodynamic atherosclerotic syndrome has been proposed as a novel clinical entity linking arterial stiffness, atherosclerosis, and hemodynamic stress, ultimately contributing to target organ damage and cardiovascular events.

Original languageEnglish
Title of host publicationTextbook of Arterial Stiffness and Pulsatile Hemodynamics in Health and Disease
PublisherElsevier
Pages609-620
Number of pages12
ISBN (Electronic)9780323913911
ISBN (Print)9780323916486
DOIs
StatePublished - 1 Jan 2022
Externally publishedYes

Keywords

  • Arterial stiffness
  • Atherosclerosis
  • Cardio-ankle vascular index
  • Cardiovascular risk
  • Hemodynamics
  • Pulse wave velocity
  • Systemic hemodynamic atherothrombotic syndrome
  • Vascular disease

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