The global effect of aortic coarctation on carotid and renal pulsatile hemodynamics.

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  • Author(s): Rafiei D;Rafiei D; Pahlevan NM; Pahlevan NM; Pahlevan NM
  • Source:
    PloS one [PLoS One] 2024 Dec 17; Vol. 19 (12), pp. e0310793. Date of Electronic Publication: 2024 Dec 17 (Print Publication: 2024).
  • Publication Type:
    Journal Article
  • Language:
    English
  • Additional Information
    • Source:
      Publisher: Public Library of Science Country of Publication: United States NLM ID: 101285081 Publication Model: eCollection Cited Medium: Internet ISSN: 1932-6203 (Electronic) Linking ISSN: 19326203 NLM ISO Abbreviation: PLoS One Subsets: MEDLINE
    • Publication Information:
      Original Publication: San Francisco, CA : Public Library of Science
    • Subject Terms:
      Aortic Coarctation*/physiopathology ; Pulsatile Flow* ; Hemodynamics*; Humans ; Kidney/physiopathology ; Renal Circulation ; Carotid Arteries/physiopathology ; Cerebrovascular Circulation/physiology ; Vascular Stiffness/physiology
    • Abstract:
      Coarctation of the aorta (CoA) is a congenital disease characterized by the narrowing of the aorta, typically the descending portion after the left subclavian artery. If left untreated, by the time individuals reach 50 years of age, the mortality rate can reach 90%. Previous studies have highlighted the adverse effects of CoA on local hemodynamics. However, no study has investigated the global hemodynamic effects of CoA in end-organ (brain and kidney) damage. Clinical studies have shown that coarctation acts as a reflection site, potentially damaging the hemodynamics of the brain and kidneys. Our goal in this study is to investigate the underlying mechanisms of these altered wave dynamics and their impacts on the pulsatile hemodynamics of end-organs. In this study, we use a physiologically accurate in-vitro experimental setup that simulates the hemodynamics of systemic circulation. Experiments are conducted across various cardiac outputs, heart rates, and coarctation degrees using aortas across a wide range of aortic stiffnesses. Our principal finding is that CoA increases cerebral blood flow and harmful pulsatile energy transmission to the brain. Conversely, both renal blood flow and pulsatile energy transmission to the kidneys are reduced in CoA at every level of aortic stiffness.
      Competing Interests: The authors have declared that no competing interests exist.
      (Copyright: © 2024 Rafiei, Pahlevan. This is an open access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.)
    • Publication Date:
      Date Created: 20241217 Date Completed: 20241217 Latest Revision: 20241217
    • Publication Date:
      20241218
    • Accession Number:
      10.1371/journal.pone.0310793
    • Accession Number:
      39689111