ArticlePloS one2024
The global effect of aortic coarctation on carotid and renal pulsatile hemodynamics.
Article in PloS one, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Stanford Type B Aortic Dissection in an Adult Patient With Unrepaired Coarctation of the Aorta.Journal of investigative medicine high impact case reportsArticle
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Authors and funding
2 authors.
Funding
No grant is acknowledged in the PubMed record.
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.
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Registered trials
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