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Biological Pathways in Adolescent Aortic Stiffness
BACKGROUND: Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflammation, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we as...
Autores principales: | , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
John Wiley and Sons Inc.
2021
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8174212/ https://www.ncbi.nlm.nih.gov/pubmed/33641350 http://dx.doi.org/10.1161/JAHA.120.018419 |
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author | Zachariah, Justin P. Wang, Yunfei Newburger, Jane W. deFerranti, Sarah D. Mitchell, Gary F Vasan, Ramachandran S. |
author_facet | Zachariah, Justin P. Wang, Yunfei Newburger, Jane W. deFerranti, Sarah D. Mitchell, Gary F Vasan, Ramachandran S. |
author_sort | Zachariah, Justin P. |
collection | PubMed |
description | BACKGROUND: Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflammation, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we assessed the relations of comprehensive measures of aortic stiffness with body mass index (BMI) and related but distinct circulating biomarkers. METHODS AND RESULTS: A convenience sample of 246 adolescents (mean age, 16±2 years; 45% female, 24% Black, and 43% Hispanic) attending primary care or preventive cardiology clinics at 2 tertiary hospitals was grouped as normal weight (N=98) or excess weight (N=148, defined as BMI ≥age‐ and sex‐referenced 85th percentile). After an overnight fast, participants underwent anthropometry, noninvasive arterial tonometry, and assays for serum lipids, CRP (C‐reactive protein), glucose, insulin, renin, aldosterone, and leptin. We used multivariable linear regression to relate arterial stiffness markers (including carotid‐femoral pulse wave velocity) to BMI z score and a biomarker panel. Carotid‐femoral pulse wave velocity was higher in excess weight compared with normal weight group (5.0±0.7 versus 4.6±0.6 m/s; P<0.01). After multivariable adjustment, carotid‐femoral pulse wave velocity was associated with BMI z score (0.09 [95% CI, 0.01–0.18]; P=0.04) and with low‐density lipoprotein cholesterol (0.26 [95% CI, 0.03–0.50]; P=0.03). CONCLUSIONS: Higher BMI and low‐density lipoprotein cholesterol were associated with greater aortic stiffness in adolescents. Maintaining optimal BMI and lipid levels may mitigate aortic stiffness. |
format | Online Article Text |
id | pubmed-8174212 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2021 |
publisher | John Wiley and Sons Inc. |
record_format | MEDLINE/PubMed |
spelling | pubmed-81742122021-06-11 Biological Pathways in Adolescent Aortic Stiffness Zachariah, Justin P. Wang, Yunfei Newburger, Jane W. deFerranti, Sarah D. Mitchell, Gary F Vasan, Ramachandran S. J Am Heart Assoc Original Research BACKGROUND: Aortic stiffening begins in youth and antedates future hypertension. In adults, excess weight, systemic inflammation, dyslipidemia, insulin resistance, neurohormonal activation, and altered adipokines are implicated in the pathogenesis of increased aortic stiffness. In adolescents, we assessed the relations of comprehensive measures of aortic stiffness with body mass index (BMI) and related but distinct circulating biomarkers. METHODS AND RESULTS: A convenience sample of 246 adolescents (mean age, 16±2 years; 45% female, 24% Black, and 43% Hispanic) attending primary care or preventive cardiology clinics at 2 tertiary hospitals was grouped as normal weight (N=98) or excess weight (N=148, defined as BMI ≥age‐ and sex‐referenced 85th percentile). After an overnight fast, participants underwent anthropometry, noninvasive arterial tonometry, and assays for serum lipids, CRP (C‐reactive protein), glucose, insulin, renin, aldosterone, and leptin. We used multivariable linear regression to relate arterial stiffness markers (including carotid‐femoral pulse wave velocity) to BMI z score and a biomarker panel. Carotid‐femoral pulse wave velocity was higher in excess weight compared with normal weight group (5.0±0.7 versus 4.6±0.6 m/s; P<0.01). After multivariable adjustment, carotid‐femoral pulse wave velocity was associated with BMI z score (0.09 [95% CI, 0.01–0.18]; P=0.04) and with low‐density lipoprotein cholesterol (0.26 [95% CI, 0.03–0.50]; P=0.03). CONCLUSIONS: Higher BMI and low‐density lipoprotein cholesterol were associated with greater aortic stiffness in adolescents. Maintaining optimal BMI and lipid levels may mitigate aortic stiffness. John Wiley and Sons Inc. 2021-03-01 /pmc/articles/PMC8174212/ /pubmed/33641350 http://dx.doi.org/10.1161/JAHA.120.018419 Text en © 2021 The Authors. Published on behalf of the American Heart Association, Inc., by Wiley. https://creativecommons.org/licenses/by-nc-nd/4.0/This is an open access article under the terms of the http://creativecommons.org/licenses/by-nc-nd/4.0/ (https://creativecommons.org/licenses/by-nc-nd/4.0/) License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non‐commercial and no modifications or adaptations are made. |
spellingShingle | Original Research Zachariah, Justin P. Wang, Yunfei Newburger, Jane W. deFerranti, Sarah D. Mitchell, Gary F Vasan, Ramachandran S. Biological Pathways in Adolescent Aortic Stiffness |
title | Biological Pathways in Adolescent Aortic Stiffness |
title_full | Biological Pathways in Adolescent Aortic Stiffness |
title_fullStr | Biological Pathways in Adolescent Aortic Stiffness |
title_full_unstemmed | Biological Pathways in Adolescent Aortic Stiffness |
title_short | Biological Pathways in Adolescent Aortic Stiffness |
title_sort | biological pathways in adolescent aortic stiffness |
topic | Original Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8174212/ https://www.ncbi.nlm.nih.gov/pubmed/33641350 http://dx.doi.org/10.1161/JAHA.120.018419 |
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