Arterial stiffness but not carotid intima-media thickness progression precedes premature structural and functional cardiac damage in youth: A 7-year temporal and mediation longitudinal study.

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  • Additional Information
    • Source:
      Publisher: Elsevier Country of Publication: Ireland NLM ID: 0242543 Publication Model: Print-Electronic Cited Medium: Internet ISSN: 1879-1484 (Electronic) Linking ISSN: 00219150 NLM ISO Abbreviation: Atherosclerosis Subsets: MEDLINE
    • Publication Information:
      Publication: Limerick : Elsevier
      Original Publication: Amsterdam, Elsevier.
    • Subject Terms:
      Insulin Resistance* ; Vascular Stiffness*/physiology ; Hypertension*; Male ; Female ; Child ; Humans ; Adolescent ; Carotid Intima-Media Thickness ; Longitudinal Studies ; Pulse Wave Analysis ; Overweight ; Blood Pressure/physiology ; Hypertrophy, Left Ventricular/epidemiology ; Obesity/complications ; Obesity/epidemiology
    • Abstract:
      Background and Aims: The longitudinal relations of cardiac indices with the aorta and carotid vessel and the time sequence for early cardiac disease development are uncharacterized in youth. We examined the temporal longitudinal associations of carotid-femoral pulse wave velocity (cfPWV) and carotid intima-media thickness (cIMT) with left ventricular hypertrophy (LVH) and diastolic dysfunction (LVDD).
      Methods: From the Avon Longitudinal Study of Parents and Children, UK birth cohort, 1856 adolescents (1011 females) at a mean (SD) age 17.7 (0.3) years were followed up for 7 years. Vicorder-measured cfPWV and ultrasound-measured cIMT were grouped in tertiles as low (reference), moderate, and high. Echocardiography measured cardiac abnormalities are left ventricular mass indexed for height 2.7 (LVMI 2.7 ) ≥51 g/m 2.7 as LVH; relative wall thickness ≥44 as hiRWT; LVD function E/A <1.5 as LVD dysfunction (LVDD); and LV filling pressure E/e' ≥8 as hiLVFP. Data were analysed with generalized logit mixed-effect models, cross-lagged path, and mediation structural equation models adjusting for cardiometabolic and lifestyle factors.
      Results: Over follow-up, LVH prevalence increased from 3.6% to 7.2% and LVDD from 11.1 to 16.3%. High cfPWV progression was associated with worsening LVH [Odds ratio 1.23 (1.13-1.35); p < 0.001] in the total cohort, males, overweight/obese, and normotensive. High cfPWV progression was associated with worsening hiLVFP in the total cohort, females, and normal weight. Likewise, high cIMT progression was associated with worsening LVH [1.27 (1.26-1.27); p < 0.0001] in the total cohort, overweight/obese and elevated BP/hypertensive. Neither cfPWV nor cIMT progression was associated with worsening hiRWT in the total cohort. In cross-lagged models, higher baseline cfPWV was associated with future LVMI 2.7 (β = 0.06, SE, 5.14, p = 0.035), RWT, LVDF, and LVFP. However, baseline LVMI 2.7 , RWT, LVDF, and LVFP were not associated with follow-up cfPWV. Baseline cIMT was not associated with follow-up cardiac indices and vice versa. Cumulative increased systolic blood pressure (34.3% mediation) and insulin resistance (15.1% mediation) mediated the direct associations of cumulative cfPWV with cumulative LVMI 2.7 .
      Conclusions: Arterial stiffness progression temporally preceded worsening structural and functional cardiac damage in youth with increased systolic blood pressure and insulin resistance partly mediating the relationships. Future interventions aimed at attenuating premature cardiac damage in adolescents and young adults may consider a simultaneous treatment of both arterial stiffness, elevated blood pressure and insulin resistance.
      Competing Interests: Declaration of competing interest The authors declare that they have no known competing financial interests or personal relationships that could have appeared to influence the work reported in this paper.
      (Copyright © 2023 The Author(s). Published by Elsevier B.V. All rights reserved.)
    • Grant Information:
      217065/Z/19/Z United Kingdom WT_ Wellcome Trust; CS/15/6/31468 United Kingdom BHF_ British Heart Foundation; MC_PC_19009 United Kingdom MRC_ Medical Research Council; MR/L010305/1 United Kingdom MRC_ Medical Research Council; MC_PC_15018 United Kingdom MRC_ Medical Research Council; G9815508 United Kingdom MRC_ Medical Research Council; MR/M006727/1 United Kingdom MRC_ Medical Research Council; R01 HL148217 United States HL NHLBI NIH HHS
    • Contributed Indexing:
      Keywords: Atherosclerosis; Left ventricular diastolic dysfunction; Left ventricular hypertrophy; Metabolic syndrome; Pediatrics
    • Publication Date:
      Date Created: 20230815 Date Completed: 20230929 Latest Revision: 20240221
    • Publication Date:
      20240221
    • Accession Number:
      10.1016/j.atherosclerosis.2023.117197
    • Accession Number:
      37582328