Abstract
Introduction: Left ventricular hypertrophy (LVH) is a marker of cardiovascular events and is driven by ventriculo-vascular interactions with stiffening arteries. But longitudinal relations of left ventricle with aorta is uncharacterized in youth. Hypothesis: Aortic stiffening, measured as change in carotid-femoral pulse wave velocity (cfPWV), and arterial thickening measured as change in carotid intima-media thickness (cIMT) each independently predicts and precedes changes in LVH indices even after adjustment for BP. Methods: From the Avon Longitudinal Study of Parents and Children, UK birth cohort, 1856 adolescents (1011 females) were assessed at mean age 17.7 years and followed 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 ) ≥51g/m 2.7 as LVH; relative wall thickness ≥44 as hiRWT; LV diastolic function E/A as ≥1.5 (LVDD); and LV filling pressure E/e’ ≥8 as hiLVFP. Data were analysed with generalized logit mixed-effect model and cross-lagged structural equation path model 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] and worsening hiLVFP [1.14 (1.13 - 1.14); p<0.0001]. Likewise, high cIMT progression was associated with worsening LVH [1.27 (1.26 - 1.27); p<0.0001] and worsening hiLVFP [1.17 (1.07 - 1.28); p<0.001]. Neither cfPWV nor cIMT progression was associated with worsening hiRWT nor LVDD. 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 . Conclusions: Youth aortic stiffness progression temporally preceded and may causally associate with worsening LVH and hiLVFP but not hiRWT. Mechanistic delineation of coupling in ventriculo-vascular remodeling and consequent physiologic dysfunction is warranted.
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