Abstract 14855: Altered Flow Hemodynamic Metrics in Descending Aorta Correlate With N-terminal Prohormone of Brain Natriuretic Peptide (NT-proBNP) in Youth With Type 1 Diabetes
Introduction: Cardiovascular disease (CVD) remains the leading cause of mortality in T1D. Early non-invasive characterization of CVD in youth with T1D is thus of great importance. Therefore we aimed to: 1) characterize sensitive wall shear stress (WSS) parameters in youth with T1D, known to promote vascular remodeling in the descending aorta (DA); 2) examine the relationship between WSS and NT-proBNP, a known marker of ventricular dysfunction.
Hypothesis: NT-proBNP will correlate with WSS in youth with T1D.
Methods: Youth with T1D (n=37, mean age 16±2 years, 46 % female) and control youth (n=23, mean age 15±2, % female) underwent phase-contrast cardiac MRI evaluation of flow hemodynamic shear stress in the DA, 10 cm below the aortic isthmus. Collected indices included peak and time-averaged WSS (dyne/cm2), and vascular strain (%). Additionally, youth with T1D underwent a fasting blood sample for NT-proBNP (median: 41 [26-53] pg/mL). Generalized linear regression models were used to examine the relationships between NT-proBNP, WSS peak and WSS time averaged, adjusted for age and sex. NT-proBNP was positively skewed and thus natural log-transformed (ln).
Results: T1D youth had greater time-averaged WSS (4.2 vs. 2.7 (dyne/cm2), p < 0.0001) and peak systolic WSS (15.5 vs. 10.7 (dyne/cm2), p < 0.0001) vs. controls. Strain in the DA also decreased in participants with T1D (22 vs. 26 (%), p = 0.048). Ln(NT-proBNP) was associated with time averaged WSS (β±SE: 1.06 ± 0.27, p = 0.0005) and peak WSS (β±SE: 2.75 ± 1.13, p = 0.02).
Conclusion: Flow hemodynamic shear was significantly increased in the DA in T1D youth, and was associated with NT-proBNP concentrations. Vascular stiffness promoting shear forces may play an important role in the development of CVD in youth with T1D, and NT-proBNP may be a potential clinical marker for early vascular dysfunction in this population.
Author Disclosures: M. Schafer: None. P. Bjornstad: None. M. McClatchey: None. K.S. Hunter: None. M. Cree-Green: None. A. Baumgartner: None. A.J. Barker: None. U. Truong: None. K.J. Nadeau: None.
- © 2016 by American Heart Association, Inc.