Abstract 19658: Descending Aortic Reverse Flow is Independently Associated with Left Ventricular Hypertrophy and Diffuse Fibrosis
Background: Disturbed aortic flow, present as flow reversal in a given aortic cross section, is, a.o.., dependent on LV function and aortic anatomy, which in turns impacts ventricular-arterial interactions. Flow reversal from disturbed flow in the descending aorta can be interrogated using phase-contrast MRI. The relationship between aortic flow abnormalities and LV remodeling has not been previously assessed.
Methods: We prospectively studied 205 subjects without significant aortic regurgitation. Descending thoracic aortic forward (Qf, caudal) and backward (Qb, cranial) flow was quantified with through-plane phase-contrast MRI. A dimensionless index of flow reversal was computed as Qb/Qf. We assessed the relationship between Qb/Qf and: (1) LV hypertrophy; (2) In a subsample (n=49), myocardial fibrosis, quantified as the extracellular volume fraction (ECV) from pre- and post-gadolinium myocardial T1 measurements (Look-Locker sequences): ECV= λ * (1-hematocrit). Lambda (λ), the Gd partition coefficient, was computed as the slope of the linear relationship between myocardial R1 versus blood R1 before and several time points after the administration of Gd.
Results: In a multivariate model adjusting for multiple risk factors, descending aortic Qb/Qf increased with age (β=0.20; P=0.012), heart rate (β=0.21; P=0.006) and carotid augmentation index, marker of wave reflections (β=0.18;P=0.025). After adjustment for age, body size, mean arterial pressure, pulse pressure, diabetes mellitus, history of hypertension, number of antihypertensive drugs, LDL and HDL cholesterol, Qb/Qf was the strongest independent predictor of LV mass (β=0.29; P<0.000). Similarly, Qb/Qf was associated with an increased ECV (β=0.40; P=0.004), even after adjustment for all other predictors of ECV (adjusted β=0.35; P=0.01).
Conclusions: Descending aortic flow reversal is independently associated with left ventricular hypertrophy and diffuse fibrosis. Our findings support the role of aortic hemodynamics in the pathogenesis of LV hypertrophy and fibrosis.
Author Disclosures: J.A. Chirinos: None. S. Peddireddy: None. P. Zamani: None. N. Vadde: None. A. Dunde: None. S. Desai: None. P. Bhattacharya: None. V. Ferrari: None. P. Segers: None. S. Akers: None.
- © 2014 by American Heart Association, Inc.