THORACIC AORTIC ANEURYSM GROWTH IN PATIENTS WITH BICUSPID AORTIC VALVES: ROLE OF AORTIC STIFFNESS AND PULSATILE HEMODYNAMICS

Abstract

Bicuspid aortic valve (BAV) is the most common congenital cardiac abnormality, and the second most common etiology for thoracic aortic aneurysm (TAA) formation. Among BAV patients, risk of aortic dissection is increased 8-fold, and 25-year risk of aortic surgery is 25%. However, there are no clinical predictors of aneurysm growth for risk stratification. Since the health of the aortic wall is directly reflected in its stiffness, which increases pulsatile hemodynamic load due to impairment of the aorta’s pressure buffering function, we evaluated whether measures of aortic stiffness and hemodynamic load are associated with TAA growth in patients with BAV. Twenty nine participants with TAA due to BAV who had serial imaging were recruited. Aneurysm size was measured systematically by an imaging cardiologist blinded to hemodynamics, and growth rate was calculated in mm/year. Central arterial hemodynamics were non-invasively determined with validated methods that integrate arterial tonometry with echocardiography, yielding measures of aortic stiffness (aortic pulse wave velocity, aPWV), steady (systemic vascular resistance) and pulsatile hemodynamic load [aortic characteristic impedance (Zc), proximal aortic (PAC) and total arterial (TAC) compliances, central systolic (cSBP) and pulse pressures, forward (Pf) and reflected pressure wave amplitudes]. Spearman correlation coefficients were calculated between TAA growth rate and brachial blood pressure, as well as the aforementioned central hemodynamic measures. Multivariable linear regression adjusted for potential confounders (Table 1 legend) assessed the independent associations of hemodynamic variables with TAA growth. Sixty six percent of participants were men. Mean±standard deviation (SD) age, baseline aneurysm size and follow-up time were 57.2±8.3 years, 46.9±3.6 mm and 2.9±3.3 years, respectively. There were significant correlations between several measures of aortic stiffness and pulsatile arterial load with TAA growth (Table1, top). There were no significant correlations between brachial blood pressure parameters or steady hemodynamic load with TAA growth (P>0.05 for each). In multivariable linear regression, measures of aortic stiffness (aPWV) and pulsatile hemodynamic load (Zc, PAC, TAC) remained independently associated with aneurysm growth (Table 1, bottom). Other hemodynamic measures were not independently associated with TAA growth. In patients with TAA due to BAV, greater aortic stiffness and central pulsatile hemodynamic load are associated with faster aneurysm growth; while brachial blood pressure and steady hemodynamic load are not. Our findings suggest that evaluating aortic stiffness and pulsatile arterial load could be useful for risk stratification of subjects with TAA due to BAV, and may provide a therapeutic target for this disease.