Thoracic Aortic Aneurysm Growth in Bicuspid Aortic Valve Patients: Role of Aortic Stiffness and Pulsatile Hemodynamics

Abstract

Background Bicuspid aortic valve ( BAV ) is the most common congenital cardiac abnormality. A thoracic aortic aneurysm ( TAA ) is present in ≈50% of BAV patients, who also have an 8‐fold higher risk of aortic dissection than the general population. Because the health of the aorta is directly reflected in its stiffness and pulsatile hemodynamics, we hypothesized that measures of aortic stiffness and arterial load would be associated with TAA growth in BAV . Methods and Results Twenty‐nine unoperated participants with TAA due to BAV who had serial imaging were recruited. Aortic stiffness and steady and pulsatile arterial load were evaluated with validated methods that integrate arterial tonometry with echocardiography. TAA growth was assessed retrospectively based on available imaging, blinded to hemodynamic status. Multivariable linear regression assessed associations of aortic stiffness and hemodynamic variables with TAA growth, adjusting for potential confounders. Overall, 66% of participants were men. Mean±SD for age, baseline aneurysm size, growth rate, and follow‐up time were 57.2±8.3 years, 46.9±3.6 mm, 0.75±0.81 mm/y, and 2.9±3.3 years, respectively. We found that greater aortic stiffness (β± SE for carotid‐femoral pulse wave velocity: 0.30±0.13. P =0.03) and aortic characteristic impedance (β± SE : 0.46±0.18, P =0.02), as well as lower total arterial and proximal aortic compliance (β± SE : −0.44±0.21, P =0.05, and −0.63±0.16, P =0.001, respectively) were independently associated with faster aneurysm growth. Conclusions In patients with TAA due to BAV , measures of greater aortic stiffness and pulsatile arterial load indicate an association with accelerated aneurysm expansion. Assessing arterial hemodynamics may be useful for risk stratification and disease monitoring in TAA patients with BAV .

Prosthetic aortic graft replacement of the ascending thoracic aorta alters biomechanics of the native descending aorta as assessed by transthoracic echocardiography

“…It is important to contextualize our findings with prior studies that have shown aortic stiffness to be increased in patients with Marfan syndrome, [32,33] and reported increased stiffness to confer risk for aortic dissection [24,34]. Our finding of increased descending aortic distention after proximal aortic graft implantation supports the notion that graft induced changes in aortic physiology are sufficient to overcome intrinsic tissue properties in patients with Marfan syndrome.…”

Biomechanical Assessment of Bicuspid Aortic Valve Phenotypes: A Fluid–Structure Interaction Modelling Approach

“…The use of indicators such as WSS may be useful to estimate the risk of dilation in BAV patients, by estimating phenotypes with a larger risk for dilation onset and progression. Aortic wall mechanics for BAV patients is fundamentally different than for TAV patients: BAV patients present with ascending aortic wall structural changes resulting in excessive stiffness and reduced compliance in comparison with patients with a normal TAV [71,72]. In fact, a previous study reported a 109.8% increase in the aortic wall stiffness index for BAV patients in comparison with TAV ones [73].…”

“…Incorporating a non-rigid wall would introduce a range of variables for which data is lacking; this would limit cross-BAV comparisons. In addition, previous studies have showed that the aortic wall in BAV patients presents with excessive stiffness and reduced compliance in comparison with patients with a TAV [71][72][73]. Hence, for these patients, it is preferable to assume the effect of wall motion in velocity and WSS fields as negligible [81].…”

Regulatory variants in TCF7L2 are associated with thoracic aortic aneurysm

“…5,6 Moreover, approximately 50% of individuals with congenital heart malformations, such as bicuspid aortic valve (BAV), later develop TAA. 7 Yet the origin of the majority of TAA cases remains unknown. It is likely that these cases have more complex origins, involving common genetic variants affecting many genes.…”