Reducing Left Ventricular Wall Stress through Aortic Valve Enlargement via Transcatheter Aortic Valve Implantation in Severe Aortic Stenosis

Abstract

Background: In aortic stenosis, the left ventricle exerts additional force to pump blood through the narrowed aortic valve into the downstream arterial vasculature. Adaptive hypertrophy helps to maintain wall stress homeostasis but at the expense of impaired compliance. Advanced ventricular deformation impacts the extent of functional recovery benefits achieved through transcatheter aortic valve implantation. Methods and Results: Subgroups were stratified based on output, with low-flow severe aortic stenosis defined as stroke volume index <35 mL· m^-2. Before intervention, the low-flow subgroup exhibited worse effective orifice area index and arterial and global impedance, along with thinner wall thickness and larger chamber volume marginally. LV performance, including stroke volume index, ventricular elastance, and ventricular-arterial coupling, were notably inferior, consistent with worse adverse remodeling. Although the effective orifice area index was similarly augmented after TAVI, inferior recovery benefits were noted. Persistently higher wall stress and energy consumption were observed, along with poorer ventricular-arterial coupling. These changes in wall stress showed an inverse relationship with alterations in wall thickness and were proportional to changes in dimension and volume. Additionally, they were proportional to changes in left ventricular end-systolic pressure, pressure-volume area, and ventricular-arterial coupling but inversely related to ventricular end-systolic elastance. Conclusions: The study revealed that aortic valve enlargement through transcatheter aortic valve implantation reduces left ventricular wall stress in severe aortic stenosis. The reduced recovery benefits in the low-flow subgroup were evident. Wall stress could serve as a marker of mechanical benefit after the intervention.

Keywords: low-flow aortic stenosis; transcatheter aortic valve implantation; ventricular–arterial coupling; wall stress.

Figure 1

Correlation in alterations of geometry and hemodynamics from baseline to post-TAVI with linear regression. (A) The relative change in posterior wall thickness is inverse relation to relative change in wall stress; (B) the relative change in end-systolic dimension is proportional to relative change in wall stress; (C) the relative change in end-systolic pressure is proportional to relative change in wall stress; (D) the relative change in end-systolic elastance is inverse relation to relative change in wall stress; (E) the relative change in pressure–volume area is proportional to relative change in wall stress; (F) the relative change in pressure–volume area is proportional to relative change in wall stress.

Figure 2

(A) The ventricular function curve shifts up and to the left (indicating from black line to red dotted line) with increased ventricular contractility, decreased afterload, and increased compliance. (B) TAVI reduces LV end-systolic pressure (LVESP), LV end-systolic volume (LVESV), and LV end-diastolic volume (LVEDV), improving afterload and compliance, ultimately resulting in decreased potential energy and stroke work and increased mechanical efficiency. Ea, arterial elastance; EDPVR, end-diastolic pressure–volume relationship; EDV, LV end-diastolic volume; Ees, LV end-systolic elastance; ESP, LV end-systolic pressure; ESPVR, end-systolic pressure–volume relationship; ESV, end-systolic volume; PE, potential energy; SW, stroke work.