# Homeometric autoregulation in severe aortic stenosis: insights from transcatheter aortic valve replacement

## TL;DR

This study explores how heart function changes after aortic valve replacement in patients with severe aortic stenosis, revealing unexpected declines in heart muscle strength.

## Contribution

The study identifies a novel autoregulatory mechanism linking high afterload and contractility in severe aortic stenosis.

## Key findings

- Contractility declined in the near-term postoperative period following TAVR.
- High afterload in severe AS augments contractility, which declines after TAVR.
- Heart rate and ventricular volumes remained unchanged post-TAVR.

## Abstract

In severe aortic stenosis (AS), relief of afterload excess would be expected to improve left ventricular ejection fraction. However, the response of LVEF to transcatheter aortic valve replacement (TAVR) is variable, with some patients even demonstrating a decline. The mechanisms underlying this phenomenon are incompletely characterized. Accordingly, we investigated changes in systolic function in the near-term postoperative period following TAVR.

We studied consecutive patients with severe AS referred for TAVR without identifiable perioperative sources of negative inotropy or ventricular dyssynchrony. Preoperative and postoperative day one echocardiograms were compared with respect to hemodynamics, LV geometry, LVEF, and midwall fractional shortening (FSmw). Contractility was assessed by comparing observed FSmw values to those predicted based on the stress-shortening relation of healthy controls.

Thirty-six patients were included (61% women; mean age 77 years; mean Society of Thoracic Surgeons mortality risk score 3.6%). Following TAVR, there was a precipitous decline in circumferential end-systolic wall stress from 122 ± 47 to 74 ± 32 kdyn/cm2 (p < 0.001) and a slight increase in LVEF. Surprisingly, however, there was also an increase in the percentage of patients with depressed contractility from 22% (8) to 78% (28) (p < 0.001). Heart rate and ventricular volumes remained unchanged.

Contractility declined in the near-term postoperative period following TAVR. We interpret this finding to suggest that contractility is augmented by high afterload in severe AS and declines in parallel with afterload reduction. We speculate that autoregulatory mechanisms triggered by high valvular resistance support LVEF in severe AS and rapidly abate following TAVR.