Previous studies have shown that, in patients with severe aortic stenosis (SAS), global longitudinal strain (GLS), as assessed by speckle tracking echocardiography (STE), is often reduced. The present study aimed to understand the mechanisms underlying this reduction by using stress-shortening relationships.

Ninety-nine patients with isolated SAS (36% men, 69±11years) and 75 healthy volunteers (HV) underwent resting 2D-echo and STE to measure GLS, global circumferential strain (GCS), rate-corrected mean velocity of fiber shortening (Vcfc), and end-systolic wall stress (ESWS). Stress-GLS, GCS or Vcfc relationships were constructed using the HV data and fitted to a linear regression. The relative position of individual SAS patients on these relationships was calculated and used as a load-independent index of myocardial contractility (unloaded GLS,GCS or Vcfc). At the time of surgery, myocardial biopsy was obtained to quantify interstitial fibrosis.

GLS and Vcfc were lower in SAS than HV (−17±3 vs. −20±2%, P<0.001; and 1.1±0.3 vs. 1.3±0.3cm/s, P<0.001). In contrast, GCS was similar in both groups (−29.04±4.7% and −29.6±4.3%, P=0.40). In HV, GLS was less afterload-dependent than Vcfc and GCS. In SAS, unloaded GLS, GCS and Vcfc were lower than 2 standard deviations of HV in respectively 40%, 18% and 35% of patients. Using multivariate analysis, unloaded GLS, GCS and Vcf correlated significantly (P<0.05) with interstitial fibrosis and LV mass. Moreover, if divided by tertiles of fibrosis (<2.3%, 2.3–5.4%, >5.4%), a real gradient is draw between the groups. The more fibrosis they have, the worse the longitudinal and circumferential functions are altered for a given afterload (Fig. 1).

In HV, longitudinal function is less afterload-dependent than circumferential function. In SAS, reduced longitudinal or circumferential function is a marker of interstitial fibrosis and LV remodeling.