One hundred and two patients (age, 70 years [range, 63-75 years]; male, 66%; aortic valve area, 0.9 cm(2) [range, 0.7-1.2 cm(2)]) underwent ECG, echocardiography, and cardiovascular magnetic resonance. They made up the mechanism cohort. Myocardial
fibrosis was determined with late
gadolinium enhancement (replacement
fibrosis) and T1 mapping (diffuse
fibrosis). The relationship between ECG strain and cardiovascular magnetic resonance was then assessed in an external validation cohort (n=64). The outcome cohort was made up of 140 patients from the Scottish
Aortic Stenosis and
Lipid Lowering Trial Impact on Regression (SALTIRE) study and was followed up for 10.6 years (1254 patient-years). Compared with those without
left ventricular hypertrophy (n=51) and
left ventricular hypertrophy without ECG strain (
n=30), patients with ECG strain (n=21) had more severe
aortic stenosis, increased left ventricular mass index, more myocardial injury (high-sensitivity plasma cardiac
troponin I concentration, 4.3 ng/L [interquartile range, 2.5-7.3 ng/L] versus 7.3 ng/L [interquartile range, 3.2-20.8 ng/L] versus 18.6 ng/L [interquartile range, 9.0-45.2 ng/L], respectively; P<0.001) and increased diffuse
fibrosis (extracellular volume fraction, 27.4±2.2% versus 27.2±2.9% versus 30.9±1.9%, respectively; P<0.001). All patients with ECG strain had midwall late
gadolinium enhancement (positive and negative predictive values of 100% and 86%, respectively). Indeed, late
gadolinium enhancement was independently associated with ECG strain (odds ratio, 1.73; 95% confidence interval, 1.08-2.77; P=0.02), a finding confirmed in the validation cohort. In the outcome cohort, ECG strain was an independent predictor of aortic valve replacement or cardiovascular death (hazard ratio, 2.67; 95% confidence interval, 1.35-5.27; P<0.01).
CONCLUSION: