Left Ventricular Hypertrophy With Strain and Aortic Stenosis

Shah, Anoop S.V., Chin, Calvin W.L., Vassiliou, Vassilios ORCID: https://orcid.org/0000-0002-4005-7752, Cowell, S. Joanna, Doris, Mhairi, Kwok, T'ng Choong, Semple, Scott, Zamvar, Vipin, White, Audrey C., McKillop, Graham, Boon, Nicholas A., Prasad, Sanjay K., Mills, Nicholas L., Newby, David E. and Dweck, Marc R. (2014) Left Ventricular Hypertrophy With Strain and Aortic Stenosis. Circulation, 130 (18). pp. 1607-1616. ISSN 0009-7322

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Background—ECG left ventricular hypertrophy with strain is associated with an adverse prognosis in aortic stenosis. We investigated the mechanisms and outcomes associated with ECG strain. Methods and Results—One hundred and two patients (age, 70 years [range, 63–75 years]; male, 66%; aortic valve area, 0.9 cm2 [range, 0.7–1.2 cm2]) 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—ECG strain is a specific marker of midwall myocardial fibrosis and predicts adverse clinical outcomes in aortic stenosis.

Item Type: Article
Uncontrolled Keywords: aortic valve stenosis,fibrosis,left ventricular hypertrophy,troponin i
Faculty \ School: Faculty of Medicine and Health Sciences > Norwich Medical School
UEA Research Groups: Faculty of Medicine and Health Sciences > Research Groups > Cardiovascular and Metabolic Health
Faculty of Science > Research Groups > Norwich Epidemiology Centre
Faculty of Medicine and Health Sciences > Research Groups > Norwich Epidemiology Centre
Faculty of Medicine and Health Sciences > Research Centres > Metabolic Health
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Depositing User: Pure Connector
Date Deposited: 23 Jun 2017 05:06
Last Modified: 19 Oct 2023 02:01
URI: https://ueaeprints.uea.ac.uk/id/eprint/63816
DOI: 10.1161/CIRCULATIONAHA.114.011085

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