Abstract
Introduction: Left ventricular hypertrophy in Aortic stenosis (AS) results from pressure overload and relates to perturbations in cardiac fatty acid metabolism with evidence of steatosis and deranged myocardial energetics in severe AS. There is, however, wide individual heterogeneity in the degree of hypertrophy and progression to myocardial fibrosis and heart failure. Underlying interplay of metabolism and hypertrophy may explain this variability. Purpose We sought to determine if a gradient of myocardial metabolic remodelling exists in AS and its relationship with AS severity, degree of hypertrophy and fibrosis. Methods: 74 asymptomatic AS participants including mild (n=18), moderate (n=38), severe (n=18), and 13 healthy volunteers underwent CMR imaging for cardiac function, myocardial PCr/ATP and triglyceride content (MTG) assessment. Participants were divided into quartile groups based on LV wall thickness (LVWT) and peak aortic valve gradient (AVG) to study relationship between cardiac metabolism and hemodynamic markers of LV structure and function. Results: There was a stepwise deterioration in LV structure and function in both the LVWT and AVG quartile groups (p values significant) with increasing AS severity, as expected. Notably, PCr/ATP was reduced early in mild-moderate AS (Q2 1.43±0.13 vs 1.80±0.14 in Q1 controls, p=0.05) with a progressive decline across groups (Q4 PCr/ATP 1.39±0.14, p=0.02 vs Q1). MTG was elevated in mild-moderate AS (Q2 1.52±0.84 vs 1.25±0.70% in Q1, p = 0.032). Global longitudinal strain was impaired across all AS groups, and was related to the degree of energetic impairment (R 0.219, p 0.03). In addition, PCr/ATP was strongly associated with the presence of myocardial fibrosis (p 0.01). Conclusion A gradient of myocardial energetic deficit and steatosis exists across the spectrum of hypertrophied AS hearts, notably these metabolic changes precede irreversible LV remodelling and subclinical dysfunction.
Published Version
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