Why the study?
There is unexplained individual heterogeneity in LV hypertrophy and progression to myocardial fibrosis and heart failure in AS; the authors sought to determine whether the cardiac metabolic state underpins this variability.
Do cardiac metabolic alterations (energetic deficit and steatosis) correlate with disease severity and precede LV remodeling in asymptomatic aortic stenosis?
Do cardiac metabolic alterations (energetic deficit and steatosis) correlate with disease severity and precede LV remodeling in asymptomatic aortic stenosis?
Myocardial energetic deficit and steatosis precede irreversible LV remodeling in asymptomatic aortic stenosis, suggesting a potential causal role in disease progression.
Answers are grounded in this paper and cite their sources.
Metabolic changes should not yet alter AS management; hypothesis-generating for energetics-targeted therapies in asymptomatic disease.
BACKGROUND: Severe aortic stenosis (AS) is associated with left ventricular (LV) hypertrophy and cardiac metabolic alterations with evidence of steatosis and impaired myocardial energetics. Despite this common phenotype, there is an unexplained and wide individual heterogeneity in the degree of hypertrophy and progression to myocardial fibrosis and heart failure. We sought to determine whether the cardiac metabolic state may underpin this variability. METHODS: We recruited 74 asymptomatic participants with AS and 13 healthy volunteers. Cardiac energetics were measured using phosphorus spectroscopy to define the myocardial phosphocreatine to adenosine triphosphate ratio. Myocardial lipid content was determined using proton spectroscopy. Cardiac function was assessed by cardiovascular magnetic resonance cine imaging. The metabolic and functional parameters showed comparable results when graded by clinical severity of AS. CONCLUSIONS: A gradient of myocardial energetic deficit and steatosis exists across the spectrum of hypertrophied AS hearts, and these metabolic changes precede irreversible LV remodeling and subclinical dysfunction. As such, cardiac metabolism may play an important and potentially causal role in disease progression.
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Monga et al. (2023) studied this question.
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