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Background  Metabolic impairment is an important contributor to heart failure ( HF ) pathogenesis and progression. Dysregulated metabolic pathways remain poorly characterized in patients with  HF  and preserved ejection fraction ( HF p EF ). We sought to determine metabolic abnormalities in  HF p EF  and identify pathways differentially altered in  HF p EF  versus  HF  with reduced ejection fraction ( HF r EF ).    Methods and Results  We identified  HF p EF  cases,  HF r EF  controls, and no‐ HF  controls from the  CATHGEN  study of sequential patients undergoing cardiac catheterization.  HF p EF  cases (N=282) were defined by left ventricular ejection fraction ( LVEF ) ≥45%, diastolic dysfunction grade ≥1, and history of  HF ;  HF r EF  controls (N=279) were defined similarly, except for having  LVEF  <45%. No‐ HF  controls (N=191) had  LVEF  ≥45%, normal diastolic function, and no  HF  diagnosis. Targeted mass spectrometry and enzymatic assays were used to quantify 63 metabolites in fasting plasma. Principal components analysis reduced the 63 metabolites to uncorrelated factors, which were compared across groups using  ANCOVA . In basic and fully adjusted models, long‐chain acylcarnitine factor levels differed significantly across groups ( P< 0.0001) and were greater in  HF r EF  than  HF p EF  ( P =0.0004), both of which were greater than no‐ HF  controls. We confirmed these findings in sensitivity analyses using stricter inclusion criteria, alternative  LVEF  thresholds, and adjustment for insulin resistance.    Conclusions  We identified novel circulating metabolites reflecting impaired or dysregulated fatty acid oxidation that are independently associated with  HF  and differentially elevated in  HF p EF  and  HF r EF . These results elucidate a specific metabolic pathway in  HF  and suggest a shared metabolic mechanism in  HF  along the  LVEF  spectrum.

journal of the american heart association

Metabolomic Profiling Identifies Novel Circulating Biomarkers of Mitochondrial Dysfunction Differentially Elevated in Heart Failure With Preserved Versus Reduced Ejection Fraction: Evidence for Shared Metabolic Impairments in Clinical Heart Failure