ABSTRACT
BACKGROUND: Understanding the pathophysiology of heart failure (HF) with preserved ejection fraction (HFpEF) continues to be challenging. Several inflammatory and metabolic biomarkers have recently been suggested to be involved in HFpEF. OBJECTIVES: The purpose of this review was to synthesize the evidence on non-traditional biomarkers from metabolomic studies that may distinguish HFpEF from heart failure with reduced ejection fraction (HFrEF) and controls without HF. METHODS: A systematic search was conducted using Medline and PubMed with search terms such as "HFpEF" and "metabolomics", and a meta-analysis was conducted. RESULTS: Myeloperoxidase (MPO) levels were significantly (p < 0.001) higher in HFpEF than controls without HF, but comparable (p = 0.838) between HFpEF and HFrEF. Carnitine levels were significantly (p < 0.0001) higher in HFrEF than HFpEF, but comparable (p = 0.443) between HFpEF and controls without HF. Derivatives of reactive oxidative metabolites (DROMs) were not significantly (p = 0.575) higher in HFpEF than controls without HF. CONCLUSION: These data suggest that MPO is operative in HFpEF and HFrEF and may be a biomarker for HF. Furthermore, circulating carnitine levels may distinguish HFrEF from HFpEF.
Subject(s)
Heart Failure , Humans , Carnitine , Stroke Volume/physiology , Biomarkers/metabolism , Peroxidase , Oxidative Stress , PrognosisABSTRACT
This review will focus on epigenetic modifications utilizing the DNA methylation mechanism, which is potentially involved in the pathogenesis of heart failure with preserved ejection fraction (HFpEF). The putative pathways of HFpEF will be discussed, specifically myocardial fibrosis, myocardial inflammation, sarcoplasmic reticulum Ca2+-ATPase, oxidative-nitrosative stress, mitochondrial and metabolic defects, as well as obesity. The relationship of HFpEF to aging and atrial fibrillation will be examined from the perspective of DNA methylation.
