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Circulating Omentin Levels in Heart Failure: A Case-Control Study
Diego Currò1, Edoardo Vergani1, Maria Anna Nicolazzi2
1Dipartimento di Medicina e Chirurgia Traslazionale, Università Cattolica del Sacro Cuore, 00136 Rome, Italy.
Insights
Lower omentin levels are observed in heart failure patients with reduced (HFrEF) and preserved ejection fraction (HFpEF). This adipokine is inversely linked to BMI and reduced in heart failure patients with COPD, suggesting a potential biomarker role.
Area of Science:
- Cardiology
- Endocrinology
- Biochemistry
Background:
- Cardiovascular diseases are a leading cause of death globally.
- Heart failure (HF) is a critical endpoint, with phenotypes like HFrEF and HFpEF presenting distinct challenges.
- HFpEF pathophysiology involves inflammation and metabolic issues, with adipokines potentially playing a role.
Purpose of the Study:
- To investigate and compare circulating omentin levels in patients with HFrEF and HFpEF.
- To explore the relationship between omentin, body mass index (BMI), and chronic obstructive pulmonary disease (COPD) in heart failure patients.
Main Methods:
- Cross-sectional study comparing omentin levels.
- Analysis of omentin in relation to BMI and COPD status in heart failure cohorts.
Main Results:
- Omentin levels were significantly lower in both HFpEF and HFrEF patients compared to controls.
- Omentin showed an inverse correlation with BMI.
- Omentin levels were significantly lower in heart failure patients with COPD.
Conclusions:
- Omentin may serve as a potential biological marker in heart failure.
- Further research in diverse populations is needed to confirm the clinical significance of omentin in heart failure.
Abstract:
Cardiovascular diseases remain the leading cause of global mortality, with heart failure (HF) representing a critical clinical endpoint. HF is traditionally classified into two distinct phenotypes based on left ventricular ejection fraction (LVEF): HF with reduced ejection fraction (HFrEF, LVEF < 40%) and HF with preserved ejection fraction (HFpEF, LVEF > 50%). While HFrEF is well-characterized and responsive to conventional pharmacological therapies, HFpEF remains therapeutically challenging due to its complex pathophysiology involving metabolic comorbidities and systemic inflammation. Emerging evidence suggests that adipokines may play a role in these inflammatory pathways. The present study aimed to evaluate and compare circulating levels of omentin, a recently discovered visceral adipose tissue-derived adipokine, in patients with HFrEF and HFpEF. This study reports that omentin levels were significantly lower in both HFpEF and HFrEF compared to controls. Moreover, omentin is inversely correlated to BMI and significantly lower in HF subjects with COPD than in those with no medical history of COPD. In conclusion, omentin may represent a potential biological signal in heart failure; however, further validation in broader populations is necessary to establish its clinical relevance.
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