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The Efficacy of Risk Factor Modification Compared to NAD+ Repletion in Diastolic Heart Failure
Yen Chin Koay1,2,3, Ren Ping Liu1,2,3, Bailey McIntosh1,2,3
1Cardiometabolic Medicine Group, The University of Sydney, Sydney, New South Wales, Australia.
Insights
Heart failure with diastolic dysfunction shows depleted nicotinamide adenine dinucleotide (NAD+). Supplementation with nicotinamide riboside (NR) restored NAD+ levels and improved heart function, offering a potential therapeutic strategy.
Area of Science:
- Cardiology
- Biochemistry
- Metabolic Diseases
Background:
- Heart failure (HF) with left ventricular diastolic dysfunction is a significant global health issue.
- Myocardial nicotinamide adenine dinucleotide (NAD+) depletion is implicated in diastolic HF pathophysiology.
- Understanding NAD+ metabolism is crucial for developing novel therapeutic interventions.
Purpose of the Study:
- To evaluate myocardial NAD+ levels in human systolic and diastolic HF.
- To investigate the therapeutic potential of NAD+ repletion using nicotinamide riboside (NR).
- To assess the efficacy of NR in a murine model of HF with preserved ejection fraction.
Main Methods:
- Quantification of myocardial NAD+ and nicotinamide phosphoribosyltransferase (NAMPT) levels in human HF patients.
- Administration of NR to human myocardial tissue samples and a murine HF model.
- Assessment of metabolic and antioxidant profiles in the murine model.
Main Results:
- Significant depletion of NAD+ and NAMPT observed in human diastolic HF myocardium.
- NR treatment successfully restored myocardial NAD+ levels in human samples.
- In murine HF with preserved ejection fraction, NR improved metabolic and antioxidant parameters, both preventively and therapeutically.
Conclusions:
- Myocardial NAD+ depletion is a key feature of diastolic HF.
- NAD+ repletion via NR demonstrates therapeutic potential for diastolic HF.
- NR warrants further investigation as a treatment for heart failure with preserved ejection fraction.
Abstract:
Heart failure (HF) with left ventricular diastolic dysfunction is a growing global concern. This study evaluated myocardial oxidized nicotinamide adenine dinucleotide (NAD+) levels in human systolic and diastolic HF and in a murine model of HF with preserved ejection fraction, exploring NAD+ repletion as therapy. We quantified myocardial NAD+ and nicotinamide phosphoribosyltransferase levels, assessing restoration with nicotinamide riboside (NR). Findings show significant NAD+ and nicotinamide phosphoribosyltransferase depletion in human diastolic HF myocardium, but NR successfully restored NAD+ levels. In murine HF with preserved ejection fraction, NR as preventive and therapeutic intervention improved metabolic and antioxidant profiles. This study underscores NAD+ repletion's potential in diastolic HF management.
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