Efficacy of Nicotinamide Adenine Dinucleotide in Heart Failure Patients: A randomized, double-blind, placebo-control clinical trial

Author:

Meng Xuyang1,Li Yi1,Weng Sixian1,Guo Ying1,Pei Zuowei2,Dong Ming1,Wang Xiang1,Xia Chenxi1,Wang Fang1

Affiliation:

1. Beijing Hospital

2. Central Hospital of Dalian University of Technology

Abstract

Abstract Background: Nicotinamide adenine dinucleotide (NAD+) is a coenzyme for most redox reactions in metabolic processes. Heart failure occurs in the end stage of various cardiovascular diseases and is associated with a deficit in NAD+. The improvement of cardiac bioenergetics and cardiac function by supplementation of NAD+ has attracted broad intensive attention. Our objective was to evaluate the efficacy of NAD+ in the treatment of heart failure. Methods: Sixty eligible participants were randomly assigned in a 1:1 ratio to NAD+ group or placebo group and administrated with Coenzyme Ⅰ for injection (Powder for Injection, 50mg/day) or same volume of normal saline for 7-10 days. All subjects were followed up for 3 months. Transthoracic Doppler Echocardiography should be examined at the time of enrollment and 3 months follow-up. Myocardial work is derived from the strain-pressure relation, integrating in its calculation the noninvasive arterial pressure. Results: In all the 55 participants who completed the study, after treatment for heart failure, LVEF improved significantly in both NAD+ and placebo groups (both P<0.0001). In per-protocol analysis, LVEF, GWI and GWE of NAD+ group were extremely increased after 3 months of follow-up compared with baseline (all P<0.05). Furthermore, only in participants with LVEF>40%, GWI, GWW and GWE provided significant differences between baseline and 3 months follow-up in NAD+ group (all P<0.05). Conclusion: This study evaluated the efficacy of NAD+ in the treatment of HF by echocardiography, and confirmed that supplementation of NAD+ was beneficial to the improvement of cardiac function in HF patients, especially in patients with LVEF>40%.

Publisher

Research Square Platform LLC

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