1. Introduction
Disrupted nicotinamide adenine dinucleotide (NAD+) metabolism is increasingly deemed to be one of risk factor for amendable cardiovascular disorders. A substantial evidence has mirrored that restoring NAD+ stock and energy metabolism may be effective in alleviating the symptoms of patients with heart failure (HF), one of the typical cardiovascular disease after myocardial infarction (MI).
2. About HF
HF has dominant clinical features of ventricular filling or ejection impairment, concomitant with abnormalities in cardiac structure/function. This disorder afflicts about 38 million patients across the world, and the number of HF patients is on the rise with the age, posing a great threat to the life of patients and bringing huge economic burden on the patient family and society.
In terms of drug therapies of HF, the "golden triangle" of beta blockers, ACEI/ARB, and aldosterone receptor antagonists has long been the preferred option. Despite significant improvement on the survival of patients, the 5-year mortality rate remains at 50%. Hence, it is of great significance to seek novel way with high efficacy and safety. NAD supplements may be an effective choice for alleviating HF.
3. Research protocol
For further verification of the efficacy of NAD+, MI-induced HF models are constructed in male Sprague-Dawley rats and beagles herein. Subsequently, the left anterior descending arteries of MI-induced HF animals are ligated for 1 week, followed by 4-week treatment with or without low/medium/high dose of NAD+ and the positive control drug LCZ696, an angiotensin receptor blocker-neprilysin inhibitor with an cardioprotective effect after MI.
4. The efficacy of NAD on rats and beagles with MI-induced HF
NAD+ shows the equivalent efficacy as LCZ696 in the treatment of MI-induced HF, or even better than LCZ696 at the medium and high doses. In rat/beagle HF models, the heart mass index, heart function, and myocardial fibrosis in the infarct marginal zone are dose-dependently improved post administration of NAD or LCZ696, as manifested by decreased end-systolic volume, end-systolic dimension, creatine kinase and lactic dehydrogenase, as well as the increased ejection fractions, fractional shortening, cardiac output, and stroke volume. In addition, the downregulation of left ventricular blood pressure in the HF model animals is ameliorated post administration of NAD or LCZ696.
5. Conclusion
In rat and beagle MI-induced HF models, NAD+ conspicuously alleviates myocardial hypertrophy and cardiac function, represses myocardial fibrosis, and reduces the myocardial infarction, laying a theoretical foundation for the clinical application of energy metabolism therapy with NAD+.
Reference
Pei Z, Yang C, Guo Y, Dong M, Wang F. The Role of NAD+ in Myocardial Ischemia-induced Heart Failure in Sprague-Dawley Rats and Beagles. Curr Pharm Biotechnol. Published online February 13, 2024. doi:10.2174/0113892010275059240103054554
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