Effect of Intravenous Nicotinamide Adenine Dinucleotide on Left Ventricular Function After Primary Percutaneous Coronary Intervention in ST-Segment Elevation Myocardial Infarction: A Randomized Controlled Trial

BACKGROUND: Despite timely reperfusion and guideline-directed therapies, the recovery of left ventricular function after ST-segment elevation myocardial infarction (STEMI) remains suboptimal. Adjunctive metabolic therapy may enhance post-infarction cardiac repair. Nicotinamide adenine dinucleotide (NAD⁺), a key regulator of cellular bioenergetics and redox homeostasis, has cardioprotective effects in experimental ischemia-reperfusion injury. However, its clinical impact in patients undergoing primary percutaneous coronary intervention (PCI) remains unclear. METHODS: In this prospective, randomized, placebo-controlled trial, 120 patients with STEMI undergoing primary PCI were assigned to receive intravenous NAD⁺ (10 mg/day) or placebo for 7 days, in addition to standard medical therapy. The primary endpoint was the left ventricular ejection fraction (LVEF) at 30 days. The secondary endpoints included N-terminal pro-B-type natriuretic peptide (NT-proBNP) levels at 7 and 30 days, echocardiographic parameters at 30 days, and major adverse cardiac and cerebrovascular events (MACCE) at 6 months. RESULTS: At 30 days, the NAD⁺ group demonstrated a modest but significant improvement in LVEF compared with the placebo group (56.32 ± 8.04% vs. 53.37 ± 8.12%, p = 0.048). NT-proBNP levels were lower in the NAD⁺ group at follow-up. However, findings for LV remodeling parameters were mixed, and no significant between-group difference was observed in 6-month MACCE rates. CONCLUSIONS: Short-term intravenous NAD⁺ therapy following primary PCI improved left ventricular systolic function and reduced NT-proBNP levels in patients with STEMI. These findings suggest that restoring NAD⁺ availability may facilitate post-ischemic cardiac recovery, potentially through mechanisms related to mitochondrial energy metabolism and NAD⁺-dependent stress-response signaling. Larger trials are required to confirm its long-term clinical benefits and elucidate the underlying biological pathways. REGISTRATION: Chinese Clinical Trial Registry identifier number ChiCTR2200059333.