Key result
Intravenous NAD+ improves 30-day LVEF by ~3 points vs. placebo following primary PCI for STEMI.
Why the study?
Left ventricular functional recovery after STEMI remains suboptimal despite timely reperfusion, and while nicotinamide adenine dinucleotide (NAD⁺) shows cardioprotective effects in experimental ischemia-reperfusion injury, its clinical impact in patients undergoing primary PCI was unclear.
Does short-term intravenous nicotinamide adenine dinucleotide (NAD+) supplementation improve 30-day left ventricular ejection fraction in patients with acute STEMI undergoing primary percutaneous coronary intervention?
RCT (n=120)
Blinded outcome assessment and placebo-controlled
1:1 computer-generated sequence
No
Does short-term intravenous nicotinamide adenine dinucleotide (NAD+) supplementation improve 30-day left ventricular ejection fraction in patients with acute STEMI undergoing primary percutaneous coronary intervention?
Short-term intravenous NAD+ supplementation for 7 days following primary PCI in STEMI patients modestly improved 30-day LVEF and lowered NT-proBNP levels, though it did not significantly reduce 6-month MACCE rates.
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. 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. 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. 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. Chinese Clinical Trial Registry identifier number ChiCTR2200059333.
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Yu et al. (2026) conducted an RCT in ST-segment elevation myocardial infarction (STEMI) undergoing primary percutaneous coronary intervention (n=120). Intravenous nicotinamide adenine dinucleotide (NAD+) vs. Placebo (100 mL of 0.9% normal saline) was evaluated on Left ventricular ejection fraction (LVEF, %) at 30 days (p=0.048). Intravenous NAD+ therapy for 7 days significantly improved 30-day LVEF compared with placebo (56.32% vs 53.37%, p=0.048) in STEMI patients after primary PCI.
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