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Niacin, a compound primarily used for its lipid altering properties, has been shown to improve endothelial function with short term administration, via the release of prostaglandins. We hypothesized that via these effects, niacin could lead to reductions in pulmonary artery pressures.
Pilot study involving 32 subjects with known tricuspid regurgitation (TR) and a Doppler jet velocity of 2.7 m/s or greater. Subjects were randomized in a 1:2:2 ratio to receive a single dose of either placebo, niacin 100mg or niacin 500mg respectively in a double blinded, acute provocation study. Following baseline assessment of TR jet velocity, blinded study drug was administered. At peak absorption of niacin and maximal flushing triggered by prostaglandin release (1 hour post-administration), TR jet velocity was re-assessed. The study was powered to detect a difference of 0.2 ± 0.2 m/s in TR jet velocity between groups.
Baseline TR jet velocity was 2.89 ± 0.30 m/s. The mean change in Doppler jet velocity was -0.024 ± 0.15 m/s in the placebo group, compared to -0.041 ± 0.27 m/s with niacin 100 mg, and -0.065 ± 0.17 m/s with niacin 500 mg. This trend was not statistically significant (ANOVA). The overall reduction in TR jet velocity observed with niacin, (2.93 ± 0.32 m/s to 2.87 ± 0.42 m/s) was small and not statistically significant (P = 0.26). There was no observed effect among subgroups with above or below median baseline TR Doppler jet velocities.
Single dose administration of immediate-release niacin 100 mg or 500 mg has no significant effect on PA pressures at 1 hour post administration.