Why the study?
Inhaled nitric oxide reduces right ventricular afterload in the immediate phase of acute PE, but whether it has pulmonary vasodilator efficacy in both the immediate and prolonged phase was unknown.
Does inhaled nitric oxide improve pulmonary hemodynamics in a porcine model of acute pulmonary embolism?
Population
18 anesthetized pigs in a porcine model of intermediate-risk PE
Comparison
iNO at 40 ppm vs vehicle vs sham
Design
Randomized preclinical animal study
Follow-up
12 hours
Key result
Inhaled nitric oxide significantly reduced mean pulmonary artery pressure at 12 hours compared to vehicle in a porcine model of acute pulmonary embolism (-3.5 vs 0.5 mmHg, p < 0.0001).
Authors
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Hypothesis-generating for inhaled nitric oxide in acute pulmonary embolism; human trials needed before clinical consideration.
RCT (n=18)
randomized
Does inhaled nitric oxide improve pulmonary hemodynamics in a porcine model of acute pulmonary embolism?
Absolute Event Rate: -3.5% vs 0.5%
p-value: p=<0.0001
Inhaled nitric oxide effectively reduces pulmonary artery pressure in both the immediate and prolonged phases of acute pulmonary embolism in a porcine model.
Kramer et al. (2020) conducted an RCT in acute pulmonary embolism (n=18). Inhaled nitric oxide (iNO) vs. Vehicle (no active treatment) and sham was evaluated on mean pulmonary artery pressure (mPAP) reduction at 12 hours (p=<0.0001). Inhaled nitric oxide significantly reduced mean pulmonary artery pressure at 12 hours compared to vehicle in a porcine model of acute pulmonary embolism (-3.5 vs 0.5 mmHg, p < 0.0001).