Key result
Inhaled nitric oxide at 10 ppm for 48 hours after cardiac surgery significantly increased cardiac index (3.93 vs 2.65 l/min/m2, p=0.03) compared to oxygen therapy in patients with mitral stenosis and severe pulmonary hypertension.
Why the study?
Does inhaled nitric oxide improve cardiac hemodynamics and short-term clinical outcomes in patients with mitral stenosis and severe pulmonary hypertension undergoing cardiac surgery?
RCT (n=27)
Does inhaled nitric oxide improve cardiac hemodynamics and short-term clinical outcomes in patients with mitral stenosis and severe pulmonary hypertension undergoing cardiac surgery?
Absolute Event Rate: 3.93% vs 2.65%
p-value: p=0.03
Inhaled nitric oxide administered immediately after surgery in patients with mitral stenosis and severe pulmonary hypertension improves cardiac index and reduces the need for vasoactive drugs.
Supports short-term use to boost cardiac index and cut vasoactive drugs post-surgery; extends limited RCT evidence in mitral stenosis with severe PH.
Mitral stenosis is frequently associated with increased pulmonary vascular resistance (PVR), pulmonary hypertension and right ventricular dysfunction that persist even after surgery. Inhaled nitric oxide (NO) has been shown to selectively reduce PVR in patients with pulmonary hypertension. We tested the hypothesis that NO would improve the hemodynamic effects and short-term clinical outcomes of patients with mitral stenosis and severe pulmonary hypertension undergoing cardiac surgery. Twenty-seven patients (three male, 24 female) with a mean age of 46.9 ± 12.9 years with mitral stenosis and elevated pulmonary artery systolic pressure (PASP) were randomly allocated to receive continuously inhaled NO at 10 parts per million (NO group) or oxygen therapy (control) for 48 hours immediately after surgery. The hemodynamic data, the number and doses of vasoactive drugs, the duration of stay in the ICU and short-term complications (infections, respiratory and/or renal failure, and death) were assessed. The mean mitral valve area, gradient and PASP were 0.88 ± 0.20 cm , 15.7 ± 5.0 mmHg and 70.9 ± 10.3 mmHg, respectively, for all patients. After 48 hours, patients receiving NO showed an increased cardiac index compared with patients receiving oxygen therapy, with a reduction in the number of vasoactive drugs used. There was a significant reduction in PASP in both groups compared with preoperative levels but no differences were observed between the groups. A tendency towards a reduction in pulmonary vascular resistance, ICU stay and acute complications was observed in the NO group but did not reach statistical significance. Use of inhaled NO immediately after surgery in patients with mitral stenosis and severe pulmonary hypertension improves cardiac hemodynamics and may have clinical benefits in short-term outcomes.
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Fernandes et al. (2005) conducted an RCT in Mitral stenosis and severe pulmonary hypertension (n=27). Inhaled nitric oxide vs. Oxygen therapy was evaluated on Cardiac index at 48 hours (l/min/m2) (p=0.03). Inhaled nitric oxide at 10 ppm for 48 hours after cardiac surgery significantly increased cardiac index (3.93 vs 2.65 l/min/m2, p=0.03) compared to oxygen therapy in patients with mitral stenosis and severe pulmonary hypertension.
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