Variable response to inhaled nitric oxide after cardiac surgery

Inhaled nitric oxide (NO) is a promising therapy that may be valuable in the control of pulmonary hypertension in cardiac surgical patients. Patients with valvular heart disease have remodeling of the pulmonary vascular bed that contributes to pulmonary hypertension. The purpose of this study was to compare the efficacy of inhaled NO in cardiac surgical patients with pulmonary hypertension with and without valvular heart disease. The effect of inhaled NO (40 ppm) on pulmonary hemodynamics in patients with pulmonary hypertension (mean pulmonary artery pressure ≥30 mm Hg) was studied in the operating room after cardiac operation. Fifteen patients with valvular heart disease comprised the study group; 25 patients undergoing aortocoronary bypass grafting were controls. In patients undergoing aortocoronary bypass grafting, inhaled NO produced a 24% decrease in mean pulmonary artery pressure (33 ± 1 to 25 ± 1 mm Hg; p < 0.05), a 36% decrease in pulmonary vascular resistance (375 ± 30 to 250 ± 30 dyne · s · cm −5; p < 0.05), and no change in systemic arterial blood pressure. On the other hand, patients with pulmonary hypertension from valvular heart disease did not respond to inhaled NO: mean pulmonary artery pressure was 39 ± 3 mm Hg and pulmonary vascular resistance was 620 ± 30 dyne · s · cm −5 before, during, and after NO. Among cardiac surgical patients with pulmonary hypertension, the response to inhaled NO is variable. Despite the promise of inhaled NO as a pulmonary vasodilator in cardiac surgical patients, these data suggest that alternative therapies are needed to control pulmonary hypertension in patients with pulmonary hypertension from valvular heart disease.