Hemodynamic effects of nitroprusside on valvular aortic stenosis

Abstract

The effects of acute reduction of left ventricular (LV) loading in valvular aortic stenosis (AS) were examined. Thirty-five consecutive patients with AS (peak-to-peak aortic valve gradient 66 ± 26 mm Hg, aortic valve area 0.65 ± 0.22 cm 2) were given intravenous sodium nitroprusside (1 to 3 μg/kg/min) to reduce systolic aortic pressures by >10 mm Hg (mean aortic pressure 99 ± 15 to 80 ± 15 mm Hg; p < 0.001). Overall, nitroprusside infusion resulted in little change in cardiac index (2.72 ± 0.61 to 2.67 ± 0.58 liters/min/m 2; p = not significant). Individual patients had a range of responses. Fourteen patients (group 1) had an increase in cardiac index (2.42 ± 0.59 to 2.74 ± 0.67 liters/min/m 2; p < 0.001), whereas 21 (group 2) had a decrease or no change (2.93 ± 0.56 to 2.61 ± 0.52 liters/min/ m 2; p < 0.001). Comparison of these subgroups showed that a cardiac index increase with nitroprusside was significantly predicted by a higher LV end-diastolic pressure (26 ± 12 vs 15 ± 6 mm Hg), lower LV ejection fraction (44 ± 18 vs 62 ± 12%), smaller aortic valve area (0.52 ± 0.12 vs 0.74 ± 0.22 cm 2) and lower cardiac index (2.42 ± 0.59 vs 2.93 ± 0.56 liters/min/m 2) (all values groups 1 and 2, respectively). It is concluded that there is a disparate response to acute vasodilatation in AS. Potentially beneficial effects are seen in a subgroup of patients, especially those with increased filling pressures and impaired LV function. It is postulated that the hemodynamic effects of sodium nitroprusside in patients with AS can be explained by the balance of effects on preload and afterload.