Effects of nitroprusside on cardiac norepinephrine spillover and isovolumic left ventricular relaxation in the normal and failing human left ventricle.

BACKGROUND

Left ventricular isovolumic relaxation responses to changes in afterload or preload may be mediated, in part, by reflex changes in sympathetic nervous system activity.

PATIENTS AND METHODS

The authors examined whether changes in left ventricular isovolumic relaxation during changes in load were associated with changes in cardiac norepinephrine spillover. Six patients with normal left ventricular function and 12 patients with congestive heart failure secondary to left ventricular systolic dysfunction were studied. Measurements of left ventricular isovolumic relaxation (Tau) were obtained using a high fidelity left ventricular pressure manometer, before, during and after infusion of nitroprusside. Total body and cardiac norepinephrine spillover were measured using a radiotracer infusion.

RESULTS

Nitroprusside caused significant reductions in systemic arterial and left ventricular end-diastolic pressures, changes that were similar in the two groups. In people with normal left ventricular systolic function, these changes were associated with significant increases in both systemic and cardiac sympathetic activity, but no change in Tau. In the group with congestive heart failure, cardiac norepinephrine spillover did not change; however, there was a significant increase in the rate of left ventricular isovolumic relaxation.

CONCLUSION

This study confirms that in the failing human left ventricular, isovolumetric relaxation is sensitive to changes in loading conditions induced by the nitrosovasodilator nitroprusside. Importantly, this load sensitivity is not associated with reflex increases in cardiac sympathetic activity.