INSIGHTS INTO THE MECHANISM OF THE NITROPRUSSIDE-INDUCED INCREASE IN CARDIAC-OUTPUT IN FAILING HEARTS - AN ATTEMPT AT ITS PREDICTION WITH DOPPLER-ECHOCARDIOGRAPHY

Increased left ventricular (LV) diastolic pressure is consistently dec reased by the administration of nitroprusside; however, nitroprusside- induced changes in cardiac output (GO) vary among patients with failin g hearts. Although the variation has been considered to be related to interindividual inhomogeneity of LV diastolic performance, nitroprussi de-induced changes in CO are not predictable before drug administratio n in individual subjects. We attempted to clarify whether nitroprussid e-induced changes in CO may be predicted by analysis of the mitral flo w velocity pattern in failing hearts. LV diastolic pressure was increa sed by the combination of the decrease in LV function and the volume e xpansion, and 15 conditions with LV end-diastolic pressure (EDP) great er than or equal to 15 mm Hg were obtained in 8 dogs. In each conditio n, pulsed Doppler mitral flow velocity patterns were recorded simultan eously with hemodynamic variables before and during intravenous nitrop russide infusion. After nitroprusside administration, LV systolic pres sure and LVEDP decreased in all dogs, and CO increased in eight condit ions but decreased in seven conditions. CO was more Likely to increase with administration of nitroprusside, and its change was greater in t he conditions in which deceleration time of the early diastolic fillin g wave before nitroprusside infusion was longer (r = 0.56, p<0.05, n = 15). Better correlation was obtained with multiple-regression analysi s, using the deceleration time and peak filling velocity at atrial con traction (r = 0.67, p<0.05, n = 15). The deceleration time correlated with LV dynamic compliance (r = 0.66, p<0.01, n = 30). Analysis of mit ral flow velocity patterns may be useful in predicting nitroprusside-i nduced changes in CO in failing hearts.