[Acute changes in the hemodynamic profile and circulating levels of atrial natriuretic peptide induced by dobutamine in severe heart failure]. / Modificazioni acute del profilo emodinamico e dei livelli circolanti di peptide natriuretico atriale indotte dalla dobutamina nello scompenso cardiaco grave.

METHODS: Sixteen patients (15 males, 1 female; mean age 63 years, range 45-78) with severe heart failure (NYHA class III = 5; class IV = 11) secondary to ischemic heart disease (8), dilated cardiomyopathy (5) and valvular heart disease (3), were evaluated for eligibility to intermittent Dobutamine (D) treatment. As a part of this evaluation, they were submitted to an acute dose-ranging test with D, up to 10 micrograms/Kg/min under hemodynamic and electrocardiographic monitoring. By inclusion criteria, all patients had:-cardiac index (CI) < 2.2 L/min/m2;-pulmonary wedge pressure (WP) > 18 mmHg;-left ventricular ejection fraction (EF) < 30%. At each step of the procedure, hemodynamic measurements and blood sampling for atrial natriuretic peptide (ANP) concentration were performed. RESULTS: Peak effect, defined as the dose corresponding to the maximum increase in CI, was reached at a mean of 7.8 +/- 0.5 micrograms/Kg/min. CI increased from 1.7 +/- 0.3 to 2.53 +/- 0.7 L/min/m2 (p < 0.001) and ANP decreased from 234 +/- 112 to 173 +/- 118 pg/ml (p < 0.001). Correspondingly, heart rate, stroke volume index and stroke work index increased, while right atrial pressure (RAP), mean pulmonary artery pressure (PAP), WP, systemic and pulmonary vascular resistance all significantly decreased. Mean arterial pressure was not affected. Changes in ANP concentration correlate significantly with changes in WP and in PAP (r = 0.65, p < 0.05 and r = 0.89, p < 0.001, respectively), but not with changes in RAP (r = 0.26, p = 0.34). Patients showing an increase > 40% in CI or a CI > or = 2.5 L/min/m2 at peak effect (responders) had significantly lower baseline PAP with respect to non-responders. Besides PAP, baseline ANP levels, end-systolic pressure/volume ratio and ejection fraction were also independent predictors of response. The test did not induce complex arrhythmias and was well tolerated in all patients. CONCLUSIONS: Patients with severe heart failure retain the ability to respond to acute administration of D. with a significant improvement in their hemodynamic profile. Response to D. administration is predicted by lower baseline pulmonary pressure and ANP levels and a lesser degree of left ventricular dysfunction. Despite high baseline ANP concentration, a significant decrease is obtained which parallels the decrease in pulmonary artery and pulmonary wedge pressure, but is not related to changes in right atrial pressure. These findings suggest that changes in left ventricular performance induced by D. are the major determinants of the decrease in ANP concentration in this clinical setting.