Physiologic Assessment of Milrinone Therapy in Severe Heart Failure Patients

To assess the inotropic, vasodilator, and afterload-reducing effects of intravenous milrinone in patients with severe congestive heart failure, a simple noninvasive echocardiographic study coupled with a right atheterization was performed in 12 patients. Milrinone was administered intravenously as a 50 $mUg $$ kg-1 bolus followed by a 24-h milrinone infusion at a rate of 5 $mUg $$ kg-1 $$ min-1 Echocardiographic left ventricular end-diastolic diameter (Ded), end-systolic diameter (Des), and wall thickness were measured at baseline and at 24 h of milrinone insusion, before and after a sublingual nitrate administration (0.8 mg of nitroglycerin) that induced load variations. Hemodynamic measurements were performed simultaneously. Left ventricular end-systolic meridionalwall stress (Ses) was then calculated. The slopes of percent fractional shortening (percent FS) Ses and Ses/Des, obtained during sublingual nitrate administration, were traced, Both end-systolic relations are an index of the contractile state. Milrinone therapy imporved hemodynamics in all patients, resulting in stabilized hemodynamic conditions between 12 and 24 h of continuous milrinone infusion. At these times, the cardiac index increased to 30% while the capillary pulmonary wedge pressure and systemic vascular resistance decreased to 26 and 24%, respectively (all p < 0.01). The average slope of Ses/Des shifted upward from 47.5 $$ 30 to 69.25 $$ 34 (p < 0.05) and the average slope of (percent FS)/Ses shifted from −0.032 $$ 0.025 to −0.082 $$ 0.061 (p < 0.01), both variations attesting the inotropic effect of milrinone. However, the decrease in systemic vascular resistance (ΔSVR) was closely correlated to the decrease in endsystolic meridional wall stress (ΔSes) (r = +0.75; p = 0.0046). This suggests a dominant vasodilator action of milrinone in severe heart failure patients. This noninvasive echocardiographic study coupled with a righ catheteriation allowed the separation of the inotropic effect of milrinone from its vasodilator action. This may have useful clinical implications for intensive care patients with severe heart failure.