Nitroprusside in critically ill patients with left ventricular dysfunction and aortic stenosis.

BACKGROUND Vasodilators are considered to be contraindicated in patients with severe aortic stenosis because of concern that they may precipitate life-threatening hypotension. However, vasodilators such as nitroprusside may improve myocardial performance if peripheral vasoconstriction is contributing to afterload. METHODS We determined the response to intravenous nitroprusside in 25 patients with severe aortic stenosis and left ventricular systolic dysfunction. Patients were included in the study if they had been admitted to the intensive care unit for invasive hemodynamic monitoring of heart failure and if they had a depressed ejection fraction (<or=0.35), severe aortic stenosis (aortic-valve area, <or=1 cm2), and a depressed cardiac index (<or=2.2 liters per minute per square meter). Patients were excluded if they had hypotension, defined as either the need for intravenous inotropic or pressor agents or a low mean systemic arterial pressure (<60 mm Hg). Patients were enrolled irrespective of other, coexisting valve disease or coronary artery disease. RESULTS At base line, the mean (+/-SD) ejection fraction was 0.21+/-0.08; the aortic-valve area was 0.6+/-0.2 cm2, with peak and mean gradients of 65+/-37 and 39+/-23 mm Hg, respectively; and the cardiac index was 1.60+/-0.35 liters per minute per square meter. After six hours of therapy with nitroprusside (at which time the dose had been increased to a mean of 103+/-67 microg per minute), the cardiac index had increased to 2.22+/-0.44 liters per minute per square meter (P<0.001 for the comparison with base line). After 24 hours of nitroprusside infusion (dose, 128+/-96 microg per minute), the cardiac index had increased further, to 2.52+/-0.55 liters per minute per square meter (P<0.001 for the comparison with base line). Nitroprusside was well tolerated and had minimal side effects. CONCLUSIONS Nitroprusside rapidly and markedly improves cardiac function in patients with decompensated heart failure due to severe left ventricular systolic dysfunction and severe aortic stenosis. It provides a safe and effective bridge to aortic-valve replacement or oral vasodilator therapy in these critically ill patients.