ADENOSINE INFUSION FOR THE REVERSAL OF PULMONARY VASOCONSTRICTION IN BIVENTRICULAR FAILURE - A GOOD TEST BUT A POOR THERAPY

Background. Elevation of pulmonary vascular resistance is an important determinant of right ventricular function in patients with end-stage biventricular heart failure. Vasodilator drug therapy directed at the pulmonary vasculature is used in the hemodynamic assessment of patients for orthotopic heart transplantation, and therapy aimed at decreasing pulmonary vascular resistance and transpulmonary pressure gradient has been advocated in patients awaiting heart transplantation. Adenosine infusion has been shown to cause selective pulmonary vasodilatation in normal subjects and in patients with primary pulmonary hypertension but has not been assessed in patients with biventricular heart failure. Methods and Results. Using two infusion doses, we studied the pulmonary and renal hemodynamic effects of adenosine on patients referred for heart transplantation (n=21) and compared it with sodium nitroprusside (n=18). Patients received 30% oxygen via face mask throughout the study. Adenosine at 100-mu-g/kg/min achieved the same percentage fall in pulmonary vascular resistance as nitroprusside (41+/-6% versus 42+/-4%) and a greater and more consistent fall in transpulmonary pressure gradient (35+/-6% versus 9+/-30%, p<0.02). The mean arterial blood pressure fell by 16 mm Hg with nitroprusside but was unchanged by adenosine, indicating that in contrast to nitroprusside, adenosine acted as a selective pulmonary vasodilator. Despite this, cardiac index showed only a modest increase with adenosine (1.73+/-0.09 to 1.89+/-0.161 . m-2,p<0.05), and there was a rise in pulmonary capillary wedge pressure from baseline at the higher dose (29.7+/-2.5 to 33.4+/-3.4 mm Hg, p<0.05). Renal blood flow was unchanged during adenosine infusion. Conclusions. Adenosine is a potent selective pulmonary vasodilator in patients with biventricular heart failure and is preferable to sodium nitroprusside as a test for the reversibility of pulmonary vasoconstriction. However, its deleterious effects on left atrial pressure make it unsuitable as a therapeutic agent in patients awaiting heart transplantation.