Objective: The objective of this study was to assess the acute hemodynamic effects of endogenous adenosine accumulation in patients with chronic heart failure. Exogenously administered adenosine has been shown to reduce pulmonary vascular resistance and to increase cardiac index in normal subjects and in patients with pulmonary hypertension or end-stage biventricular heart failure. Endogenous adenosine accumulation can be provoked by dipyridamole.
Methods and results: Ultra-low-dose dipyridamole (0.07 mg/kg/min for 4 minutes) was administered in 20 patients with either symptomatic idiopathic (n = 12) or ischemic (n = 8) dilated cardiomyopathy and reduced left ventricular ejection fraction (mean 25%+/-5%). Hemodynamic variables were measured before and within 1 minute from the end of dipyridamole infusion. After dipyridamole administration, a mild but significant increase in heart rate (4.5%; p = 0.03) and reduction in mean blood pressure (6.8%; p < 0.001) without changes in right atrial pressure (p = NS) were detected. Dipyridamole increased cardiac output by 26.6% (p < 0.001), cardiac index by 24% (p < 0.001), and stroke volume by 19.8% (p < 0.001), with concomitant 24.6% reduction of systemic vascular resistance (p < 0.001). Moreover, dipyridamole reduced mean pulmonary artery pressure by 8.3% (p < 0.01) and pulmonary vascular resistance by 33.3% (p = 0.001), without changes in pulmonary wedge pressure (p = NS). A significant correlation between percent decrease from baseline in pulmonary and systemic vascular resistance (r = 0.66; p = 0.002) was found after administration of dipyridamole.
Conclusions: Endogenous adenosine accumulation induced by ultra-low-dose dipyridamole infusion acutely improves the hemodynamic profile, decreasing pulmonary and, to a lower extent, systemic vascular resistance and increasing cardiac index in patients with severe chronic heart failure.