Left ventricular chamber function during inhaled nitric oxide in patients with dilated cardiomyopathy

Inhaled nitric oxide is a potent and selective pulmonary vasodilator. Howev er, when used in patients with congestive cardiac failure, the decrease in pulmonary vascular resistance is associated with an increase in pulmonary c apillary wedge pressure (PCWP). This study examined load-independent indexe s of left ventricular chamber function during inhaled nitric oxide in 10 pa tients with dilated cardiomyopathy (mean ejection fraction, 30.2 +/- 7.8%, mean +/- SD). Etiology of cardiomyopathy was idiopathic in six and ischemic in four. Pulmonary hemodynamics in seven patients revealed normal resting pulmonary vascular resistance. Chamber function was defined by recording pr essure-volume loops at steady state and during inferior vena caval occlusio n during inhalation of 20 ppm nitric oxide for 10 min. We found no effect o f inhaled nitric oxide on steady-state left ventricular pressures, volumes, contractility (end-systolic elastance or preload recruitable stroke work), contraction duration, or active (tau, dP/dt(min)) or passive (end-diastoli c pressure-volume relation) diastolic function. Right heart filling pressur es did not change. We therefore conclude that 20 ppm inhaled nitric oxide d oes not affect left ventricular chamber function in patients with controlle d heart failure. Previously described elevations in PCWP during inhaled nit ric oxide are most likely due to altered left ventricular loading condition s related to secondary pulmonary hypertension in severe heart failure.