• C S Hayward, W V Kalnins, P Rogers, M P Feneley, P S Macdonald, and R P Kelly.
• Cardiology Department of St. Vincent's Hospital Darlinghurst NSW, Australia. c.s.hayward@ic.ac.uk
• J. Cardiovasc. Pharmacol. 1999 Nov 1; 34 (5): 749-54.

AbstractInhaled nitric oxide is a potent and selective pulmonary vasodilator. However, when used in patients with congestive cardiac failure, the decrease in pulmonary vascular resistance is associated with an increase in pulmonary capillary wedge pressure (PCWP). This study examined load-independent indexes of left ventricular chamber function during inhaled nitric oxide in 10 patients 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 pressure-volume loops at steady state and during inferior vena caval occlusion during inhalation of 20 ppm nitric oxide for 10 min. We found no effect of 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-diastolic pressure-volume relation) diastolic function. Right heart filling pressures did not change. We therefore conclude that 20 ppm inhaled nitric oxide does not affect left ventricular chamber function in patients with controlled heart failure. Previously described elevations in PCWP during inhaled nitric oxide are most likely due to altered left ventricular loading conditions related to secondary pulmonary hypertension in severe heart failure.

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