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J Am Coll Cardiol, 2005; 45:965-966, doi:10.1016/j.jacc.2004.12.032 © 2005 by the American College of Cardiology Foundation |
* Cardiology Division, Massachusetts General Hospital, Bigelow 842, 32 Fruit Street, Boston, MA 02114 (Email: msemigran{at}partners.org).
Dr. Bendjelid also raises the concern that positive pressure ventilation may act to prevent the development of acute left ventricular (LV) failure that may occur during NO inhalation, and that LV failure may arise in nonventilated patients. Left ventricular filling pressures have been found to increase during NO inhalation in patients with severe LV systolic dysfunction (2,3). The RVMI patients in our study had primarily RV dysfunction, and the degree of LV dysfunction was not as severe as in those patients in whom the pulmonary capillary wedge pressure (PCWP) has been reported to increase during NO inhalation. Furthermore, we excluded patients with a PCWP >25 mm Hg from study. In the three nonventilated RVMI patients in our study, we did not observe an increase in their PCWP while they were breathing NO for 10 min.
In future studies of the effects of sustained NO inhalation in RVMI patients, it will be important to observe the hemodynamic effects of this agent in patients who receive positive pressure ventilation as well as those who do not. Patients with severe LV systolic function should be monitored carefully during chronic NO inhalation because of the possibility of their developing pulmonary venous hypertension.
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