Abstract
Background: Pulmonary vascular resistance (PVR) is frequently elevated in patients with advanced heart failure. Nitric oxide (NO), which contributes to the activity of endothelium-derived relaxing factor, causes relaxation of pulmonary arteries and veins in vitro. Inhalation of NO gas causes pulmonary vasodilation in patients with primary and secondary forms of pulmonary hypertension. Methods and Results: To test the hypothesis that inhalation of NO gas lowers PVR in patients with heart failure, we studied the hemodynamic effects of a 10-minute inhalation of NO (80 ppm) in 19 patients with New York Heart Association class III (n=5) and class IV (n=14) heart failure due to left ventricular (LV) dysfunction. Although inhalation of NO had no effect on pulmonary artery pressures, the PVR decreased by 31±7% (P<.001) due to a 23±7% increase (P<.001) in pulmonary artery wedge pressure and despite a (P<.05) decrease in cardiac index. The magnitude of the decrease in PVR with inhaled NO was inversely related (r=-.713; P<.001) to the baseline PVR. Inhaled NO had no effect on heart rate, systemic arterial pressure, systemic vascular resistance, or LV peak +dP/dt or -dP/dt. Conclusions: In patients with heart failure due to LV dysfunction, inhalation of NO causes a decrease in the PVR associated with an increase in LV filling pressure. These findings predict that inhaled NO, if used alone at this dose (80 ppm), may have adverse effects in patients with LV failure.
| Original language | English |
|---|---|
| Pages (from-to) | 2780-2785 |
| Number of pages | 6 |
| Journal | Circulation |
| Volume | 90 |
| Issue number | 6 |
| State | Published - Dec 1 1994 |
| Externally published | Yes |
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Keywords
- endothelium-derived factors
- heart failure
- lung
- nitric oxide
ASJC Scopus subject areas
- Physiology
- Cardiology and Cardiovascular Medicine
Cite this
Cardiovascular effects of inhaled nitric oxide in patients with left ventricular dysfunction. / Loh, Evan; Stamler, Jonathon S.; Hare, Joshua; Loscalzo, Joseph; Colucci, Wilson S.
In: Circulation, Vol. 90, No. 6, 01.12.1994, p. 2780-2785.Research output: Contribution to journal › Article
}
TY - JOUR
T1 - Cardiovascular effects of inhaled nitric oxide in patients with left ventricular dysfunction
AU - Loh, Evan
AU - Stamler, Jonathon S.
AU - Hare, Joshua
AU - Loscalzo, Joseph
AU - Colucci, Wilson S.
PY - 1994/12/1
Y1 - 1994/12/1
N2 - Background: Pulmonary vascular resistance (PVR) is frequently elevated in patients with advanced heart failure. Nitric oxide (NO), which contributes to the activity of endothelium-derived relaxing factor, causes relaxation of pulmonary arteries and veins in vitro. Inhalation of NO gas causes pulmonary vasodilation in patients with primary and secondary forms of pulmonary hypertension. Methods and Results: To test the hypothesis that inhalation of NO gas lowers PVR in patients with heart failure, we studied the hemodynamic effects of a 10-minute inhalation of NO (80 ppm) in 19 patients with New York Heart Association class III (n=5) and class IV (n=14) heart failure due to left ventricular (LV) dysfunction. Although inhalation of NO had no effect on pulmonary artery pressures, the PVR decreased by 31±7% (P<.001) due to a 23±7% increase (P<.001) in pulmonary artery wedge pressure and despite a (P<.05) decrease in cardiac index. The magnitude of the decrease in PVR with inhaled NO was inversely related (r=-.713; P<.001) to the baseline PVR. Inhaled NO had no effect on heart rate, systemic arterial pressure, systemic vascular resistance, or LV peak +dP/dt or -dP/dt. Conclusions: In patients with heart failure due to LV dysfunction, inhalation of NO causes a decrease in the PVR associated with an increase in LV filling pressure. These findings predict that inhaled NO, if used alone at this dose (80 ppm), may have adverse effects in patients with LV failure.
AB - Background: Pulmonary vascular resistance (PVR) is frequently elevated in patients with advanced heart failure. Nitric oxide (NO), which contributes to the activity of endothelium-derived relaxing factor, causes relaxation of pulmonary arteries and veins in vitro. Inhalation of NO gas causes pulmonary vasodilation in patients with primary and secondary forms of pulmonary hypertension. Methods and Results: To test the hypothesis that inhalation of NO gas lowers PVR in patients with heart failure, we studied the hemodynamic effects of a 10-minute inhalation of NO (80 ppm) in 19 patients with New York Heart Association class III (n=5) and class IV (n=14) heart failure due to left ventricular (LV) dysfunction. Although inhalation of NO had no effect on pulmonary artery pressures, the PVR decreased by 31±7% (P<.001) due to a 23±7% increase (P<.001) in pulmonary artery wedge pressure and despite a (P<.05) decrease in cardiac index. The magnitude of the decrease in PVR with inhaled NO was inversely related (r=-.713; P<.001) to the baseline PVR. Inhaled NO had no effect on heart rate, systemic arterial pressure, systemic vascular resistance, or LV peak +dP/dt or -dP/dt. Conclusions: In patients with heart failure due to LV dysfunction, inhalation of NO causes a decrease in the PVR associated with an increase in LV filling pressure. These findings predict that inhaled NO, if used alone at this dose (80 ppm), may have adverse effects in patients with LV failure.
KW - endothelium-derived factors
KW - heart failure
KW - lung
KW - nitric oxide
UR - http://www.scopus.com/inward/record.url?scp=0028610499&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0028610499&partnerID=8YFLogxK
M3 - Article
C2 - 7994821
AN - SCOPUS:0028610499
VL - 90
SP - 2780
EP - 2785
JO - Circulation
JF - Circulation
SN - 0009-7322
IS - 6
ER -