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Exhaled nitric oxide: a marker of pulmonary hemodynamics in heart failure

Joshua M. Hare, MD, FACC^*,*, Geoffrey C. Nguyen, MD^*, Anthony F. Massaro, MD, Jeffrey M. Drazen, MD, Lynne W. Stevenson, MD, FACC, Wilson S. Colucci, MD, FACC, James C. Fang, MD, FACC, Wendy Johnson, MD, FACC, Michael M. Givertz, MD, FACC and Caroline Lucas, MD

^* Johns Hopkins Medical Institutions, Baltimore, Maryland, USA
Brigham and Women’s Hospital, Boston, Massachusetts, USA
Boston University, Boston, Massachusetts, USA

View larger version (14K): [in a new window]   Figure 1 Comparison of baseline exhaled nitric oxide (NO) in patients with heart failure versus normal control subjects. The baseline exhaled NO was significantly increased in the heart failure group. *p = 0.0002.

View larger version (17K): [in a new window]   Figure 2 Scatterplot demonstrating the correlation (r = – 0.81, p < 0.00001) between levels of exhaled nitric oxide (NO) and systolic pulmonary artery pressure (PAP) in patients with compensated heart failure (open circles). Linear regression lines with 95% confidence intervals are depicted for patients with compensated heart failure. Patients with decompensated heart failure at baseline (solid squares) deviated from this curve, did not exhibit an inverse correlation between eNO and PAP, and eliminated the linear relationship between PAP and eNO. The relationship between these two variables was restored toward normal after tailored therapy (solid inverted triangles). With inclusion of the post-treatment data, the linear regression between NO and PAP persisted (r = –0.66, p = 0.00005).

View larger version (22K): [in a new window]   Figure 3 Individual nitric oxide (NO) curves among patients with heart failure (n = 7) in response to tailored therapy showing a progressive decline in exhaled NO concentrations during heart failure treatment.

View larger version (12K): [in a new window]   Figure 4 Scatterplot demonstrating the inverse correlation between the change in pulmonary artery pressure (PAP) and exhaled nitric oxide (eNO) in response to acute administration of milrinone (r = –0.61, p = 0.027). A decrease in PAP caused by milrinone was associated with a rise in eNO, consistent with the inverse relationship depicted in Figure 1. In patients in whom PAP remained unchanged or rose slightly with milrinone, eNO actually fell, consistent with the notion that these patients have a defect in nitric oxide pathway activity.