OBJECTIVES. We compared the ability of inhaled nitric oxide (NO), oxygen (O
-2) and nitric oxide in oxygen (NO+O-2) to identify reactive pulmonary vasc
ulature in pulmonary hypertensive patients during acute vasodilator testing
at cardiac catheterization.
BACKGROUND. In patients with pulmonary hypertension, decisions regarding su
itability for corrective surgery, transplantation and assessment of long-te
rm prognosis are based on results obtained during acute pulmonary vasodilat
or testing.
METHODS. In group 1, 46 patients had hemodynamic measurements in room air (
RA), 100% O-2, return to RA and NO (80 parts per million [ppm] in Rtl). In
group 2, 25 additional patients were studied in RA, 100% O-2 and 80 ppm NO
in oxygen (NO+O-2).
RESULTS. In group 1, O-2 decreased pulmonary vascular resistance (PVR) (mea
n +/- SEM) from 17.2 +/- 2.1 U.m(2) to 11.1 +/- 1.5 U.m(2) (P < 0.05). Nitr
ic oxide caused a comparable decrease from 17.8 +/- 2.2 U.m(2) to 11.7 +/-
1.7 U.m(2) (p < 0.05). In group 2, PVR decreased from 20.1 +/- 2.6 U.m(2) t
o 14.3 +/- 1.9 U.m(2) in O-2 (p < 0.05) and further to 10.5 +/- 1.7 U.m(2)
in NO+O-2, (p < 0.05). A response of 20% or more reduction in PVR was seen
in 22/25 patients with NO+O-2 compared with 16/25 in O-2 alone (p = 0.01).
CONCLUSIONS. Inhaled NO and O-2 produced a similar degree of selective pulm
onary vasodilation. Our data suggest that combination testing with NO+O-2 p
rovides additional pulmonary vasodilation in patients with a reactive pulmo
nary vascular bed in a selective, safe and expeditious fashion during cardi
ac catheterization. The combination of NO+O-2 identifies patients with sign
ificant pulmonary vasoreactivity who might not be recognized if O-2 or NO w
ere used separately.(C) 1999 by the American College of Cardiology.