A diagnosis of pulmonary arterial hypertension (PAH) implies a mean pulmonary artery pressure (mPAP) >25 mm Hg and normal LV filling pressures (<15 mmHg). Higher LV pressures suggest pulmonary venous hypertension (PVH) and preclude the use of PAH-specific therapies. However, some patients with PVH present with severe PH that seems “out-of-proportion” to the elevation in LV pressures, suggesting the presence of both PVH and PAH. We hypothesize that a trial of NTP - administered in an attempt to normalize left ventricular end-diastolic pressure (LVEDP) and assess the degree of residual PH- can help in differentiating those with predominant PVH from those with an additional component of PAH.
We reviewed the cardiac catheterization records and tracings of eight patients with PH in whom it was questioned whether PVH alone could be causative. All patients underwent a right heart catheterization that included an intravenous (IV) NTP trial. Hemodynamic measurements at baseline and while receiving NTP were compared and analyzed. In two patients the NTP trial was conducted after a trial of prostacyclin and nitric oxide failed to show a significant reduction in pulmonary pressures. LV ejection fraction was >50% in all patients but one (45%). Average NTP dose and time to response was 1.8 mcg/kg/min and 6.8 minutes, respectively.
IV NTP resulted in a significant decrease in LV filling pressures and mPAP, without deleterious changes in blood pressure or heart rate. LVEDP was normalized (<15 mmHg) in all patients and in 7/8 patients the mPAP became <30 mmHg.
This preliminary study demonstrates that use of NTP during a diagnostic catheterization provides valuable information for differentiating between PH due to PVH alone and that due to a combination of PVH and PAH. This occurs predominantly by decreasing LVEDP.
Near normalization of pulmonary arterial pressures after reduction of LV filling pressures during a trial of NTP suggests a predominant component of PVH and thus guides treatment decisions.
Zouras Wendy, None.