Nitric Oxide Attenuates Arterial Pulse Wave Reflection in a Vasodilator Responding Pulmonary Arterial Hypertension Patient
This article requires a subscription to view the full text. If you have a subscription you may use the login form below to view the article. Access to this article can also be purchased.
Pulmonary arterial hypertension (PAH) is characterized by distal vasoconstriction, vascular remodeling, microvascular injury, and thrombosis leading to increased pulmonary vascular resistance (PVR) and elevated mean pulmonary arterial pressure (PAPm). A small subset (<10%) of patients with idiopathic PAH (IPAH) respond profoundly (≥10 mm Hg drop in PAPm to ≤40 mm Hg with stable or increased cardiac output) to acute vasodilators, such as inhaled nitric oxide (NO).1 These patients have an excellent prognosis when treated with high-dose calcium channel blockers.1 The principal disease mechanism in this rare subtype of IPAH may be vasoconstriction with limited vascular remodeling. Here, we describe for the first time how inhaled NO influences arterial pulse wave propagation in such a vasoreactive IPAH patient.
The patient was a 33-year-old woman undergoing right heart catheterization, which was performed using a dual-tipped pressure and Doppler flow sensor wire to acquire simultaneous pressure and flow velocity measurements in the right pulmonary artery at rest and during NO inhalation (20 PPM). Wave intensity analysis (with and without subtraction of reservoir pressure) and pressure separation were performed.2,3
During vasoreactivity testing, PAPm and PVR decreased (31→17 mm Hg and 4.1→1.0 Wood U, respectively), whereas …