LAUSR

We read with great interest the recent article by Gerges et al. [1] on partitioning pulmonary vascular resistance (PVR) at baseline and after inhaled nitric oxide (iNO) in patients with pulmonary hypertension associated with left heart disease (PH-LHD). The study highlighted that the increase of right ventricular (RV) afterload in isolated post-capillary PH (Ipc-PH) primarily depended on a passive backward transmission of left ventricular filling pressure and left atrial (LA) function, explaining the very high upstream resistance (Rup). Further afterload increase secondary to an elevated vessel resistance in combined post- and pre-capillary pulmonary hypertension (Cpc-PH), was associated with a lower Rup similar to that seen in idiopathic pulmonary arterial hypertension (iPAH) patients. Upstream impedance could characterise the RV afterload and the relative contribution of large and small vessel disease in PH, regardless of the PAOP, including the inverse relationship with HR as an indirect RV functional response http://ow.ly/fqvN30nbNFo