In-depth haemodynamic phenotyping of pulmonary hypertension due to left heart disease
| Autor: | David S. Celermajer, Anna Maria Pistritto, Mario Gerges, Irene M. Lang, Nicholas P. Konowitz, Johannes Jakowitsch, Pierre Fesler, Christian Gerges |
|---|---|
| Přispěvatelé: | Université médicale de Vienne, Autriche, Centre Hospitalier Régional Universitaire [Montpellier] (CHRU Montpellier), Physiologie & médecine expérimentale du Cœur et des Muscles [U 1046] (PhyMedExp), Institut National de la Santé et de la Recherche Médicale (INSERM)-Université de Montpellier (UM)-Centre National de la Recherche Scientifique (CNRS), Ferrarotto University Hospital, The University of Sydney |
| Rok vydání: | 2018 |
| Předmět: |
Pulmonary and Respiratory Medicine
Adult Male medicine.medical_specialty [SDV]Life Sciences [q-bio] Hypertension Pulmonary Hemodynamics 030204 cardiovascular system & hematology Pulmonary Artery Nitric oxide 03 medical and health sciences chemistry.chemical_compound Ventricular Dysfunction Left 0302 clinical medicine Internal medicine medicine.artery medicine Humans Prospective Studies Pulmonary Wedge Pressure Pulmonary wedge pressure Aged Aged 80 and over Inhalation business.industry Middle Aged medicine.disease Pulmonary hypertension Compliance (physiology) medicine.anatomical_structure 030228 respiratory system chemistry Pulmonary artery Cardiology Vascular resistance Linear Models Female Vascular Resistance business |
| Zdroj: | European Respiratory Journal European Respiratory Journal, European Respiratory Society, 2018, ⟨10.1183/13993003.00067-2018⟩ |
| ISSN: | 1399-3003 0903-1936 |
| DOI: | 10.1183/13993003.00067-2018⟩ |
| Popis: | The commonest cause of pulmonary hypertension (PH) is left heart disease (LHD). The current classification system for definitions of PH-LHD is under review. We therefore performed prospective in-depth invasive haemodynamic phenotyping in order to assess the site of increased pulmonary vascular resistance (PVR) in PH-LHD subsets.Based on pulmonary artery occlusion waveforms yielding an estimate of the effective capillary pressure, we partitioned PVR in larger arterial (Rup, upstream resistance) and small arterial plus venous components (Rds, downstream resistance). In the case of small vessel disease,Rupdecreases andRdsincreases. Inhaled nitric oxide (NO) testing was used to assess acute vasoreactivity.Right ventricular afterload (PVR, pulmonary arterial compliance and effective arterial elastance) was significantly higher in combined post- and pre-capillary PH (Cpc-PH, n=35) than in isolated post-capillary PH (Ipc-PH, n=20). Right ventricular afterload decreased during inhalation of NO in Cpc-PH and idiopathic pulmonary arterial hypertension (n=31), but remained unchanged in Ipc-PH.Rupwas similar in Cpc-PH (66.8±10.8%) and idiopathic pulmonary arterial hypertension (65.0±12.2%; p=0.530) suggesting small vessel disease, but significantly higher in Ipc-PH (96.5±4.5%; pRight ventricular afterload is driven by elevated left atrial pressure in Ipc-PH and is further increased by elevated small vessel resistance in Cpc-PH. Cpc-PH is responsive to inhaled NO. Our data support current definitions of PH-LHD subsets. |
| Databáze: | OpenAIRE |
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