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Eur Respir J. 2018 May 24;51(5). pii: 1800067. doi: 10.1183/13993003.00067-2018. Print 2018 May.

In-depth haemodynamic phenotyping of pulmonary hypertension due to left heart disease.

Author information

1
Dept of Internal Medicine II, Division of Cardiology, Vienna General Hospital, Medical University of Vienna, Vienna, Austria.
2
PhyMedExp, University of Montpellier, CNRS, INSERM and Dept of Internal Medicine Lapeyronie, CHU Montpellier, Montpellier, France.
3
Dept of Internal Medicine, Division of Cardiology, Ferrarotto Hospital, University of Catania, Catania, Italy.
4
Dept of Cardiology, Sydney Medical School, University of Sydney, Sydney, Australia.

Abstract

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, Rup decreases and Rds increases. 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. Rup was 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%; p<0.001) suggesting upstream transmission of elevated left atrial pressure.Right 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.

PMID:
29599186
DOI:
10.1183/13993003.00067-2018
[Indexed for MEDLINE]

Conflict of interest statement

Conflict of interest: C. Gerges reports grants from United Therapeutics Corporation, Bayer HealthCare and Actelion Pharmaceuticals, during the conduct of the study. He has also received personal fees (for scientific symposia) from GlaxoSmithKline, AOP Orphan and Actelion, outside the submitted work. Conflict of interest: M. Gerges reports grants from United Therapeutics Corporation, Bayer HealthCare and Actelion Pharmaceuticals, during the conduct of the study. He has also received personal fees (for scientific symposia) from GlaxoSmithKline, AOP Orphan and Actelion, outside the submitted work. Conflict of interest: P. Fesler reports personal fees (travel and accommodation support) from Actelion, outside the submitted work. Conflict of interest: I.M. Lang reports grants from United Therapeutics Corporation, Bayer AG and Actelion Pharmaceuticals, during the conduct of the study. She also received grants, personal fees and nonfinancial support from Actelion, AOP Orphan Pharmaceuticals, Bayer AG, GlaxoSmithKline, Pfizer and United Therapeutics Corporation, as well as honoraria from AstraZeneca, Servier, Cordis, Medtronic and Novartis, outside the submitted work.

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