Quantitative CT assessment of bronchial and vascular alterations in severe precapillary pulmonary hypertension

Abstract

Background

Little is known about in vivo alterations at bronchial and vascular levels in severe pulmonary hypertension (PH) of different etiologies. We aimed to compare quantitative computed tomography (CT) data from the following three groups of severe precapillary PH patients: COPD, idiopathic pulmonary arterial hypertension (iPAH), and chronic thromboembolic PH (CTEPH).

Patients and methods

This study was approved by the institutional review board. Severe PH patients (mean pulmonary arterial pressure [mPAP] ≥35 mmHg) with COPD, iPAH, or CTEPH (n=24, 16, or 16, respectively) were included retrospectively between January 2008 and January 2017. Univariate analysis of mPAP was performed in each severe PH group. Bronchial wall thickness (WT) and percentage of cross sectional area of pulmonary vessels less than 5 mm² normalized by lung area (%CSA_<5) were measured and compared using CT, and then combined to arterial partial pressure of oxygen (PaO₂) to generate a “paw score” compared within the three groups using Kruskal–Wallis and its sensitivity using Fisher’s exact test.

Results

WT was higher and %CSA_<5 was lower in the COPD group compared to iPAH and CTEPH groups. Mosaic pattern was higher in CTEPH group than in others. In severe PH patients secondary to COPD, mPAP was positively correlated to %CSA_<5. By contrast, in severe iPAH, this correlation was negative, or not correlated in severe CTEPH groups. In the COPD group, “paw score” showed higher sensitivity than in the other two groups.

Conclusion

Unlike in severe iPAH and CTEPH, severe PH with COPD can be predicted by “paw score” reflecting bronchial and vascular morphological differential alterations.

Keywords:

• computed tomography
• pulmonary hypertension
• COPD
• prediction
• quantitative

Data availability

The datasets used and/or analyzed during the current study are available from the corresponding author on reasonable request.

Acknowledgments

Berger reports grants from Laboratory of Excellence (LabEx) Transitional Research International Laboratory (TRAIL, Université de Bordeaux, France) ANR-10-LABX-57, during the conduct of the study. Laurent reports grants from TRAIL ANR-10-LABX-57, during the conduct of the study. Coste reports funding for salary from LabEx TRAIL ANR-10-LABX-57, during the conduct of the study. This study has received funding from the LabEx TRAIL, ANR-10-LABX-57.

Author contributions

Conception and design: FC, GD, FL, PB; analysis and interpretation: FC, IB, GD, FL, PB; drafting the manuscript for important intellectual content: FC, IB, GD, FL, PB; revising the manuscript for important intellectual content: FC, IB, GD, RM, FL, PB; and final approval of the manuscript: FC, IB, GD, CD, EB, POG, MM, FB, FP, RM, FL, PB. All authors contributed to data analysis, drafting and revising the article, gave final approval of the version to be published, and agree to be accountable for all aspects of the work.

Disclosure

Berger reports personal fees, nonfinancial support from Novartis, Boehringer Ingelheim, AstraZeneca, and GSK outside the submitted work; in addition, he has a patent EP N°15152886.6, ie, new compositions and methods of treating and/or preventing COPD, which is pending. Laurent reports personal fees from Boehringer Ingelheim, Roche, Novartis, Bayer, Guerbet, and Chiesi outside the submitted work. Girodet reports personal fees and nonfinancial support from Novartis, Chiesi, Takeda, Boehringer Ingelheim, and AstraZeneca outside the submitted work. The other authors report no conflicts of interest in this work.