Bronchial thermoplasty reduces airway resistance

David Langton,Peter Noble,Virginia Plummer,Kim Bennetts,Francis Thien

doi:10.1186/s12931-020-1330-5

Abstract

BackgroundThe mechanism for symptomatic improvement after bronchial thermoplasty (BT) is unclear, since spirometry reveals little or no change. In this study, the effects of BT on airway resistance were examined using two independent techniques.MethodsEighteen consecutive patients, with severe asthma (57.6 ± 14.2 years) were evaluated by spirometry and plethysmography at three time points: (i) baseline, (ii) left lung treated but right lung untreated and (iii) 6 weeks after both lungs were treated with BT. At each assessment, total and specific airway resistance (Raw, sRaw) were measured. High resolution CT scans were undertaken at the first two assessments, and measurements of lobar volume, airway volume and airway resistance were made. The Asthma Control Questionnaire (ACQ) was administered at each assessment.ResultsThe baseline ACQ score was 3.5 ± 0.9, and improved progressively to 1.8 ± 1.2 (p < 0.01). At baseline, severe airflow obstruction was observed, FEV1 44.8 ± 13.7% predicted, together with gas trapping, and elevated Raw at 342 ± 173%predicted. Following BT, significant improvements in Raw and sRaw were observed, as well as a reduction in Residual Volume, increase in Vital Capacity and no change in FEV1. The change in Raw correlated with the change in ACQ (r = 0.56, p < 0.05).CT scans demonstrated reduced airway volume at baseline, which correlated with the increased Raw determined by plethysmography (p = − 0.536, p = < 0.05). Following BT, the airway volume increased in the treated lung, and this was accompanied by a significant reduction in CT-determined local airway resistance.ConclusionSymptomatic improvement after BT is mediated by increased airway volume and reduced airway resistance.

Highlights

The mechanism for symptomatic improvement after bronchial thermoplasty (BT) is unclear, since spirometry reveals little or no change
Plethysmography has demonstrated a reduction in the degree of gas trapping after BT, but the magnitude of this change was modest [11]
The first compelling evidence for an improvement in lung physiology after BT was presented in our recent paper, which used a Computerized Tomography (CT)-based segmentation methodology to demonstrate that the volume of air in the airways increased following BT treatment [12]

Summary

Introduction

The mechanism for symptomatic improvement after bronchial thermoplasty (BT) is unclear, since spirometry reveals little or no change. Human histological studies clearly demonstrate that BT is effective at its target site, the airway smooth muscle layer. This layer is characteristically hypertrophied in asthma, and BT induces its thinning and atrophy [7, 8]. Spirometry has been our gold standard for 100 years in the assessment of airflow obstruction, yet the anticipated changes in spirometry following BT have either been small or non-existent [4,5,6] This discrepancy of symptom improvement without spirometry-based validation has been labelled a clinical paradox, and needs to be addressed to reduce physician scepticism regarding BT [9]. The first compelling evidence for an improvement in lung physiology after BT was presented in our recent paper, which used a CT-based segmentation methodology to demonstrate that the volume of air in the airways increased following BT treatment [12]

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