Tjeerd van der Veer, Anastasia Kimberley Ay-Lan Kwee, Leticia Gallardo Estrella, Elrozy R. Andrinopoulou, Jean Paul Charbonnier, Stephen M. Humphries, Pim A. De Jong, David A. Lynch, Harm A. W. M. Tiddens, Esther Pompe
{"title":"CT-quantified pulmonary artery volume associates independently with higher mortality in smokers with and without COPD","authors":"Tjeerd van der Veer, Anastasia Kimberley Ay-Lan Kwee, Leticia Gallardo Estrella, Elrozy R. Andrinopoulou, Jean Paul Charbonnier, Stephen M. Humphries, Pim A. De Jong, David A. Lynch, Harm A. W. M. Tiddens, Esther Pompe","doi":"10.1183/13993003.congress-2023.pa2284","DOIUrl":null,"url":null,"abstract":"<b>Aims:</b> Emphysema in COPD can lead to loss of microscopic pulmonary arteries and secondary pulmonary hypertension. <b>Aim:</b> To determine the association between pulmonary artery volume on CT and mortality. <b>Methods:</b> The artery-vein phenotyping analysis (AVX) was performed using the AI-based lung quantification platform LungQ (Thirona, The Netherlands). AVX quantified total volume of small (diameter <2mm; AVX<sub>SA</sub>) and large (≥2mm; AVX<sub>LA</sub>) pulmonary arteries from inspiratory CT in 7903 participants in the COPDGene study, normalized for body height. Cox regression analysis was used to analyze associations between AVX scores and mortality. Corrections were made for age, sex, BMI, FEV1%predicted, mMRC, 6MWT, smoking status, emphysema, airway wall thickness, coronary artery calcium score, severe exacerbations, and scanner model. <b>Results:</b> Average age was 60.1±9.0 years, 3594 (45.5%) subjects had COPD. AVX<sub>SA</sub> was 103.3±21.5 mm3/cm and AVX<sub>LA</sub> was 201.9±68.1 mm3/cm. Higher AVX<sub>SA</sub> and AVX<sub>LA</sub> were both associated with higher mortality, HR 1.23 (CI 1.10-1.38) and HR 1.17 (CI 1.12-1.22) per 50 mm3/cm increase, respectively. <b>Conclusions:</b> An increased pulmonary arterial volume is associated with mortality, independent of emphysema. AVX<sub>SA</sub> and AVX<sub>LA</sub> may be markers of secondary blood flow redistribution and arterial dilatation due to destruction of more distal arterioles, potentially leading to pulmonary hypertension.","PeriodicalId":34850,"journal":{"name":"Imaging","volume":"1 1","pages":"0"},"PeriodicalIF":0.7000,"publicationDate":"2023-09-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"Imaging","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.1183/13993003.congress-2023.pa2284","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q3","JCRName":"MEDICINE, GENERAL & INTERNAL","Score":null,"Total":0}
引用次数: 0
Abstract
Aims: Emphysema in COPD can lead to loss of microscopic pulmonary arteries and secondary pulmonary hypertension. Aim: To determine the association between pulmonary artery volume on CT and mortality. Methods: The artery-vein phenotyping analysis (AVX) was performed using the AI-based lung quantification platform LungQ (Thirona, The Netherlands). AVX quantified total volume of small (diameter <2mm; AVXSA) and large (≥2mm; AVXLA) pulmonary arteries from inspiratory CT in 7903 participants in the COPDGene study, normalized for body height. Cox regression analysis was used to analyze associations between AVX scores and mortality. Corrections were made for age, sex, BMI, FEV1%predicted, mMRC, 6MWT, smoking status, emphysema, airway wall thickness, coronary artery calcium score, severe exacerbations, and scanner model. Results: Average age was 60.1±9.0 years, 3594 (45.5%) subjects had COPD. AVXSA was 103.3±21.5 mm3/cm and AVXLA was 201.9±68.1 mm3/cm. Higher AVXSA and AVXLA were both associated with higher mortality, HR 1.23 (CI 1.10-1.38) and HR 1.17 (CI 1.12-1.22) per 50 mm3/cm increase, respectively. Conclusions: An increased pulmonary arterial volume is associated with mortality, independent of emphysema. AVXSA and AVXLA may be markers of secondary blood flow redistribution and arterial dilatation due to destruction of more distal arterioles, potentially leading to pulmonary hypertension.