Electronic Thesis and Dissertation Repository

Degree

Master of Science

Program

Medical Biophysics

Supervisor

Dr. Grace Parraga

Abstract

Chronic obstructive pulmonary disease (COPD) is a major contributor to hospitalizations and healthcare costs in North America. While the hallmark of COPD is airflow limitation, it is also associated with abnormalities of the cardiovascular system. Enlargement of the pulmonary artery (PA) is a morphological marker of pulmonary hypertension, and was previously shown to predict acute exacerbations using a one-dimensional (1D) diameter measurement of the main PA. We hypothesized that a three-dimensional (3D) quantification of PA size would be more sensitive than 1D methods and encompass morphological changes along the entire central PA. Hence, we developed a 3D measurement of the main (MPA), left (LPA) and right (RPA) pulmonary arteries as well as total PA volume (TPA) volume from thoracic x-ray computed tomography (CT) imaging. Three observers performed five repeated measurements for 15 ex-smokers. There was a strong agreement (r2 = 0.76) between PA volume and PA diameter measurements, which was used as the gold standard. Intra-rater measurement reproducibility was evaluated by calculating the coefficient of variation (CV) using five rounds of measurements and revealed excellent agreement (CV < 8%) between measurements. Inter-rater measurement variability was also evaluated using intraclass correlation analysis which revealed strong agreement (ICCMPA=0.98) between observers.

In an application of this tool, we sought to explore the relationship between PA volumes and lung structure-function as determined by spirometry, hyperpolarized helium-3 magnetic resonance imaging (MRI) and CT in 124 ex-smokers, with (n=68) and without (n=56) airflow limitation, and in a control group of 35 healthy never-smokers. We observed significantly greater MPA (p=.014), RPA (p=.001) and TPA (p=.003) volumes in ex-smokers with airflow limitation when compared to ex-smokers without airflow limitation. We also observed significantly greater PA volumes in both ex-smoker subgroups when compared with the never-smoker control group. Modest but significant correlations were observed for PA volumes and measurements of lung structure and function. However, this was not observed when analyzing ex-smokers with airflow limitation alone, suggesting that pulmonary artery enlargement may occur secondary to COPD in our subject group. Multivariate zero-inflated Poisson regression analysis revealed TPA volume to be a significant (p=.03) predictor of acute exacerbations of COPD.

In conclusion, we developed a reproducible technique for quantifying the volume of the PA. We showed that pulmonary artery enlargement may be secondary to COPD in our subject group. We also showed that total pulmonary artery volume was a significant predictor of COPD exacerbations and could be considered as a biomarker for predicting the occurrence of exacerbation events. Automated measurements of pulmonary artery abnormalities once developed, can be used to further evaluate healthy volunteers and patients with COPD.

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