Pulmonary Arterial Remodeling in Chronic Obstructive Pulmonary Disease is Lobe Dependent

Abstract

Pulmonary arterial remodeling has been demonstrated in patients with severe chronic obstructive pulmonary disease (COPD), but it is not known whether lobar heterogeneity of remodeling occurs. Furthermore, the relationship between pulmonary hypertension (PH) and pulmonary arterial remodeling in COPD has not been established. Muscular pulmonary arterial remodeling in arteries 0.10-0.25 mm in diameter was assessed in COPD-explanted lungs and autopsy controls. Remodeling was quantified as the percentage wall thickness to vessel diameter (%WT) using digital image analysis. Repeat measures mixed-effects remodeling for %WT was performed according to lobar origin (upper and lower), muscular pulmonary arterial size (small, medium, and large), and echocardiography-based pulmonary arterial pressure (no PH, mild PH, and moderate-tosevere PH). Lobar perfusion and emphysema indices were determined from ventilationperfusion and computed tomography scans, respectively. Overall, %WT was greater in 42 subjects with COPD than in 5 control subjects (P < 0:0001 ). Within the COPD group, %WT was greater in the upper lobes (P < 0:0001 ) and in the small muscular pulmonary arteries (P < 0:0001 ). Lobar differences were most pronounced in medium and large arteries. Lobar emphysema index was not associated with arterial remodeling. However, there was a significant positive relationship between the lobar perfusion index and pulmonary arterial remodeling (P ¼ 0:024). The presence of PH on echocardiography showed only a trend to a small effect on lower lobe remodeling. The pattern of pulmonary arterial remodeling in COPD is complicated and lobe dependent. Differences in regional blood flow partially account for the lobar heterogeneity of pulmonary arterial remodeling in COPD.

Intrapulmonary vascular remodeling: MSCT-based evaluation in COPD and alpha-1 antitrypsin deficient subjects

“…This could be explained by the fact that the basal parenchymal and vascular remodeling may induce an apical vascular redistribution, thus increasing the number of vessels of large caliber. However, these results are in contradiction to the findings of Wrobel et al who evaluated the vascular remodeling on anatomical specimens of [0.10 -0.25] mm arteries of severe COPDs in terms of ratio of wall thickness to vessel diameter (WT%), and showed a larger WT% in the upper lung lobes [9]. This could be explained by the fact that the patients recruited in our study had severe emphysema predominating in the lower part of the lungs, which is unusual in COPD.…”

Pulmonary Hypertension in COPD: A Case Study and Review of the Literature

“…In PH secondary to COPD, ongoing chronic hypoxic pulmonary vasoconstriction leads to changes that produce fixed remodeling of the pulmonary vasculature, namely fibromuscular intimal thickening and an increase in smooth muscle of the media of the pulmonary arterioles and arteries [7]. These same changes have also been noted in the pulmonary vasculature of smokers even without the presence of airflow obstruction [8].…”

<p>Assessing pulmonary hypertension in COPD. Is there a role for computed tomography?</p>

“…Those vessel alterations are multiples and can happen at initial stage of COPD71 with endothelial dysfunction, inflammation, suggesting that the history of PH in COPD might be related with cigarette-smoke-induced endothelial alterations 73,74. The quantitative amount of emphysema in COPD was often negatively correlated to pulmonary microvasculature abnormalities measured using CT,75–79 except for Wrobel et al,72 which did not find any significant correlation.…”

“…It has been shown that the toxicity of tobacco smoke affects bronchi and parenchyma, but can also directly alter pulmonary vessels both in animals70 and humans 6,71. At histological level, pulmonary arterial remodeling appeared to be more important in COPD than in control subjects, and is particularly important in upper lobe and in small muscular pulmonary arteries 72. Those vessel alterations are multiples and can happen at initial stage of COPD71 with endothelial dysfunction, inflammation, suggesting that the history of PH in COPD might be related with cigarette-smoke-induced endothelial alterations 73,74.…”