Pulmonary hypertension in COPD

Abstract

Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema.A small proportion of COPD patients may present with ''out-of-proportion'' pulmonary hypertension, defined by a mean pulmonary artery pressure .35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-ofproportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension.Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements.The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.

Pulmonary vascular changes in asthma and COPD

“…The two circulatory systems are quite different physiologically and pharmacologically, including muscularisation at different levels and different arterial pressures: bronchial arterial (mean arterial) pressure and pulmonary artery pressure (~20 mmHg) [14,16].…”

“…The pulmonary arteries are relatively thin-walled vessels with elastic fibres and relatively less smooth muscle than systemic arteries [16]. During hypoxic conditions in the alveolar compartments, the pulmonary arteries respond by constricting [14] causing the terminal bronchioles to dilate.…”

“…Thereafter, a number of studies reported the involvement of specific growth factors, such as fibroblast growth factor (FGF), transforming growth factor (TGF) β1 and vascular endothelial growth factor (VEGF), during vascular remodelling in asthma and COPD [9][10][11][12]. Vascular remodelling, including thickening of the intimal and medial layers due to vascular smooth muscle (VSM) cell hypertrophy, is reported to progressively decline lung function [10,13] and vascular alterations in the pulmonary circulation may impair gas exchange in the alveolar compartments that result in pulmonary hypertension in some COPD patients [14]. Previous research has focused on the …”

Exercise‐induced pulmonary hypertension associated with systemic sclerosis: Four distinct entities

“…Abnormal exercise physiology has been recognized in SSc, idiopathic PAH, idiopathic pulmonary fibrosis (IPF), and chronic obstructive pulmonary disease (21,28,(34)(35)(36)(37)(38)(39)(40). Studies have described exerciseinduced PH in 46-59% of patients with scleroderma spectrum disorders, characterized by Doppler echocardiogram pulmonary artery systolic pressure Ͼ40 mm Hg during exercise (23,41,42).…”

Hypoxia: good guy or bad guy?

“…Types of exposures and individual responses to hypoxia are so multifaceted that much more systematic research will be necessary to find conclusive answers. Nevertheless, sometimes hypoxia is undoubtedly a bad guy as it is the case at very high altitude, in obstructive sleep apnea or in severe chronic obstructive pulmonary disease (COPD) [1][2][3]. However, there are also examples for hypoxia as a good guy, e.g., the planned exposures to hypoxia have been proved to support the high-altitude acclimatization or preacclimatization processes [4,5].…”