Abstract
[No abstract. Showing first paragraph of article]Pulmonary hypertension (PH) associated with hypoxia and lung disease, first identified as Group 3 in the 2008 Dana Point classification of PH, is the second most common form of PH and is associated with increased morbidity and mortality. The most common lung diseases resulting in PH are chronic obstructive pulmonary disease (COPD), interstitial lung disease (ILD) and obstructive sleep apnoea (OSA) but is also associated with other diseases, such as cysticfibrosis and high altitude exposure. Those with PH in the setting of obstructive or restrictive lung disease have worse outcomes, but it is not clear if the PH causes increased mortality or whether it is a marker for the severe end of the lung disease spectrum. Patients with Group 3 disease have a worse outcome than Group 1 IPAH. Those patients with Group 1 disease pulmonary arterial hypertension (PAH) but with minor associated lung disease also suffer from worse outcomes.
Highlights
Pulmonary hypertension (PH) associated with hypoxia and lung disease, first identified as Group 3 in the 2008 Dana Point classification of PH1, is the second most common form of PH and is associated with increased morbidity and mortality (Figure 1)[2]
The role of pulmonary rehabilitation is well established in parenchymal lung disease and in pre-capillary pulmonary hypertension, but further work is required on its efficacy in PH complicating lung disease
Group 3 PH is common and is associated with increased mortality rates compared to IPAH
Summary
Pulmonary hypertension (PH) associated with hypoxia and lung disease, first identified as Group 3 in the 2008 Dana Point classification of PH1, is the second most common form of PH and is associated with increased morbidity and mortality (Figure 1)[2]. There is significant variability between patients’ responses to hypoxia The reasons for this variability, which is seen between species[23], are not clear, but some patients have a greater increase in PAP when hypoxic, resulting in a higher risk of vascular remodeling over the longer term. There are several reasons why this is thought to be the case: firstly, histological samples of patients of idiopathic pulmonary fibrosis show evidence of vascular remodeling in areas of preserved lung[24] and, secondly, severity of pulmonary hypertension does not correlate well with abnormalities in lung function, suggesting there is an additional mechanism leading to rises in pressure[25,26]. This imbalance between natural vasodilators and vasoconstrictors creates an environment that is conducive to the development of pulmonary hypertension
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