Pulmonary hypertension in chronic obstructive pulmonary disease

Abstract

Pulmonary hypertension in chronic obstructive pulmonary disease. J.A. Barberà, V.I. Peinado, S. Santos. #ERS Journals Ltd 2003. ABSTRACT: Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). Its presence is associated with shorter survival and worse clinical evolution. In COPD, pulmonary hypertension tends to be of moderate severity and progresses slowly. However, transitory increases of pulmonary artery pressure may occur during exacerbations, exercise and sleep. Right ventricular function is only mildly impaired with preservation of the cardiac output.Structural and functional changes of pulmonary circulation are apparent at the initial stages of COPD. Recent investigations have shown endothelial dysfunction and changes in the expression of endothelium-derived mediators that regulate vascular tone and cell growth in the pulmonary arteries of patients with mild disease. Some of these changes are also present in smokers with normal lung function. Accordingly, it has been postulated that the initial event in the natural history of pulmonary hypertension in COPD could be the lesion of pulmonary endothelium by cigarettesmoke products.Long-term oxygen administration is the only treatment that slows down the progression of pulmonary hypertension in chronic obstructive pulmonary disease. Nevertheless, with this treatment pulmonary artery pressure rarely returns to normal values and the structural abnormalities of pulmonary vessels remain unaltered. Vasodilators are not recommended on the basis of their minimal clinical efficacy and because they impair pulmonary gas exchange. Recognition of the role of endothelial dysfunction in the physiopathology of pulmonary hypertension in chronic obstructive pulmonary disease opens new perspectives for the treatment of this complication. Eur Respir J 2003; 21: 892-905.

Association of ex vivo vascular and bronchial dysfunctions in smokers

“…We observed that one quarter of our COPD patients displayed pulmonary endothelial dysfunction, which is in agreement with our subsequent results observed in a larger series [8]. No data are available in the literature for further comparison, but a ~30% incidence of pulmonary hypertension in COPD patients has been reported [10]. In the study of Peinado and colleagues in mild COPD patients (mean ± SD: 24.9 ± 22.9 %), the dilator response to acetylcholine was diminished as compared to non smokers (40.1 ± 22.0 %), without reaching statistical significance.…”

“…We suggest that in former smokers, endothelial dysfunction of pulmonary arteries is associated with impairment of both spontaneous resting tone and cGMP-mediated dilation of airways, establishing a biological link between pulmonary arterial and bronchial functions. To our best knowledge, comparison of arterial and bronchial pharmacological functions obtained from the same lung sample has never been made, and the description of dysfunction of pulmonary arteries has been assessed in a very limited number of studies [4,10,11]. A recent pulmonary perspective supported by the National Heart, Lung, and Blood Institute stated that there is a need for methods linking in vitro observations to in vivo disease state with regard to airway smooth muscle function [12].…”

Pulmonary haemodynamic changes in patients with severe COPD

“…An important cause of V' A /Q' inequality might be the change of pulmonary blood flow distribution due to a vasoconstrictive reaction that includes HPV, endothelial dysfunction and inflammation. 5,9 The obviously increased PVRI and the during rest, exercise and exacerbation in patients with severe COPD.…”

“…9 Among all of the possible mechanisms, hypoxic pulmonary vasoconstriction (HPV) might play an important role in inducing PH during exercise, because exercise-induced PH was improved by supplemental oxygen. The significant decrease of PvO 2 during exercise might enhance HPV resulting in significant PH.…”

“…9 Pulmonary hypertension usually develops at the latter stage of COPD. 5 Although pulmonary hemodynamics during exercise have been well investigated, 7,10 the present study examined differences in pulmonary hemodynamics during exercise and exacerbation status in patients with severe COPD.…”