Pulmonary hypertension at exercise in COPD: does it matter?

Abstract

Listen

Translate article

Pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD). In these patients, the increase in pulmonary artery pressure (PAP) is usually mild, in the range of 20 to 30 mmHg mean PAP (mPAP) with little progression over the years, on average 0.4 mmHg per year, and is preventable and sometimes partially reversible with chronic oxygen therapy [1, 2]. Sharp increases in PAP may occur during sleep or episodes of acute respiratory failure, and also during exercise [1, 2]. Pulmonary hypertension in COPD is explained by the combined effects of hypoxia, inflammation, hyper-inflation of the lungs and an increase in left ventricular end-diastolic pressure [2, 3]. Increased PAP is associated with decreased survival, may be the cause of clinical right heart failure, particularly in hypoxaemic patients with associated salt and water retention, and is thought to limit exercise capacity [1, 2]. Right heart catheterisations to evaluate the pulmonary circulation used to be common practice in patients with advanced COPD. The procedure is nowadays limited to the work-up of lung transplantation or lung volume reduction surgery, or for the understanding of symptoms that appear out of proportion with the lung function impairment [2, 4]. Some rare patients with COPD, approximately 1% of those referred to expert centres, present with “out of proportion pulmonary hypertension”. This entity is defined by a particular combination of mPAP >35–40 mmHg, only moderate airflow obstruction, hypoxaemia and hypocapnia [2–5]. Whether “out of proportion pulmonary hypertension” actually represents a form of pulmonary arterial hypertension (PAH) triggered by altered blood gases or inflammation associated with COPD remains unclear [5]. But there has been no reported evidence until now that targeted therapies shown effective in the …