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Pulmonary Hypertension in Patients with COPD

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Pulmonary Hypertension in Patients with COPD EDITORIAL 283 Pulmonary hypertension in COPD with severe COPD.10 11 A degree of pulmo- ................................................................................... nary hypertension was observed in 55% Thorax: first published as 10.1136/thorax.58.4.284 on 1 April 2003. Downloaded from of consecutive respiratory outpatients using Doppler echocardiography.12 The Pulmonary hypertension in patients presence of pulmonary hypertension in patients with COPD is associated with with COPD: NO treatment? increased mortality11 13 and an increase in exacerbation rate and length of hospi- J Pepke-Zaba, N W Morrell tal stay, independent of the degree of air- flow obstruction.14 Although often in- ................................................................................... ferred, the precise contribution of pulmonary hypertension to exercise The application of “pulsed” NO combined with LTOT may limitation or quality of life in stable have a role in treating pulmonary hypertension secondary to COPD patients is unknown. Mean pul- COPD. monary artery pressure in patients with COPD is typically mild (in the region of ollowing the identification of nitric exchange based on low ventilation/ 25 mm Hg) at rest but can rise to abnor- oxide (NO) in 1986 as “endothelium perfusion (V/Q) ratios. This includes the mally high levels on exercise. derived relaxing factor”, there has use of NO in patients in intensive care, At present there are no specific treat- F ments recommended for the reduction of been an exponential growth in our neonates with persistent pulmonary understanding of the physiological role hypertension, and in postoperative set- pulmonary artery pressure in COPD. Although long term oxygen therapy of NO culminating in the award of a tings where NO is used to reduce pulmo- (LTOT) improves survival in hypoxaemic Nobel Prize, and the naming of NO as nary vascular resistance and/or improve patients with COPD, it has a negligible “molecule of the decade”.1 Considerable oxygenation—for example, pulmonary effect on pulmonary haemodynamics. research has subsequently been devoted thromboendarterectomy, heart and lung Clearly, other factors in addition to to understanding the role of this mol- transplantation, acute lung injury. alveolar hypoxia contribute to the devel- ecule in vascular biology in general, and In the lungs, one important molecule opment of pulmonary hypertension in the pulmonary vascular system in par- with which NO reacts is oxyhaemoglobin COPD. For example, remodelling of the ticular. (HbO ). The affinity of HbO for NO is 106 2 2 pulmonary vessels is present in many NO is an unstable radical with a low times greater than its affinity for 6 patients with mild COPD who are not blood gas partition coefficient. For dec- oxygen. Oxidative reactions of NO with hypoxaemic and appears to be related to ades NO was considered an environmen- haemoglobin largely limit the effects of cigarette smoking.15 tal contaminant produced by bacteria inhaled NO to the lung vasculature. There are several reports of the use of and internal combustion engines. Be- However, there are reports that high inhaled NO in patients with stable lieved to be highly toxic, it appeared an concentrations of inhaled NO have per- COPD.16–19 NO inhalation alone may unlikely candidate for a major role as a ipheral vascular effects when peripheral worsen V/Q relationships and exacerbate http://thorax.bmj.com/ biological mediator. However, within the endothelial NO synthesis is blocked, systemic hypoxaemia while lowering pul- last 15 years it has become clear that suggesting that at least a portion of monary vascular resistance. However, endogenously produced NO is ubiqui- inhaled NO survives long enough to when NO is delivered to well ventilated 7 tous in mammalian systems, playing an reach tissue remote from the lungs. The alveolar units with fast time constants, important role in both health and major immediate breakdown products of the deleterious impact on gas exchange is disease: in the regulation of blood NO in human plasma are inactive nitrox- avoided.19 This effect can also be achieved – pressure and flow, inflammatory re- ides such as nitrite (NO2 ). The rate of by using “pulsed” delivery of NO where sponses, and neurotransmission. Insight this reaction increases exponentially spikes of NO are added at the beginning into these physiological roles has led to with the concentration of both oxygen of inspiration. The addition of oxygen to on September 23, 2021 by guest. Protected copyright. 8 its use as a therapeutic agent in a and NO. This has several consequences. NO further prevents hypoxaemia. number of clinical settings. Firstly, low NO concentrations or oxygen The study reported in this issue of There are ample data to support a free environments permit relatively long Thorax by Vonbank et al20 shows that long major role for NO in the regulation of term persistence of NO. Secondly, the term use of pulsed NO with oxygen tone and vascular remodelling in the therapeutic efficacy of inhaled NO may leadstosustainedimprovementinpulmo- normal and diseased pulmonary circula- not rise dramatically with increased nary haemodynamics without worsen- tion. Endothelial NO contributes signifi- doses as the more NO given, the faster it ing hypoxaemia in patients with stable cantly to the normally low pulmonary is oxidised.9 In fact, higher doses of NO COPD. Benefits of the pulsed method vascular tone,2 and dysfunction of en- result in a relatively greater proportion of include the reduced formation of nitro- dothelial NO release has been docu- toxic products with little incremental gen dioxide and methaemoglobinaemia. mented in patients with chronic obstruc- yield of intact NO. Finally, the rapid A further safety issue that needs to be tive pulmonary disease (COPD).34 inactivation of inhaled NO in an oxygen addressed is whether discontinuation of Although nitro-vasodilatation (acting rich environment is what makes NO a long term inhaled NO can lead to severe through the intracellular generation of selective pulmonary vasodilator. Inhala- rebound pulmonary hypertension. Al- NO) has been used effectively since the tion delivers NO to the pulmonary though the results presented by Vonbank 1800s for systemic arterial dilatation resistance vessels before it is oxidised. et al show promise, it remains to be (delivered sublingually, orally, and intra- The seconds before the inhaled NO determined whether pulsed NO/oxygen venously), the prospect of selective pul- enters the systemic circulation are treatment will lead to an improvement in monary nitro-vasodilatation only be- enough for its breakdown by interaction exercise tolerance, quality of life, and came evident in the early 1990s.5 with oxygen and haemoglobin. survival in patients with hypoxaemic Treatment with inhaled NO has subse- Pulmonary hypertension secondary to COPD. Potential disadvantages of the quently been applied in a variety of lung COPD is probably more common than is approach include the delivery system diseases which have in common a degree generally appreciated. Right heart cath- and monitoring systems necessary to of pulmonary vascular endothelial dys- eterisation studies suggest a prevalence ensure accurate dosing and safety. In function and/or abnormalities of gas of up to 40% in selected series of patients addition, long term gas therapies are far www.thoraxjnl.com 284 EDITORIAL from convenient for the patient. NO 3 Dinh-Xuan AT, Higenbottam TW, Clelland pulmonary hypertension secondary to COPD. CA, et al. Impairment of Eur Respir J 2001;17:350–5. reduces pulmonary vascular resistance Thorax: first published as 10.1136/thorax.58.4.284 on 1 April 2003. Downloaded from endothelium-dependent pulmonary artery 13 Incalzi RA, Fuso L, De Rosa M, et al. by increasing cyclic GMP levels in vascu- relaxation in chronic obstructive lung disease. Electrocardiographic signs of chronic cor lar smooth muscle cells. This effect can N Engl J Med 1991;324:1539–47. pulmonale: a negative prognostic finding in also be achieved by inhibition of the 4 Peinado VI, Barbera JA, Ramirez J, et al. chronic obstructive pulmonary disease. Endothelial dysfunction in pulmonary arteries enzymes that metabolise cyclic GMP. Circulation 1999;99:1600–5. of patients with mild COPD. Am J Physiol Lung 14 Kessler R,FallerM,FourgautG,et al. Inhibitors of the type 5 cyclic GMP phos- Cell Mol Physiol 1998;274:L908–13. Predictive factors of hospitalization for acute phodiesterase such as sildenafil may 5 Pepke-Zaba J, Higenbottam TW, Dinh-Xuan exacerbation in a series of 64 patients with have some selectivity for the pulmonary AT, et al. Inhaled nitric oxide as a cause of chronic obstructive pulmonary disease. Am J selective pulmonary vasodilatation in Respir Crit Care Med 1999;159:158–64. circulation, and it remains to be seen pulmonary hypertension. Lancet 15 Santos S, Peinado VI, Ramirez J, et al. 338 whether these drugs administered orally 1991; :1173–4. Characterization of pulmonary vascular Carlsen E may have an effect equivalent to inhaled 6 , Comroe JH. The rate of uptake of remodelling in smokers and patients with mild carbon monoxide and of nitric oxide by COPD. Eur Respir J 2002;19:632–8. NO. normal human erythrocytes and 16 Zhang W, Yatskievych TA, Cao X, et al. experimentally produced spherocytes. JGen Regulation of Hex gene expression by a Thorax 2003;58:283–284 Physiol 1958;42:83–107. Smads-dependent signaling pathway. J Biol 7 Cannon RO III, Schechter AN, Panza JA, et Chem 2002;277:45435–41. ..................... al. Effects of inhaled nitric oxide on regional 17 Germann P, Ziesche R, Leitner C, et al. Authors’ affiliations blood flow are consistent with intravascular nitric oxidedelivery. J Clin Invest Addition of nitric oxide to oxygen improves J Pepke-Zaba, N W Morrell, Pulmonary 2001;108:279–87. cardiopulmonary function in patients with 114 Vascular Diseases Unit, Papworth Hospital, 8 Ford PC, Wink DA, Stanbury DM. severe COPD. Chest 1998; :29–35. Papworth Everard, Cambridgeshire CB3 8RE, Autoxidation kinetics of aqueous nitric oxide. 18 Katayama Y, Higenbottam TW, Diaz de UK FEBS Lett 1993;326:1–3.
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