Medical treatment of pulmonary hypertension in chronic lung disease

Weitzenblum, E; Kessler, Romain; Oswald, M.; Fraisse, P.

doi:10.1183/09031936.94.07010148

Cited by 39 publications

(23 citation statements)

References 25 publications

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“…Taken together, the present and previous data suggest that factors other than severity of COPD are contributors to the pathogenesis of PH. These factors may include nocturnal desaturation, frequent exacerbations, changes in haematocrit and ventilatory response to hypoxia [7,18]. Data is currently limited, but it is also possible that genetic influences are involved [27,28], acting synergistically with the effects of chronic hypoxia and predisposing certain COPD patients to PH.…”

Section: Discussionmentioning

confidence: 99%

“…mean pulmonary arterial pressure in the region of 25 mmHg) and slowly progressive (y1 mmHg . yr -1 ) [6], but dramatic elevations of pulmonary arterial pressure are observed on exercise, during nocturnal desaturations and during acute exacerbations [7]. Pulmonary arterial pressure is an important prognostic indicator in COPD, which has been underlined by a recent study demonstrating that PH predicts the number of exacerbations and length of hospital stay in COPD patients [8].…”

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confidence: 88%

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Utility of echocardiography in assessment of pulmonary hypertension secondary to COPD

Higham¹,

Dawson²,

Joshi³

et al. 2001

Eur Respir J

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Studies have confirmed the close correlation of echocardiographically estimated pulmonary arterial pressure with invasive measurements in patients with chronic obstructive pulmonary disease (COPD), but there are few data on utility of echocardiographic measurement in assessing pulmonary arterial hypertension (PH) in COPD and correlation with pulmonary function tests.Presence or absence of tricuspid regurgitation (TR) was determined by Doppler echocardiography in 73 consecutive COPD patients attending a hospital outpatient clinic. Transtricuspid pressure gradient (TTPG) was calculated. PH was defined as TTPG ¢30 mmHg. Patients also underwent spirometry, forced expiratory volume in one second (FEV1), single breath gas transfer (carbon monoxide transfer coefficient; (KCO) and carbon monoxide diffusing capacity of the lung; DL,CO) and arterial blood gas measurement.Measurable TR was observed in 56/73 patients (77%). There were no differences between the group in which TR was observed compared to that in which it was absent, with regard to age, smoking history nor pulmonary function variables. PH was seen in 31/56 cases (55%), with good reproducibility. There were statistically significant correlations of TTPG with FEV1 (r~-0.26, p~0.05), KCO (r~-0.31, p~0.04) and DL,CO (r~-0.42, p~0.006) expressed as % pred. Stepwise regression analysis showed that age and KCO combined provide a multivariate model for prediction of TTPG.It is concluded the presence and degree of pulmonary arterial hypertension is readily and reliably determined by echocardiography in the majority of chronic obstructive pulmonary disease patients. Pulmonary arterial hypertension is common in severe chronic obstructive pulmonary disease and transtricuspid pressure gradient correlates with spirometry and indices of gas transfer, similar to previous invasive studies. In view of the adverse effects of pulmonary arterial hypertension on morbidity and mortality routine echocardiography in patients with severe chronic obstructive pulmonary disease may be warranted. Eur Respir J 2001; 17: 350-355.

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Section: Discussionmentioning

confidence: 99%

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confidence: 88%

Utility of echocardiography in assessment of pulmonary hypertension secondary to COPD

Higham¹,

Dawson²,

Joshi³

et al. 2001

Eur Respir J

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“…However, recent advances in knowledge of the pathogenesis of pulmonary hypertensive states, along with the development of new and effective strategies in the treatment of pulmonary hypertension, open a new perspective that could be applicable in COPD. Therefore, it is appropriate to revisit this old topic [1,2] in the light of new discoveries in this field. In this report the different aspects of pulmonary hypertension associated with COPD are reviewed with special emphasis placed on the recent advances in the knowledge of the pathogenesis of COPD and the potential implications of these findings in treatment perspectives.…”

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confidence: 99%

Pulmonary hypertension in chronic obstructive pulmonary disease

Barberà

Peinado²,

Santos³

2003

Eur Respir J

390

299

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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.

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“…There remains, therefore, a need to identify the underlying mechanisms of these diseases, in the hope that new treatments can be developed. A previous review series in the Journal has already highlighted new insights into clinical and basic knowledge of major conditions associated with pulmonary hypertension [1][2][3][4][5]. However, certain areas have not been covered by the previous series.…”

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confidence: 99%