Development of Pulmonary Hypertension after Lung  Volume Reduction Surgery

Weg, Ira L.; Rossoff, Leonard J.; McKEON, Kerri; Graver, L. Michael; Scharf, Steven M.

doi:10.1164/ajrccm.159.2.9802056

Cited by 57 publications

(26 citation statements)

References 7 publications

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“…The development of secondary pulmonary hypertension in chronic obstructive pulmonary disease (e.g., emphysema) is ominous and denotes patients at greater risk for hospitalization (26), reduced exercise tolerance (27), and higher mortality (28,29). Several authors have reported that LVRS worsens pulmonary hemodynamics (16,17). Similarly, in emphysematous animal models, LVRS produced increases in pulmonary arterial pressure that varied with the extent of resection (30,31).…”

Section: Discussionmentioning

confidence: 99%

“…Several authors have reported improvement in RV function after LVRS (11), a decrease in pulmonary capillary wedge pressure (PCWP) (12), decreased respiratory swings in pulmonary arterial diastolic pressure (13), and improvements in RV and LV diastolic filling and function (14,15). Others have reported an increase in resting pulmonary arterial systolic pressures (16) and PVR (17), or no effect on the development of exercise-induced pulmonary hypertension (18) after LVRS. None of the above studies, however, examined the effects of LVRS in a prospective, randomized, and controlled trial.…”

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

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Effect of Lung Volume Reduction Surgery on Resting Pulmonary Hemodynamics in Severe Emphysema

Criner

Scharf

Falk

et al. 2007

Am J Respir Crit Care Med

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Rationale:To determine the effect of medical treatment versus lung volume reduction surgery (LVRS) on pulmonary hemodynamics. Methods: Three clinical centers of the National Emphysema Treatment Trial (NETT) screened patients for additional inclusion into a cardiovascular (CV) substudy. Demographics were determined, and lung function testing, six-minute-walk distance, and maximum cardiopulmonary exercise testing were done at baseline and 6 months after medical therapy or LVRS. CV substudy patients underwent right heart catheterization at rest prerandomization (baseline) and 6 months after treatment. Measurements and Main Results:A total of 110 of the 163 patients evaluated for the CV substudy were randomized in NETT (53 were ineligible), 54 to medical treatment and 56 to LVRS. Fifty-five of these patients had both baseline and repeat right heart catheterization 6 months postrandomization. Baseline demographics and lung function data revealed CV substudy patients to be similar to the remaining 1,163 randomized NETT patients in terms of age, sex, FEV 1 , residual volume, diffusion capacity of carbon monoxide, Pa O 2 , Pa CO 2 , and six-minute-walk distance. CV substudy patients had moderate pulmonary hypertension at rest (Ppa, 24.8 ؎ 4.9 mm Hg); baseline hemodynamic measurements were similar across groups. Changes from baseline pressures to 6 months post-treatment were similar across treatment groups, except for a smaller change in pulmonary capillary wedge pressure at end-expiration post-LVRS compared with medical treatment (؊1.8 vs. 3.5 mm Hg, p ϭ 0.04). Conclusions: In comparison to medical therapy, LVRS was not associated with an increase in pulmonary artery pressures.

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Section: Discussionmentioning

confidence: 99%

Section: What This Study Adds To the Fieldmentioning

confidence: 99%

Effect of Lung Volume Reduction Surgery on Resting Pulmonary Hemodynamics in Severe Emphysema

Criner

Scharf

Falk

et al. 2007

Am J Respir Crit Care Med

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“…The effects of LVRS on pulmonary haemodynamics have been analysed occasionally. WEG et al [126] reported an increase of Ppa after LVRS, which was attributed to the reduction of pulmonary capillary bed. Contrasting with this, SCIURBA et al [127] showed an improvement in right-ventricular systolic function.…”

Section: Lung Volume Reduction Surgerymentioning

confidence: 96%

Pulmonary hypertension in chronic obstructive pulmonary disease

Barberà

Peinado²,

Santos³

2003

Eur Respir J

389

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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“…LVRS may have adverse effects on pulmonary haemodynamics owing to the reduction of the vascular bed after the resection of lung tissue. Early studies have shown conflicting results, with increases in Ppa after LVRS in one study [130] but not in others [127,128]. A recent study as part of the National Emphysema Treatment Trial has shown no significant differences in terms of P pa and PVR, 6 months after medical treatment or LVRS [129].…”

Section: Lvrs and Lung Transplantationmentioning

confidence: 99%

Pulmonary hypertension in COPD

Chaouat¹,

Naeije²,

Weitzenblum³

2008

European Respiratory Journal

532

418

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Mild-to-moderate pulmonary hypertension is a common complication of chronic obstructive pulmonary disease (COPD); such a complication is associated with increased risks of exacerbation and decreased survival. Pulmonary hypertension usually worsens during exercise, sleep and exacerbation. Pulmonary vascular remodelling in COPD is the main cause of increase in pulmonary artery pressure and is thought to result from the combined effects of hypoxia, inflammation and loss of capillaries in severe emphysema.A small proportion of COPD patients may present with ''out-of-proportion'' pulmonary hypertension, defined by a mean pulmonary artery pressure .35-40 mmHg (normal is no more than 20 mmHg) and a relatively preserved lung function (with low to normal arterial carbon dioxide tension) that cannot explain prominent dyspnoea and fatigue. The prevalence of out-ofproportion pulmonary hypertension in COPD is estimated to be very close to the prevalence of idiopathic pulmonary arterial hypertension.Cor pulmonale, defined as right ventricular hypertrophy and dilatation secondary to pulmonary hypertension caused by respiratory disorders, is common. More studies are needed to define the contribution of cor pulmonale to decreased exercise capacity in COPD. These studies should include improved imaging techniques and biomarkers, such as the B-type natriuretic peptide and exercise testing protocols with gas exchange measurements.The effects of drugs used in pulmonary arterial hypertension should be tested in chronic obstructive pulmonary disease patients with severe pulmonary hypertension. In the meantime, the treatment of cor pulmonale in chronic obstructive pulmonary disease continues to rest on supplemental oxygen and a variety of measures aimed at the relief of airway obstruction.

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Development of Pulmonary Hypertension after Lung Volume Reduction Surgery

Cited by 57 publications

References 7 publications

Effect of Lung Volume Reduction Surgery on Resting Pulmonary Hemodynamics in Severe Emphysema

Effect of Lung Volume Reduction Surgery on Resting Pulmonary Hemodynamics in Severe Emphysema

Pulmonary hypertension in chronic obstructive pulmonary disease

Pulmonary hypertension in COPD

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