[Show abstract][Hide abstract] ABSTRACT: Severe pulmonary hypertension occurs occasionally in patients with chronic obstructive pulmonary disease (COPD), but no detailed description of these patients is available.
To identify and characterize patients with COPD and severe pulmonary hypertension.
Retrospective study of 27 patients with COPD with severe pulmonary hypertension (pulmonary artery mean pressure [Ppa], > or = 40 mm Hg) among 998 patients who underwent right heart catheterization between 1990 and 2002 as part of a workup for chronic respiratory failure during a period of disease stability.
Of the 27 patients, 16 had another disease capable of causing pulmonary hypertension. The remaining 11 (11 of 998, 1.1%) patients had COPD as the only cause of pulmonary hypertension, with a median Ppa of 48 mm Hg (interquartile range, 46-50). They had an unusual pattern of cardiopulmonary abnormalities with mild to moderate airway obstruction, severe hypoxemia, hypocapnia, and a very low diffusing capacity for carbon monoxide (p < 0.01 compared with a control group of patients with COPD). Exertional dyspnea was more severe (p < 0.01) and survival was shorter (p = 0.0026) than in the control subjects.
Severe pulmonary hypertension is uncommon in patients with COPD. When it occurs, another cause must be sought. COPD with severe pulmonary hypertension and no other possible cause shares features with pulmonary vascular diseases, such as idiopathic pulmonary hypertension.
American Journal of Respiratory and Critical Care Medicine 07/2005; 172(2):189-94. · 11.04 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The aim of the present study was to compare the evolution of pulmonary haemodynamics and of arterial blood gases in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate hypoxaemia, with or without sleep-related oxygen desaturation. COPD patients with daytime arterial oxygen partial pressure in the range 56-69 mmHg were included prospectively. Sleep-related oxygen desaturation was defined as spending > or = 30% of the nocturnal recording time with arterial oxygen saturation <90%. From the 64 patients included, 35 were desaturators (group 1) and 29 were nondesaturators (group 2). At baseline (t0), patients with sleep-related desaturation had a significantly higher daytime (mean +/- SD) arterial carbon dioxide partial pressure (Pa,CO2) (44.9 +/- 4.9 mmHg versus 41.0 +/- 4.1 mmHg, p=0.001) whereas mean pulmonary artery pressure (mPAP) was similar in the two groups. After 2 yrs (t2) of follow-up, 22 desaturators and 14 nondesaturators could be re-evaluated, including pulmonary haemodynamic measurements. None of the nondesaturator patients became desaturators at t2. The difference between the two groups in terms of daytime Pa,CO2 was still present at t2. The mean changes in mPAP from t0 to t2 were similar between the two groups, as were the rates of death or requirement for long-term oxygen therapy (American Thoracic Society criteria) during follow-up of up to 6 yrs. The presence of sleep-related oxygen desaturation is not a transitional state before the worsening of daytime arterial blood gases, but is a characteristic of some chronic obstructive pulmonary disease patients who have a higher daytime arterial carbon dioxide partial pressure. Such isolated nocturnal hypoxaemia or sleep-related worsening of moderate daytime hypoxaemia does not appear to favour the development of pulmonary hypertension, nor to lead to worsening of daytime blood gases.
European Respiratory Journal 06/2001; 17(5):848-55. · 6.36 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: The beneficial effects of nocturnal oxygen therapy (NOT) in chronic obstructive pulmonary disease (COPD) patients with mild-to-moderate daytime hypoxaemia (arterial oxygen tension (Pa,O2) in the range 7.4-9.2 kPa (56-69 mmHg)) and exhibiting sleep-related oxygen desaturation remains controversial. The effectiveness of NOT in that category of COPD patients was studied. The end points included pulmonary haemodynamic effects after 2 yrs of follow-up, survival and requirement for long-term oxygen therapy (LTOT). Seventy-six patients could be randomized, 41 were allocated to NOT and 35 to no NOT (control). The goal of NOT was to achieve an arterial oxygen saturation of >90% throughout the night. All these patients underwent polysomnography to exclude an associated obstructive sleep apnoea syndrome. The two groups exhibited an identical meansD daytime Pa,O2 of 8.4+/-0.4 kPa (63+/-3 mmHg) at baseline. Twenty-two patients (12 in the NOT group and 10 in the control group, p=0.98) required LTOT during the whole follow-up (35+/-14 months). Sixteen patients died, nine in the NOT group and seven in the control group (p=0.84). Forty-six patients were able to undergo pulmonary haemodynamic re-evaluation after 2 yrs, 24 in the NOT and 22 in the control group. In the control group, mean resting pulmonary artery pressure increased from 19.8+/-5.6 to 20.5+6.5 mmHg, which was not different from the change in mean pulmonary artery pressure in the NOT group, from 18.3+/-4.7 to 19.5+/-5.3 mmHg (p= 0.79). Nocturnal oxygen therapy did not modify the evolution of pulmonary haemodynamics and did not allow delay in the prescription of long-term oxygen therapy. No effect of NOT on survival was observed, but the small number of deaths precluded any firm conclusion. These results suggest that the prescription of nocturnal oxygen therapy in isolation is probably not justified in chronic obstructive pulmonary disease patients.
European Respiratory Journal 11/1999; 14(5):1002-8. · 6.36 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Cushing's syndrome is infrequently associated with adenocarcinomas of the lung. We present the clinical features of this syndrome in one case report. The pathogenesis of the syndrome explains the clinical signs, rather different from classical Cushing's disease and also the highly suggestive biological features. Ketoconazole improves clinical signs and biological abnormalities when etiological treatment is not effective.
Revue des Maladies Respiratoires 07/1999; 16(3):395-7. · 0.50 Impact Factor
[Show abstract][Hide abstract] ABSTRACT: Pulmonary hypertension at the end stage of chronic liver disease is not an uncommon situation. This association termed portopulmonary hypertension raises the question of the feasibility of performing orthotopic liver transplantation (OLT). In the case reported herein, there was a favorable outcome after OLT, even though the mean pulmonary artery pressure (MPAP) before transplantation was increased to 45 mm Hg. Before OLT, the cardiac index (CI) was considerably elevated (7.69 L/min/m2), giving evidence of a marked hyperdynamic circulatory state. The CI decreased significantly after OLT (3.38 L/min/m2), and this produced a significant decrease in the MPAP. Our observation suggests that portopulmonary hypertension due to a marked increase in the CI can be managed successfully by OLT.
[Show abstract][Hide abstract] ABSTRACT: Can daily short-duration hypoxemia (4-8 hours) induce pulmonary hypertension and right ventricular hypertrophy? A clinical model of this type of hypoxemia does exist: isolated nocturnal hypoxemia in patients with obstructive sleep apnea syndrome (OSAS) or chronic obstructive pulmonary disease (COPD). By investigating the pulmonary hemodynamics of these patients, it should be possible to determine whether nocturnal hypoxemia alone can induce pulmonary hypertension. Although nocturnal hypoxemia (in OSAS as well as in COPD) can induce acute episodes of pulmonary hypertension, it would not appear that nocturnal hypoxemia alone would be sufficient to provoke permanent diurnal pulmonary hypertension. This is the conclusion of recent studies concerning diurnal pulmonary hemodynamics in OSAS and COPD patients exhibiting minimal hypoxemia during the day but significant nocturnal desaturation. The therapeutic consequences of these data, particularly in COPD are important: current evidence is insufficient to treat with nocturnal oxygen therapy COPD patients who have minimal diurnal hypoxemia but significant nocturnal desaturation.
Revue des Maladies Respiratoires 01/1999; 15(6):743-51. · 0.50 Impact Factor