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Biomedical subjects

A Chaouat

Publications and source records attributed to A Chaouat.

At least 19 recordsLinked to original sources

"Natural history" of pulmonary hypertension in a series of 131 patients with chronic obstructive lung disease.

The prognostic value and the evolution of pulmonary hypertension (PH) in patients with markedly hypoxemic chronic obstructive pulmonary disease (COPD), treated or not with long-term oxygen therapy (LTOT), has been extensively investigated. However, little is known in patients with mildly or moderately hypoxemic COPD not requiring LTOT. Therefore, we assessed the evolution of pulmonary hemodynamics in 131 patients with stable COPD by performing two right heart catheterizations at a mean (+/- SD) time interval of 6.8 +/- 2.9 yr. At inclusion (T0), no patient had PH (i.e., the mean pulmonary artery pressure [Ppa] at rest was < 20 mm Hg). Group 1 included 55 patients without exercising PH and group 2 included 76 patients with exercising PH, defined by a pulmonary arterial pressure (Ppa) > 30 mm Hg during a steady-state 40-W exercise. Group 2 patients compared with group 1 patients had a significantly higher resting Ppa (16 +/- 3 mm Hg versus 14 +/- 2 mm Hg, p = 0.001). At the second catheterization, 33 (25%) patients (9 of 55 in group 1, 24 of 76 in group 2, p = 0.048) showed a resting Ppa > 20 mm Hg, but PH was generally mild, ranging from 20 to 42.5 mm Hg. The mean Ppa at second evaluation was 16 +/- 5 mm Hg in group 1 and 19 +/- 7 mm Hg in group 2 (p = 0.01). The patients who developed resting PH at the second catheterization (T1) had higher resting and exercising Ppa (p = 0.001 and p = 0.002, respectively), and significantly lower resting and exercising Pa(O(2)) (p = 0.005 and p = 0.012, respectively) at T0. Logistic regression analysis showed that resting and exercising Ppa were independent predictors (at T0) for the subsequent development of PH (p = 0.029 and p = 0.027, respectively). The patients who developed resting PH (T1) had a significantly worsening of Pa(O(2)) (from 63.5 mm Hg at T0 to 60 mm Hg at T1, p = 0.047), whereas the Pa(O(2)) as a mean was stable in the remainder (69.5 mm Hg at T0 and T1). These results show the following. The progression of Ppa over time in patients with COPD with mild to moderate hypoxemia is rather slow, the average change for the group as a whole being of + 0.4 mm Hg/yr. Only about 25% of patients with COPD with mild to moderate hypoxemia and without resting PH at the onset will develop PH during a 6-yr follow-up. The patients with exercising PH at the onset have a significantly increased risk of developing PH over time. Only resting and exercising Ppa at the onset are independently related to the subsequent development of PH. However, in individual cases, the models of linear or logistic regression do not allow a pertinent prediction of the level of Ppa or the presence of PH at the second right heart catheterization.

Blood Pressure↗

Outcome of COPD patients with mild daytime hypoxaemia with or without sleep-related oxygen desaturation.

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.

Adult↗

The obesity-hypoventilation syndrome revisited: a prospective study of 34 consecutive cases.

STUDY OBJECTIVES: Obesity has many detrimental effects on the respiratory function and may lead to chronic hypoventilation in some patients, an association known as the obesity-hypoventilation syndrome (OHS). In many cases, patients with OHS also have sleep apneas. Hereafter, we describe several features of a cohort (n = 34) of patients with OHS and show the comparisons with a large cohort (n = 220) of patients with obstructive sleep apnea syndrome (OSAS). We compare also OHS patients with a group of patients with the association of OSAS and COPD, also known as "overlap" patients. DESIGN: Descriptive analysis of prospectively collected clinical data. SETTING: Respiratory care unit and sleep laboratory of university hospital. RESULTS: In OHS patients, OSAS was present in most of the cases (23 of 26 patients). However, in three patients, OHS was not associated with OSAS, showing that obesity per se may lead to chronic hypoventilation. As expected by definition, OHS patients had, on average the worst diurnal arterial blood gas measurements, compared to the other groups. For the OHS patients, the mean diurnal PaO(2) was 59 +/- 7 mm Hg, which was significantly different from the PaO(2) of the OSAS patients (75 +/- 10 mm Hg; p = 0,001) but also from the overlap patients (66 +/- 10 mm Hg; p = 0.015). Pulmonary hypertension (ie, mean pulmonary artery pressure > 20 mm Hg) was more frequent in OHS patients than in "pure" OSAS patients (58% vs 9%; p = 0.001). CONCLUSION: Patients with OSAS and chronic respiratory insufficiency had in most cases an associated OHS or COPD. Patients with OHS were older than patients with pure OSAS. They had mild-to-moderate degrees of restrictive ventilatory pattern due to obesity. Severe gas exchange impairment and pulmonary hypertension were quite frequent. The association of OHS and OSAS was the rule. However, in three patients, OHS was not associated with OSAS, suggesting that OHS is an autonomous disease.

Chronic Disease↗

Platypnea-orthodeoxia syndrome related to an aortic aneurysm combined with an aneurysm of the atrial septum.

We report the case of a 71-year-old man bearing a severe right-to-left shunt through a patent foramen ovale in the absence of elevated right-sided heart or pulmonary artery pressures. He presented with platypnea-orthodeoxia syndrome, but he had no pulmonary or extracardiac diseases that are known to be associated with this syndrome. Chest radiography showed a bulky aneurysm of the thoracic aorta. A peripheral contrast transesophageal echocardiography demonstrated a large right-to-left shunt through a patent foramen ovale. In addition, the atrial septum was severely deformed by an aneurysm including this patent foramen ovale. We hypothesized that the opening of the foramen ovale was the result of a mechanical deformation of the atrial septum by two contributing factors: the aneurysm of the thoracic aorta and the aneurysm of the septum itself.

Aged↗

Prognostic value of lung function and pulmonary haemodynamics in OSA patients treated with CPAP.

The aim of the present study was to determine survival rates of obstructive sleep apnoea patients treated with continuous positive airway pressure (CPAP) and to investigate the prognostic value of pretreatment lung function and pulmonary haemodynamics. Two hundred and ninety-six patients, exhibiting > or = 20 apnoeas plus hypopnoeas per hour of sleep, were included. Patients were treated with nasal CPAP and regularly followed up. The cumulative survival rates were 0.96 (95% confidence interval (CI): 0.94-0.99) at 3 yrs and 0.93 (95% CI: 0.91-0.97) at 5 yrs. Most patients died from cardiovascular disease. Apart from age, covariates associated with a lower survival were the presence of a heavy smoking history, a low vital capacity, a low forced expiratory volume in one second (FEV1) and a high mean pulmonary artery pressure. Only three covariates were included by forward stepwise selection in the multivariate analysis, smoking habit (>30 pack-yrs), age and FEV1. The observed survival rates of the group as a whole were similar to those of the general population matched in terms of age, sex and smoking habit, except for patients between 50 and 60 yrs old who had reduced survival. This difference disappeared when patients of the present study with an associated chronic obstructive pulmonary disease were excluded from the comparison. In conclusion, survival of obstructive sleep apnoea patients treated with nasal continuous positive airway pressure is near to that of the general population. The prognosis is worse in subgroups of patients with a history of heavy smoking and with an associated chronic obstructive pulmonary disease.

Female↗

A randomized trial of nocturnal oxygen therapy in chronic obstructive pulmonary disease patients.

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.

Follow-Up Studies↗

Improvement of pulmonary hypertension after liver transplantation.

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.

Adult↗

[Paraneoplastic hypercorticism associated with a bronchial adenocarcinoma].

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.

Adenocarcinoma↗

[Chronic thromboembolic pulmonary arterial hypertension].

Chronic thromboembolic pulmonary hypertension (CTEPH) is an uncommon disease with a severe prognosis. Initially considered as a constantly fatal disease, it can be cured since the advent in the late 80's of thromboendarterectomy. CTEPH occurs in approximately 0.1% of patients who survive acute pulmonary embolism. Such outcome is due to the failure of the normal thrombi resolution in the pulmonary circulation. This disease is observed in both sexes and occasionally as early as in the third decade. Many patients have no history of acute venous thromboembolism which is responsible for the frequent diagnosis delay. Therefore, it is of paramount importance to search for pulmonary vascular disease when patients complain solely of dyspnea on exertion. These patients should undergo echocardiography and, if necessary, right heart catheterization. Once the diagnosis of pulmonary hypertension is established the next step is to find the cause. Ventilation-perfusion scanning is probably the most sensitive non-invasive test to provide evidence that pulmonary hypertension is related to chronic thromboembolism. Angiography and helical computed tomography allow to confirm the diagnosis of CTEPH and to determine whether it is accessible or not to thromboendarterectomy. Most patients who undergo thromboendarterectomy improve clinically and in terms of gas exchange and pulmonary hemodynamics. When thrombi are inaccessible surgically, patients should be placed on the list for lung transplantation if they fulfill the criteria established for primary pulmonary hypertension. When all surgical procedures are contraindicated, anticoagulant and oxygen therapy remain the sole possibility of treatment.

Anticoagulants↗

[Chronic respiratory insufficiency: evaluation, evolution, prognosis].

Chronic respiratory failure (CRF) is a major cause of morbidity and mortality. It is estimated that in France at least 60,000 patients exhibit severe CRF and that about 15,000 patients die each year from CRF. Chronic obstructive pulmonary disease (COPD) (chronic obstructive bronchitis, emphysema and their association) is by far the first cause of CRF (90% of the cases). The clinical picture of CRF depends on the causal disease, but exertional dyspnea is observed in almost all patients. Pulmonary function testing allows to assess whether the ventilatory defect is obstructive (COPD), restrictive or mixed. Severe CRF is usually defined by a Pa02 < 55 mmHg, in a stable state of the disease, with or without hypercapnia (PaC02 > 45 mmHg). The two major complications of CRF are acute exacerbations of the disease, with clinical and gasometric worsening, and pulmonary hypertension which may lead with time to right heart failure. Prognosis is poor in CRF since the 5 year survival rate is of 50% in COPD patients. Under long-term oxygen therapy (LTOT) the survival rate has been somewhat improved, being of 60-65% at 5 years. The best prognostic indices in CRF complicating COPD are the level of FEV1, Pa02, PaC02, the level of pulmonary artery mean pressure (PAP) and age. In COPD patients under LTOT the best prognostic indices are PAP and age.

Chronic Disease↗

[Short-duration nocturnal hypoxemia and persistent pulmonary hypertension].

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.

Hemodynamics↗