Cor pulmonale.

The term "cor pulmonale" is still popular but there is presently no consensual definition and it seems more appropriate to define the condition by the presence of pulmonary hypertension (PH) resulting from diseases affecting the structure and/or the function of the lungs: PH results in right ventricular enlargement and may lead with time to right heart failure (RHF). Chronic obstructive pulmonary disease (COPD) is the first cause of cor pulmonale, far before idiopathic pulmonary fibrosis and obesity-hypoventilation syndrome. In chronic respiratory disease (CRD) PH is "pre-capillary," due to an increase of pulmonary vascular resistance (PVR). The first cause of increased PVR is chronic long-standing alveolar hypoxia which induces pulmonary vascular remodeling. The main characteristic of PH in CRD and particularly in COPD is its mild to moderate degree, resting pulmonary artery mean pressure (PAP) in a stable state of the disease usually ranging between 20 and 35 mmHg. However, PH may worsen during exercise, sleep, and exacerbations of the disease. These acute increases in afterload can favor the development of RHF. A minority (<5%) of COPD patients exhibit severe or "disproportionate" PH (PAP >40 mmHg), the mechanism of which is not well understood. At present long-term oxygen therapy (LTOT) is the logical treatment of PH since alveolar hypoxia is considered to be the major determinant of the elevation of PAP and PVR. LTOT stabilizes or at least attenuates and sometimes reverses the progression of PH, but PAP seldom returns to normal. Vasodilators (prostacyclin, endothelin receptor antagonists, sildenafil, nitric oxide) could be considered in patients with severe PH but controlled studies in this field are presently lacking.

Pulmonary hypertension in COPD.

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-of-proportion 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.

[Obesity-hypoventilation syndrome]. / Syndrome obésité-hypoventilation.

INTRODUCTION: The obesity-hypoventilation syndrome (OHS), or alveolar hypoventilation in the obese, has been described initially as the "Pickwickian syndrome". It is defined as chronic alveolar hypoventilation (PaO2<70 mmHg, PaCO2 > or =45 mmHg) in obese patients (body mass index>30 kg/m2) who have no other respiratory disease explaining the hypoxemia-hypercapnia. BACKGROUND: The large majority of obese subjects are not hypercapnic, even in case of severe obesity (>40 kg/m2). There are three principal causes, which can be associated, explaining alveolar hypoventilation in obese subjects: high cost of respiration and weakness of the respiratory muscles (probably the major cause), dysfunction of the respiratory centers with diminished chemosensitivity, long-term effects of the repeated episodes of obstructive sleep apneas observed in some patients. The role of leptin (hormone produced by adipocytes) in the pathogenesis of this syndrome, has been recently advocated. OHS is generally observed in subjects over 50 years. Its prevalence has markedly increased in recent years, probably due to the present "epidemic" of obesity. The diagnosis is often made after an episode of severe respiratory failure. Comorbidities, favored by obesity, are very frequent: systemic hypertension, left heart diseases, diabetes. VIEWPOINT: OHS must be distinguished from obstructive sleep apnea syndrome (OSAS) even if the two conditions are often associated. OSAS may be absent in certain patients with OHS (20% of the patients in our experience). On the other hand obesity may be absent in certain patients with OSAS. CONCLUSION: Losing weight is the "ideal" treatment of OHS but in fact it cannot be obtained in most patients. Nocturnal ventilation (continuous positive airway pressure and mainly bilevel non invasive ventilation) is presently the best treatment of OHS and excellent short and long-term results on symptoms and arterial blood gases have been recently reported.

[Pulmonary hypertension of chronic respiratory disease]. / Hypertension pulmonaire des affections respiratoires chroniques.

Pulmonary hypertension of chronic respiratory disease is defined as elevation of the mean resting pulmonary artery pressure to over 20 mm Hg. It is the commonest cause of pre-capillary pulmonary hypertension on account of the high prevalence of chronic obstructive pulmonary disease. It is primarily due to alveolar hypoxia that leads to remodelling of the distal pulmonary vasculature and consequently to an increase in pulmonary resistance. It is not as severe as idiopathic pulmonary hypertension. The mean pulmonary artery pressure is usually moderately increased (20-35 mm Hg) when patients are seen during a stable period of the disease. There are, however, more severe cases of pulmonary hypertension called, in some cases, disproportionate but these are uncommon. Increased right ventricular afterload can lead to the development of right ventricular failure that is a definite prognostic factor. The clinical symptoms of pulmonary hypertension are at a secondary level compared with those of the causal disease. Non-invasive diagnosis depends on Doppler echocardiography. Currently the most effective treatment is long term oxygen therapy (16-18 hr/24 hr). This improves or, at least stabilises, the pulmonary hypertension.

[Pleural effusion complicating a totally implanted venous device]. / Un épanchement pleural liquidien compliquant une chambre à cathéter implantable.

INTRODUCTION: Totally implanted venous devices (TIVD) are an essential tool for repeated intravenous treatments such as chemotherapy for cancer and antibiotics for cystic fibrosis. CASE REPORT: A woman of 76 years was treated for bronchiectasis, colonised by Pseudomonas aeruginosa, with courses of intravenous antibiotics. On account of poor peripheral veins a TIVD was implanted. The implantation and subsequent antibiotic injections were uncomplicated. Three years later a further course of antibiotics was prescribed. As no reflux of blood was obtained on puncturing the device the position of the catheter was checked radiologically. The patient complained of right shoulder pain following each infusion. The chest x-ray showed a pleural effusion. The sudden onset of the effusion, the absence of signs of infection and the patient's good clinical condition suggested pleural extravasation of the antibiotic infusion from the TIVD. Pleural aspiration yielded 1400 mls of watery fluid. Injection of contrast into the TIVD confirmed intra-pleural extravasation. CONCLUSION: When using a TIVD it is important to bear in mind the possibility of late pleural complications.

[Use of linezolid for the treatment of lung infections in adults with cystic fibrosis]. / Utilisation du linézolide dans le traitement des infections broncho-pulmonaires du patient adulte atteint par la mucoviscidose.

INTRODUCTION: Linezolid, a new antistaphylococcal agent for oral or intravenous administration is active against Staphylococcus aureus with limited sensitivity to glycopeptides. The purpose of the present work was to compare data in the literature with practical clinical experience with the use of linezolid for lung infections in adult cystic fibrosis patients with the objective of developing local guidelines for use. MATERIAL AND METHODS: This retrospective clinical study was conducted in the adult pneumology department of a university hospital. RESULTS: The main clinical signs leading to prescription of linezolid were aggravating cough, bronchial obstruction, and exercise-induced fatigue. Among 42 cystic fibrosis patients, six aged 24+/-3 years were given 22 treatments of linezolid. Two patients were given the drug once and the others 2, 4, 5, and 9 times, 600 mg b.i.d. Mean duration of treatment with linezolid was 16+/-5 days. Among the six patients, two presented meti-R S. aureus infection. For twelve cases, clinical improvement was observed; and in two others the situation worsened leading to interruption of linezolid. CONCLUSIONS: There are few reports in the literature on use of linezolid in cystic fibrosis patients. Writing internal guidelines for our department has enabled standardized use: 600 mg b.i.d. p.o. for 14 days as second-line treatment for bronchial exacerbation of S. aureus infection.

Polymorphism of the serotonin transporter gene and pulmonary hypertension in chronic obstructive pulmonary disease.

BACKGROUND: The serotonin transporter (5-HTT) is involved in the pulmonary artery smooth muscle hyperplasia that leads to pulmonary hypertension (PH). Because hypoxia and 5-HTT gene polymorphism control 5-HTT expression, we examined 5-HTT gene polymorphism and PH in hypoxemic patients with advanced chronic obstructive pulmonary disease (COPD). METHODS AND RESULTS: In 103 patients with COPD recruited in France (n=67) and the UK (n=36), we determined 5-HTT gene polymorphism and pulmonary artery pressure (PAP) measured during right heart catheterization (France) or Doppler echocardiography (UK). Ninety-eight subjects from the 2 countries served as control subjects. The distribution of 5-HTT gene polymorphism did not differ between patients and control subjects. In patients carrying the LL genotype, which is associated with higher levels of 5-HTT expression in pulmonary artery smooth muscle cells than the LS and SS genotypes, PH was more severe than in LS or SS patients. Mean PAP values in patients from France with the LL, LS, and SS genotypes were 34+/-3, 23+/-1, and 22+/-2 mm Hg (mean+/-SEM), respectively (P<0.01). Corresponding systolic PAP values in the UK were 40+/-3, 28+/-3, and 24+/-3 mm Hg, respectively (P<0.01). Compared with control subjects, platelet 5-HTT protein was increased in COPD patients in proportion to the hypoxemia level, and strong 5-HTT immunostaining was observed in remodeled pulmonary arteries from COPD patients. CONCLUSIONS: 5-HTT gene polymorphism appears to determine the severity of PH in hypoxemic patients with COPD. Because PH is an important prognostic factor in this disease, recognition of patients at risk for PH should be helpful in managing COPD.

[Pulmonary hypertension associated with disorders of the respiratory system]. / Hypertension pulmonaire des affections respiratoires chroniques.

Pulmonary hypertension associated with disorders of the respiratory system is defined by a pulmonary artery mean pressure above 20 mmHg at rest in stable disease. The most frequent form of precapillary pulmonary hypertension is associated with chronic obstructive pulmonary disease, because of its high prevalence. Pulmonary vascular remodeling occurs in the small pulmonary arteries and is due mainly to chronic alveolar hypoxia. Pulmonary hypertension associated with disorders of the respiratory system is usually mild to moderate, with resting pulmonary artery mean pressure ranging between 20 and 35 mm Hg. It may increase markedly during sleep, exercise or exacerbation of respiratory failure, however. Abrupt postload elevation can lead to right heart failure, an indisputable indicator of prognosis. Because the symptoms of pulmonary hypertension are minimal relative to those of the chronic hypoxic lung disease, noninvasive diagnosis is difficult, particularly in patients with chronic obstructive pulmonary disease. Oxygen therapy (at least 16 h/day) is currently the best treatment for this type of pulmonary arterial hypertension.

[Physiological functional tests to evaluate pulmonary arterial hypertension]. / Explorations fonctionnelles dans l'hypertension artérielle pulmonaire.

INTRODUCTION: Pulmonary arterial hypertension (PAH) is a rare and complex disease, which requires careful diagnostic evaluation. STATE OF THE ART: Most patients have a mild decrease in lung volumes and a moderate decrease in carbon monoxide transfer factor. Mild to moderate arterial hypoxaemia, is often present, associated with a mild respiratory alkalosis. When hypoxaemia is severe, it may represent an intracardiac shunt. Right heart catheterisation is required to confirm the diagnosis and in most cases shows a significant elevation of pulmonary artery pressure due to an increase in pulmonary vascular resistance. The haemodynamic profile and the response to an acute pulmonary vasodilator challenge are determinants of prognosis. Finally, exercise capacity which is usually assessed by the six minute walk test provides an overall functional measure of disease severity, response to therapy, and progression. PERSPECTIVES: Functional evaluation of the heart using echocardiography will play an increasing role in the evaluation of PAH. CONCLUSIONS: Physiological measurements in PAH have several objectives. They form part of the diagnostic definition, allow the exclusion of other conditions and are tools for the assessment of severity, prognosis and response to therapy.

Allelic imbalance at loci containing FGFR, FGF, c-Met and HGF candidate genes in non-small cell lung cancer sub-types, implication for progression.

Fibroblast growth factors (FGF), hepatocyte growth factor (HGF) and their receptors, FGFR and c-Met, are essential components of the regulatory networks between the epithelium and mesenchyme in embryonic lung, but their respective roles in tumour growth are not clear. We performed allelotyping at loci containing the candidate genes FGFR-1-2-3-4, FGF-1-2-7-10, c-Met and HGF in 36 non-small cell lung cancer (NSCLC) (20 squamous-cell carcinomas (SQC) and 16 adenocarcinomas (ADC)), by surrounding each locus with two microsatellites (MS), as close as possible to the genes of interest. Unexpectedly, SQC and ADC were frequently altered at all of these loci, and SQC showed more simultaneously altered loci. In ADC, alterations at the 15q13-22 locus (FGF7 candidate gene) were significantly more frequent. Thus, these loci showed different patterns of molecular alterations between SQC and ADC. Finally, alterations at loci containing FGFR and HGF candidate genes were inversely correlated to the lymph node status in SQC and ADC, respectively.

Chronic obstructive pulmonary disease and sleep apnea syndrome.

The term "overlap syndrome" was introduced by Flenley to describe the association of sleep apnea syndrome (SAS) with chronic obstructive pulmonary disease (COPD). Epidemiologic data on the prevalence of the overlap syndrome are not available, but the frequency of an associated COPD in SAS patients has been emphasized in almost all the studies analyzing the development of respiratory insufficiency in SAS patients. In a large series (n = 264) of unselected SAS patients who had undergone detailed pulmonary function tests, we observed an obstructive ventilatory defect (FEV1/VC < 60%) in 30 of 264 patients (11%). These patients had lower daytime PaO2 and higher PaCO2 than the other patients and they had higher resting and exercising pulmonary artery mean pressure (right heart catheterization was performed in 215 of 264 patients). We conclude that the risk of developing respiratory insufficiency and cor pulmonale is higher in overlap patients.

Daytime hypoventilation in obstructive sleep apnoea syndrome.

Chronic alveolar hypoventilation is a classic feature of the "pickwickian syndrome" (i.e. obesity-hypoventilation syndrome) but in fact hypercapnia is observed in a minority of obstructive sleep apnoea syndrome (OSAS) patients. Most recent studies having included large numbers of unselected, consecutive OSAS patients agree on a prevalence of 10-20% of alveolar hypoventilation. The mechanisms of hypercapnia in OSAS are not fully understood but the determining factors of daytime respiratory insufficiency are probably the presence of a marked obesity, leading to the obesity hypoventilation syndrome and, principally, the association of OSAS with chronic obstructive pulmonary disease. This association (the so-called "overlap syndrome") is observed in >10% of OSAS patients. Bronchial obstruction is generally mild to moderate and may be asymptomatic. The severity of the nocturnal events (apnoeas, hypopnoeas) and a (possible) diminished chemosensitivity to hypercapnic and hypoxic stimuli do not appear to be determining factors of hypercapnia. The most important consequence of chronic alveolar hypoventilation is pulmonary hypertension which is only observed in patients with daytime arterial blood gases disturbances, and which can lead to right heart failure. When nasal continuous positive airway pressure fails to correct sleep-related hypoxaemia, supplementary O, must be given or another way of assisted ventilation (BIPAP) must be considered. In the most severe patients (diurnal PaO(2) <55 mmHg) conventional O(2) therapy (>or=16h/24h) is required in addition to nocturnal ventilation.

A life-threatening tracheal localization of lymphoma in a patient with AIDS.

Lymphoma is a frequent complication of HIV infection, but we report a rare localization in the subglottic tracheal area. A case of tracheal stenosis due to lymphoma in an HIV-infected patient is presented. The main complaint was severe dyspnea. Chemotherapy was ineffective but radiotherapy improved the patient's condition and increased the caliber of the tracheal lumen.

Pulmonary hemodynamics in patients with chronic obstructive pulmonary disease before and during an episode of peripheral edema.

We have investigated pulmonary hemodynamics in 16 patients with COPD with respiratory insufficiency, exhibiting marked peripheral edema. All the patients had previously undergone, within the last 6 months (T1), a right heart catheterization, in a stable state of their disease, when they were free of edema. Patients were subdivided into two groups according to the level of right ventricular end-diastolic pressure (RVEDP) during the episode of edema (T2): patients with a markedly elevated RVEDP (> 12 mm Hg) indicating the presence of right ventricular failure (RVF) = group 1, n = 9; patients with a normal or slightly elevated RVEDP (< 12 mm Hg) = group 2 (no RVF), n = 7. In group 1 pulmonary artery mean pressure (PAP) increased very significantly from T1 (27 +/- 5) to T2 (40 +/- 6 mm Hg, p < 0.001) as did RVEDP, from 7.5 +/- 3.9 to 13.4 +/- 1.2 mm Hg (p < 0.001). These hemodynamic changes paralleled a marked worsening of arterial blood gases, PaO2 falling from 63 +/- 4 to 49 +/- 7 mm Hg (p < 0.01) and PaCO2 increasing from 46 +/- 7 to 59 +/- 14 mm Hg (p < 0.01). On the other hand, in group 2, PAP was stable during the episode of edema (from 20 +/- 6 to 21 +/- 5 mm Hg), as was RVEDP (from 5.5 +/- 2.4 to 5.1 +/- 1.5 mm Hg), and changes in arterial blood gases from T1 to T2 were small and nonsignificant. It is concluded that RVF is effectively present in at least some patients with COPD with peripheral edema and is associated with a significant increase of PAP from baseline, probably accounted for by hypoxic vasoconstriction. Thus, pressure overload may contribute to the development of RVF. In other patients there are no hemodynamic signs of RVF, PAP is stable, and the origin of edema is not well understood.

Pulmonary hemodynamics in the obstructive sleep apnea syndrome. Results in 220 consecutive patients.

We have investigated pulmonary hemodynamics in a large series of consecutive, unselected patients with obstructive sleep apnea syndrome (OSAS). The aims of this study were to evaluate the frequency of pulmonary artery hypertension (PH) in OSAS and to analyze, as far as possible, its mechanisms. Two hundred twenty patients were included on the basis of a polysomnographic diagnosis of OSAS (apnea+hypopnea index > 20). PH, defined by a resting mean pulmonary artery mean pressure (PAP) of at least 20 mm Hg, was observed in 37 of 220 patients (17%). Patients with PH differed from the others with regard to pulmonary volumes (vital capacity [VC], FEV1) and the FEV1/VC ratio that were significantly lower (p < 0.001); PaO2 (64.4 +/- 9.3 vs 74.7 +/- 10.1 mm Hg; p < 0.001); PaCO2 (43.8 +/- 5.4 vs 37.6 +/- 3.9 mm Hg; p < 0.001), apnea+hypopnea index (100 +/- 33 vs 74 +/- 32; p < 0.001), and mean nocturnal arterial oxygen saturation (SaO2) (88 +/- 6% vs 94 +/- 2%; p < 0.001). Patients with PH were also more overweight (p < 0.001). Multiple regression analysis showed that 50% of the variance of PAP could be predicted by an equation including PaCO2 (accounting for 32% of the variance), FEV1 (12%), airway resistance (4%), and mean nocturnal SaO2 (2%). In conclusion, PH is observed, in agreement with previous studies, in less than 20% of OSAS patients. PH is strongly linked to the presence of an obstructive (rather than restrictive) ventilatory pattern, hypoxemia, and hypercapnia, and is generally accounted for by an associated obstructive airways disease. In this regard, the severity of OSAS plays only a minor role.

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.

Flow-volume curve abnormalities and obstructive sleep apnea syndrome.

Recent reports have suggested that flow volume curve abnormalities may be of interest in the diagnosis of obstructive sleep apnea syndromes by showing either extrathoracic airway obstruction (ratio of expiratory flow to inspiratory flow at 50 percent of forced vital capacity [FEF50/FIF50] exceeding 1) or upper airway fluttering (indicated by a sawtooth aspect on the mid-half of the inspiratory part of the curve) or both. In our study, 57 patients referred for a suspected sleep apnea syndrome (SAS) underwent conventional spirometry, assessment of flow-volume curves, ENT examination, and polysomnography. Thirty patients had an obstructive SAS, four patients a central SAS, and 23 patients no SAS. Signs of upper airway fluttering (the sawtooth sign) were present in 61 percent of the patients with obstructive SAS and in 46 percent of the patients without obstructive SAS (central SAS or no SAS). Signs of extrathoracic upper airway obstruction (FEF50/FIF50 greater than 1) were present in 67 percent of the patients with obstructive SAS and in 71 percent of the patients without obstructive SAS. These results suggest that upper airway abnormalities, as reflected by abnormal flow volume curves, are not always associated with obstructive SAS; they favor the hypothesis of a central component in the mechanism of upper airway occlusion during sleep.

Course of pulmonary hemodynamics in patients with chronic obstructive pulmonary disease.

Eighty-five patients with chronic obstructive pulmonary disease, mainly chronic bronchitis (71 patients), who had arterial hypoxemia and moderate to severe obstruction of the airways underwent at least two right cardiac catheterizations in a clinical steady state, with a delay of three years or more between the first and the last catheterization. The average delay was 60 +/- 19 months (range, 36 to 119 months). Patients were regularly examined (quarterly clinical and functional checkups). The changes in pulmonary hemodynamic data were small. In the group of 53 patients with an initial mean pulmonary arterial pressure of 20 mm Hg or less, this pressure varied from 15.4 +/- 3.1 to 18.3 +/- 6.6 mm Hg (P less than 0.001); in the group of 32 patients with an initial mean pulmonary arterial pressure greater than 20 mm Hg, this pressure varied from 27.7 +/- 6.0 to 31.0 +/- 9.3 mm Hg (P less than 0.05). The mean pulmonary arterial pressure increased by 5 mm Hg or more in only 28 patients. In these patients with hemodynamic "worsening," the final arterial oxygen pressure (PaO2) was lower and the final arterial carbon dioxide tension was higher than in the remaining patients. A significant negative correlation (r = -0.39; P less than 0.001) was observed between changes in PaO2 and mean pulmonary arterial pressure. There was a generally good agreement between the course of pulmonary hemodynamics (mean pulmonary arterial pressure), on the one hand, and the clinical, radiologic (transverse diameter of the heart), and electrocardiographic evolution, on the other hand. In the 33 patients who died, a relatively long survival was observed after the first episode of right-sided heart failure or after ascertaining pulmonary hypertension.

Detection of right ventricular pressure overloading by thallium-201 myocardial scintigraphy. Results in 57 patients with chronic respiratory diseases.

The diagnostic value of thallium 201 (201Tl) myocardial imaging was studied in 57 patients with chronic respiratory diseases, most with COPD (n = 46), by comparing the results to hemodynamic findings. In healthy subjects, the right ventricle (RV) is not visualized; therefore, any recorded activity of the RV was considered as indicating RV hypertrophy due to RV pressure overloading (RVPO). RV activity was graded from 0 (no activity) to 3 (activity greater than or equal to that of the left ventricle). Patients were divided into three groups according to the level of the pulmonary artery mean pressure (PPA): PPA less than or equal to 20 mm Hg (no pulmonary arterial hypertension [PAH] ) = group 1, n = 20; PPA ranging from 21 to 30 mm Hg (mild to moderate PAH) = group 2, n = 20; PPA greater than 30 mm Hg (marked PAH) = group 3, n = 17. RV was visualized in 14 patients in group 3 (82 percent) and in 13 patients in group 2 (65 percent). For all patients with PAH (2 + 3) the sensitivity of 201Tl imaging for the diagnosis of RVPO was of 73 percent, higher than that of ECG and echocardiography (both 51 percent). The sensitivity of 201Tl, even if moderate (65 percent) was better than that of ECG (30 percent) or echo (40 percent) in patients with mild-to-moderate PAH (group 2). A high RV activity (grade 3) was observed in only three patients. The specificity of this method (obtained from results in group 1) was of 80 percent vs 89 percent for echo and 100 percent for ECG. These results suggest that 201Tl myocardial imaging is a rather sensitive method and could be of interest for the noninvasive diagnosis of RVPO in COPD patients.

Prognostic factors in COPD patients receiving long-term oxygen therapy. Importance of pulmonary artery pressure.

Prognostic factors in COPD patients receiving long-term oxygen (LTO) therapy were recently analyzed, but very few studies considered the prognostic value of pulmonary artery pressure (PAP) in these patients. We investigated 84 patients who had undergone a right heart catheterization just before the onset of LTO. There were 75 men and 9 women, with a mean age of 63.0 +/- 9.9 (SD) years, at the onset of LTO. When PaO2 was persistently less than 55 mm Hg, LTO was initiated. This therapy was started in some patients with PaO2 in the range of 55 to 60 mm Hg if they had signs of cor pulmonale or a resting PAP of 25 mm Hg or greater at right heart catheterization. The daily duration of LTO was 16 h/d or more. Oxygen flow was adapted to achieve a PaO2 of 65 mm Hg or more. The patients were subdivided into subgroups according to the median value of age (cutoff value = 63 years); vital capacity (2,250 mL); FEV1 (800 mL); residual volume-total lung capacity ratio (58%); PaO2 value (52 mm Hg), PaCO2 level (45 mm Hg); and PAP (25 mm Hg). The cumulative 5-year survival rate was 48% for the group as a whole. Actuarial survival curves were plotted for the two subgroups of patients subdivided according to the initial median value of the variables just listed. There was no significant difference in survival rate between subgroups except when taking into account the level of PAP and age. In patients with an initial PAP of 25 mm Hg or less (n = 44), the 5-year survival was of 62.2 vs 36.3% in the remainder (n = 40) [p < 0.001]. We performed a multivariate analysis of survival using Cox's model of the proportional hazards regression including sex and the variables with the same categorization in the stepwise procedure: PAP and age were the only variables included in the final model. We conclude that the best prognostic factor in COPD patients receiving LTO is not the FEV1, nor the degree of hypoxemia or hypercapnia, but the level of PAP.