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Biomedical subjects

Emmanuel Weitzenblum

Publications and source records attributed to Emmanuel Weitzenblum.

13 recordsLinked to original sources
PubMed2006

Renal hyporesponsiveness to brain natriuretic peptide: both generation and renal activity of cGMP are decreased in patients with pulmonary hypertension.

We examined the mechanisms of renal resistance to atrial and brain natriuretic peptides (ANP and BNP) in pulmonary hypertension (PH). Compared to eight controls, nine PH patients showed a reduced ability to excrete an acute sodium load despite increased circulating ANP, BNP and cyclic guanosine monophosphate (cGMP), their second messenger. Patients' reduced urinary cGMP/BNP and natriuresis/urinary cGMP ratios demonstrated impaired generation of and reduced renal response to cGMP, respectively. Therefore, PH patients hyporesponsiveness to cardiac natriuretic peptides is likely located both upstream and downstream cGMP generation. Natriuretic peptide signalling pathway disruptions might be accessible to therapy.

Adult↗
PubMed2006

Pulmonary arterial hypertension in France: results from a national registry.

RATIONALE: Pulmonary arterial hypertension (PAH) is an orphan disease for which the trend is for management in designated centers with multidisciplinary teams working in a shared-care approach. OBJECTIVE: To describe clinical and hemodynamic parameters and to provide estimates for the prevalence of patients diagnosed for PAH according to a standardized definition. METHODS: The registry was initiated in 17 university hospitals following at least five newly diagnosed patients per year. All consecutive adult (> or = 18 yr) patients seen between October 2002 and October 2003 were to be included. MAIN RESULTS: A total of 674 patients (mean +/- SD age, 50 +/- 15 yr; range, 18-85 yr) were entered in the registry. Idiopathic, familial, anorexigen, connective tissue diseases, congenital heart diseases, portal hypertension, and HIV-associated PAH accounted for 39.2, 3.9, 9.5, 15.3, 11.3, 10.4, and 6.2% of the population, respectively. At diagnosis, 75% of patients were in New York Heart Association functional class III or IV. Six-minute walk test was 329 +/- 109 m. Mean pulmonary artery pressure, cardiac index, and pulmonary vascular resistance index were 55 +/- 15 mm Hg, 2.5 +/- 0.8 L/min/m(2), and 20.5 +/- 10.2 mm Hg/L/min/m(2), respectively. The low estimates of prevalence and incidence of PAH in France were 15.0 cases/million of adult inhabitants and 2.4 cases/million of adult inhabitants/yr. One-year survival was 88% in the incident cohort. CONCLUSIONS: This contemporary registry highlights current practice and shows that PAH is detected late in the course of the disease, with a majority of patients displaying severe functional and hemodynamic compromise.

Adolescent↗
PubMed2005

Reduced pulsatility does not explain renal hyporesponsiveness to cardiac natriuretic peptides in pulmonary hypertension.

A pulsatile secretory pattern is assumed to improve hormonal efficiency. We examined the short-term time courses of circulating atrial (ANP) and brain natriuretic peptides (BNP) in patients with pulmonary hypertension (PH) and reduced renal efficiency of ANP-BNP, reflected by low natriuresis/ANP or BNP ratios. Compared to controls, we observed a persistence of ANP and BNP pulsatility in PH patients with a similar periodicity of 20min. Pulse amplitude increased proportionally to the rise in mean plasma level observed in patients (around 27%). In PH patients, the decrease in ANP-BNP renal efficiency is not attributable to a loss of the rhythmic pulsatility of these hormones.

Cardiac Catheterization↗
PubMed2005

Severe pulmonary hypertension and chronic obstructive pulmonary disease.

RATIONALE: Severe pulmonary hypertension occurs occasionally in patients with chronic obstructive pulmonary disease (COPD), but no detailed description of these patients is available. OBJECTIVES: To identify and characterize patients with COPD and severe pulmonary hypertension. METHODS: 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. RESULTS: 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. CONCLUSIONS: 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.

Aged↗
PubMed2005

Obstructive sleep apnea syndrome and the pulmonary circulation.

The pulmonary hemodynamic consequences of obstructive sleep apneas have been investigated by several groups during the last 30 years. The earlier data have been obtained by measuring the intravascular pulmonary arterial pressure (PAP) and have shown a rise of PAP during apneas, the highest PAP being observed at the end of apneas. Actually, during obstructive apneas the only reliable measurements are those of transmural PAP which increases throughout the apneas, as a consequence of hypoxic vasoconstriction, and decreases after ventilation has resumed. The link between episodic (nighttime) and permanent (daytime) pulmonary hypertension is poorly understood. Recent studies have clearly indicated that daytime hypoxemia, generally due to an associated chronic airflow obstruction, is the major determinant of permanent pulmonary hypertension and cor pulmonale, and that nocturnal hypoxemia is not sufficient per se.

Circadian Rhythm↗
PubMed2004

[COPD: from early symptoms to chronic respiratory failure].

COPD is a frequent and progressive disease, which can lead to severe respiratory impairment. Smoking is the main causal factor. Therefore, respiratory symptoms should not be underestimated in smokers. Chronic cough, chronic sputum, persistent dyspnea on exercise (even for sustained efforts) need further investigations. Each smoker has to be considered as potentially having COPD. Lung function measurements are required in these patients.

Cough↗
PubMed2004

Sleep and chronic obstructive pulmonary disease.

Patients with COPD who are hypoxaemic during wakefulness become more hypoxaemic during sleep. The most severe episodes of nocturnal desaturation generally occur during REM sleep. There is a strong relationship between nocturnal O2 saturation and the level of daytime PaO2: the more pronounced daytime hypoxaemia, the more severe nocturnal hypoxaemia. The worsening of hypoxaemia is due to a variable combination of alveolar hypoventilation and ventilation-perfusion mismatching, alveolar hypoventilation being the predominant mechanism, at least during REM sleep. The consequences of sleep-related hypoxaemia include peaks of pulmonary hypertension due to hypoxic pulmonary vasoconstriction, generally observed in patients with marked daytime hypoxaemia. Cardiac arrhythmias have been described but their clinical relevance has not been established. The prevalence of obstructive sleep apnoea syndrome (OSAS) is not greater in chronic obstructive pulmonary disease (COPD) patients than in the general population, but this association (Overlap Syndrome) is not rare since COPD and OSAS are both frequent diseases. Overlap patients are at a higher risk of developing respiratory insufficiency than are pure OSAS patients. Polysomnography is only indicated in COPD patients who are suspected of having OSAS. The treatment of nocturnal hypoxaemia is conventional O2 therapy (> or = 16/24 h) in COPD patients with marked daytime hypoxaemia (PaO2 < 55-60 mmHg) and conventional O2 therapy plus nocturnal non-invasive ventilation in some patients with marked hypercapnia. At present data are not sufficient for justifying the use of isolated nocturnal oxygen therapy in COPD patients with nocturnal desaturation but with mild daytime hypoxaemia (PaO2 > 60 mmHg).

Arrhythmias, Cardiac↗
PubMed2003

Plasma DNA microsatellite panel as sensitive and tumor-specific marker in lung cancer patients.

The majority of lung cancer patients have tumor-derived genetic alterations in circulating plasma DNA that could be exploited as a diagnostic tool. We used fluorescent microsatellite analysis to detect alterations in plasma and tumor DNA in 34 patients who underwent bronchoscopy for lung cancer, including 11 small cell lung cancer (SCLC) and 23 nonsmall cell lung cancer (NSCLC) (12 adenocarcinomas, 11 squamous cell carcinomas) and 20 controls. Allelotyping was performed with a selected panel of 12 microsatellites from 9 chromosomal regions 3p21, 3p24, 5q, 9p, 9q, 13q, 17p, 17q and 20q. Plasma DNA allelic imbalance (AI) was found in 88% (30 of 34 patients), with a similar sensitivity in SCLC and NSCLC. In the 24 paired available tumor tissues, 83% (20 of 24) presented at least 1 AI. Among these patients, 85% (17 of 20) presented also at least 1 AI in paired plasma DNA, but the location of the allelic alterations in paired plasma and tumor DNA could differ, suggesting the presence of heterogeneous tumor clones. None of the 20 controls displayed plasma or bronchial DNA alteration. A reduced panel of six markers (at 3p, 5q, 9p, 9q) showed a sensitivity of 85%. Moreover, a different panel of microsatellites at 3p and 17p13 in SCLC and at 5q, 9p, 9q and 20q in NSCLC patients could be specifically used. Analysis of plasma DNA using this targeted panel could be a valuable noninvasive test and a useful tool to monitor disease progression without assessing the tumor.

Adenocarcinoma↗
PubMed2003

Evaluation of unattended automated titration to determine therapeutic continuous positive airway pressure in patients with obstructive sleep apnea.

BACKGROUND: Determination of the therapeutic pressure during continuous positive airway pressure (CPAP) therapy is usually performed by a technician during polysomnography. In recent years, several devices for automated adjustment of the therapeutic pressure by the means of computerized algorithms were developed. The aims of the present study were to compare two different devices for automated titration and to verify if unattended automated titration is a feasible strategy to determine the therapeutic CPAP. METHODS: We enrolled 16 consecutive patients with obstructive sleep apnea syndrome (OSAS) defined by an apnea-hypopnea index > 20/h. Automated titration was performed in the hospital using two CPAP devices (Autoset; Resmed; North Ryde, Australia; and Somnosmart; Weinmann; Hamburg, Germany) in random order for 2 consecutive nights, based on different signals for the detection of respiratory events. During titration, there was no direct supervision by a technician, and polysomnography was not recorded. We defined the therapeutic pressure as the 95th percentile of the airway pressure over time (P95). RESULTS: We observed significant differences of the P95 between the two devices, with an average of 7.0 +/- 2.5 cm H(2)O for the Somnosmart and 9.9 +/- 2.6 cm H(2)O for the Autoset (p = 0.005) [mean +/- SD]. There was a considerable lack of agreement between the two devices, with a bias of 3.0 cm H(2)O and limits of agreement ranging from + 9.3 to - 3.2 cm H(2)O. We found no significant correlation between the paired differences of P95 and either indexes of severity of OSAS or lung function variables. CONCLUSION: Automated titration based on the analyses of flow (Autoset) or forced oscillations (Somnosmart) predicted significant different therapeutic pressures for fixed CPAP therapy. Thus, unattended automated titration performed during 1 night of hospital stay with commercially available devices cannot be used to determine accurately the therapeutic CPAP in patients with OSAS.

Automation↗
PubMed2002

Dry powder ipratropium bromide is as safe and effective as metered-dose inhaler formulation: a cumulative dose-response study in chronic obstructive pulmonary disease patients.

A multi-center, open, randomized, 2-way crossover study was conducted with chronic obstructive pulmonary disease (COPD) patients to compare the safety and efficacy of cumulative doses of ipratropium bromide administered from a pressurized metered-dose inhaler (MDI) or from a breath-activated dry powder inhaler (DPI). Enrolled in the study were 39 patients with moderate to severe COPD and who showed a > or= 15% increase in baseline forced expiratory volume in the first second (FEV(1)) after 80 microg of ipratropium bromide. Thirty-six patients were evaluable for efficacy analysis, and 38 patients were included in the safety analysis group. A significant improvement in pulmonary function was observed following inhalation of cumulative doses of ipratropium bromide (from 20 to 320 microg), but no statistically significant difference was found between the 2 formulations. The dose-response curves were similar. There was no statistical difference in area-under-the-curve during the 180 min period after the last dose for any of the pulmonary function variables. Overall, effects on pulse rate, blood pressure, and QT interval on electrocardiogram were no different between the devices. Six mild adverse events occurred in 4 patients: ventricular ectopic beats on electrocardiogram at 270 min with MDI, bad taste with both MDI and DPI, slight transient increase in blood pressure in the same patient during each study day with both MDI and DPI. Two moderate adverse events occurred in 2 patients: transient ventricular ectopic beats on electrocardiograms with DPI at 270 min, moderate bronchospasm with MDI at 200 min. Patients expressed a preference for DPI, which was found to have a better acceptability and appeared to be easier to use than MDI. The new lactose powder formulation of ipratropium bromide inhaled via the breath-activated DPI is a safe and effective alternative to the chlorofluorocarbon-propelled MDI.

Adult↗