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Biomedical subjects

E Weitzenblum

Publications and source records attributed to E Weitzenblum.

At least 73 records · Page 4Linked to original sources
PubMed1996

Pulmonary hypertension in the obstructive sleep apnoea syndrome: prevalence, causes and therapeutic consequences.

"Cor pulmonale" is a classic feature of the "Pickwickian syndrome". Earlier studies have reported a high prevalence of pulmonary hypertension (PH) in obstructive sleep apnoea (OSA) patients, but this has not been confirmed by recent studies with a more adequate methodology, including larger groups of patients. The first part of this review is devoted to the prevalence of PH in OSA; most recent studies agree on prevalence of 15-20%. The second (and major) part of the study deals with the causes and mechanisms of PH in OSA. Pulmonary hypertension is rarely observed in the absence of day-time hypoxaemia, and the severity of nocturnal events (apnoea index (AI), apnoea+ hypopnoea index (AHI) does not appear to be the determining factor of PH. Diurnal arterial blood gas disturbances and PH are most often explained by the presence of severe obesity (obesity-hypoventilation syndrome) and, principally, by association of OSA with chronic obstructive pulmonary disease (the so called "overlap syndrome"). Bronchial obstruction is generally of mild-to-moderate degree and may be asymptomatic. The final part of the review analyses the therapeutic consequences of the presence of PH in OSA patients. Pulmonary hypertension, which is generally mild-to-moderate, does not need a specific treatment. When nasal continuous positive airway pressure (CPAP) fails to correct sleep-related hypoxaemia, supplementary oxygen must be administered. In patients with marked daytime hypoxaemia (arterial oxygen tension (Pa,O2), < or = 7.3 kPa (55 mmHg) conventional O2 therapy (nocturnal + diurnal) is required.

Adult↗
PubMed1996

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.

Adult↗
PubMed1996

[Iatrogenic pulmonary artery hypertension].

Primary pulmonary arterial hypertension (PPH) is a rare disorder with a predilection for young subjects (most commonly of 20-40 years) and of the female sex. The prognosis is very poor because the average life expectancy is of the order of two to three years from the time of diagnosis. Since the epidemic of PPH observed in Switzerland, Austria and Germany in the years between 1968 and 1970, following the arrival of a derivative of amphetamine, Aminorex, it was realised that certain medications, notably appetite suppressants, might play an initiating role. More recently, fenfluramine and dexfenfluramine have been incriminated: in a significant statistic of A-beclere's team, around 20% of cases of PPH were observed in patients who had taken fenfluramine or dexfenfluranime for more than three months. A very recent case-control study has shown that any use of anorexic drugs (mainly fenfluramine derivatives) was associated with an increased risk of PPH (odds ratio: 6/1), and particularly when the duration of treatment exceeds 3 months. Outside the group of appetite suppressants few medications are capable of favouring the development of PPH, the cases are sporadic and the relationship between cause and effect is hardly established.

Appetite Depressants↗
PubMed1995

[Sleep and COPD].

In COPD patients hypoxaemia does worsen during sleep and particularly during REM sleep. However, severe sleep-related O2 desaturation is only observed in patients who exhibit a marked daytime hypoxaemia. Nocturnal desaturation is due to the combination of alveolar hypoventilation and ventilation-perfusion mismatch; alveolar hypoventilation is the predominant mechanism, at least during REM sleep. Sleep-related hypoxaemia leads to peaks of pulmonary hypertension but also to cardiac arrhythmias. Hypoxaemia can be particularly severe when COPD is associated with a sleep apnoea syndrome (this association is rather frequent). A severe nocturnal desaturation needs a treatment with prolonged oxygen therapy, especially if daytime hypoxaemia (PaO2 < 55-60 mmHg) is present. The real benefit from oxygen therapy limited to sleep time in nocturnal desaturators who have not a significant daytime hypoxaemia, has not been yet demonstrated.

Humans↗
PubMed1995

Association of chronic obstructive pulmonary disease and sleep apnea syndrome.

The association of chronic obstructive pulmonary disease (COPD) and sleep apnea syndrome (SAS), which are both frequent diseases, is likely to occur in a number of patients. We have prospectively investigated a large series (n = 265) of patients who were selected solely on the basis of a confirmed diagnosis of SAS (apnea + hypopnea index > 20/hr). An obstructive spirographic pattern, defined by an FEV1/VC ratio < or = 60%, was observed in 30 of 265 patients (11%). These patients (subgroup "overlap") were older (58 +/- 9) versus 53 +/- 10 yr, p = 0.01) than the remainder of the study population, and all were male patients. Body mass index (BMI) was identical in overlap patients to that in the remainder. Vital capacity and FEV1 were lower, by definition, in the overlap group. PaO2 was lower (66 +/- 10 versus 74 +/- 10 mm Hg, p < 0.001) and PaCO2 higher (42 +/- 6 versus 38 +/- 4 mm Hg, p < 0.001) in the overlap group. Hypoxemia (Pao2, < or = 65 mm Hg) was observed in 17 of 30 overlap patients and in 54 of 235 of the remainder. Hypercapnia (Paco2 > or = 45 mm Hg) was observed in 8 of 30 overlap patients and in 19 of 235 of the remainder. The pulmonary artery mean pressure (PAP) was higher in overlap patients both at rest (20 +/- 6 versus 15 +/- 5 mm Hg, p < 0.01) and during steady-state exercise (37 +/- 12 versus 29 +/- 10 mm Hg, p = 0.01).(ABSTRACT TRUNCATED AT 250 WORDS)

Cardiac Catheterization↗
PubMed1995

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.

Actuarial Analysis↗
PubMed1995

Treatment of pulmonary hypertension in patients with chronic obstructive pulmonary disease: position of vasodilators with special focus on urapidil.

Pulmonary hypertension, generally defined by a resting pulmonary artery mean pressure higher than 20 mmHg, is a common complication of advanced chronic obstructive pulmonary disease (COPD). Pulmonary hypertension in COPD is of the "precapillary type" and is almost exclusively accounted for by the increased pulmonary vascular resistance (PVR). Among the factors leading to an increased PVR, acute as well as chronic alveolar hypoxia is by far the most important. Pulmonary hypertension is usually mild (between 20 and 35 mmHg) in COPD patients, but pulmonary artery pressure (PAP) may increase markedly and suddenly during exercise, sleep and episodes of acute respiratory failure. These acute increases of afterload can favour the development of right heart failure. Furthermore, even if the progression of pulmonary hypertension is rather slow (PAP increases by + 0.5 mmHg/year as a mean), the level of PAP is a good indicator of prognosis in COPD patients. Consequently the treatment of pulmonary hypertension is justified in COPD. There are two treatments available so far, which are not mutually exclusive: vasodilators and long-term oxygen therapy (LTOT). LTOT may partly reverse hypoxic pulmonary vasoconstriction but is not always effective in reducing PAP in COPD. Patients with severe and persistent pulmonary hypertension despite oxygen and bronchodilator may be candidates for vasodilator therapy. Numerous vasodilators have been tested, but none has proved entirely satisfactory. Ideally the predominant vasodilator effect would occur in the pulmonary rather than in the systemic vascular bed, and systemic blood pressure should be maintained. The drug should not cause tachycardia and should be well tolerated. At the present time, inhaled nitric oxide (NO) is the only selective pulmonary vasodilator currently available, but NO inhalation is limited by toxicological consideration. Urapidil is known to be an alpha 1-adrenoceptor antagonist and an agonist of central 5HT1A-receptors, and should be considered as a vasodilator. Several studies have already demonstrated that this antihypertensive agent exerts favourable effects on pulmonary and cardiac haemodynamics when administered intravenously or orally to COPD patients with secondary pulmonary hypertension or cor pulmonale. Furthermore in patients with COPD or bronchial hyperreactivity no adverse effect is observed on ventilatory function, bronchial reactivity and gas exchange. Nevertheless, the potential benefit of this vasodilator needs to be confirmed in combination with LTOT by a pragmatic evaluation of its clinical efficacy and safety in COPD patients with secondary pulmonary hypertension.

Antihypertensive Agents↗
PubMed1995

[Obstructive sleep apnea syndrome and cardiovascular diseases].

Obstructive sleep apnoea syndrome is due to pharyngeal obstruction of inspiratory airflow with preservation of thoraco-abdominal respiratory movements. This disease has been described for about thirty years, but is now the subject of growing interest. According to the increasingly abundant literature on this subject, OSAS is associated with essentially cardiovascular morbidity and mortality (systemic hypertension, pulmonary hypertension, heart failure, coronary heart disease, arrhythmias, cerebral vascular accidents and sudden death). The pathophysiology of its underlying mechanisms and its complications is complex and multifactorial. The diagnosis of this syndrome should be suspected on clinical interview (snoring, excessive daytime drowsiness, and apnoea during sleep) and is confirmed by polysomnography. Nasal continuous positive pressure with elimination of aggravating factors is the reference treatment in 1994. The diagnosis and management of this syndrome requires a multidisciplinary approach with collaboration between general practitioners, neurologists, maxillofacial/ENT surgeons, cardiologists and respiratory physicians.

Cardiovascular Diseases↗
PubMed1994

Antitumoral potential of aerosolized interferon-gamma in mice bearing lung metastases.

Cytokines and immune cells are likely to be involved in the control of lung metastasis. We have therefore investigated the possibility of inhibiting lung metastases by the means of interferon-gamma (IFN-gamma) aerosolizations in a murine model of lung cancer. A Lewis lung carcinoma (3LL) was inoculated in the thigh of C57BL/6 mice. Randomized groups of 10 mice each were then treated by repeated aerosols of IFN-gamma (4,000 U/mouse) of aerosols of a Hanks' solution as controls. When the animals were killed at 18 days, the number of lung metastatic nodules was significantly reduced (by 50%; P < 0.01) after IFN-gamma aerosols, compared with controls. When the primary tumor was resected at 18 days and aerosols were continued, in the absence of local recurrence, mice treated by IFN-gamma aerosols survived longer than did controls (P < 0.05). In vitro, IFN-gamma exerted no direct antitumoral effect on 3LL cells in culture. Macrophages recovered from mice receiving IFN-gamma aerosols showed a higher antiproliferative effect on 3LL cells in vitro than did controls. Nevertheless, the higher antiproliferative effect of activated macrophages seems insufficient to explain the difference of survival that we observed between IFN-gamma-treated mice and controls.

Administration, Inhalation↗
PubMed1994

Medical treatment of pulmonary hypertension in chronic lung disease.

In chronic respiratory diseases, especially chronic obstructive pulmonary disease (COPD) pulmonary arterial hypertension is generally mild to moderate and the necessity for treating it can, therefore, be questioned. In fact, pulmonary hypertension, even when modest, may worsen markedly during acute episodes, exercise and sleep. These acute increases in mean pulmonary artery pressure (PAP) could contribute to the development of right heart failure. Therefore, the medical treatment of pulmonary hypertension is justified. There are, at the present time, no selective pulmonary vasodilators, with the exception of inhaled nitric oxide. Indeed, vasodilators appear less effective in COPD compared to primary pulmonary hypertension. Thus, there is, at present, no justification for the long-term use of vasodilators in COPD patients. Long-term oxygen therapy (LTOT) attenuates and sometimes reverses the progression of pulmonary hypertension, although the condition rarely returns to normal. We do not know whether the structural changes of the pulmonary vasculature in COPD patients are potentially reversible with LTOT. The longer the daily duration of LTOT the better are the haemodynamic results. At present, LTOT remains the best treatment for pulmonary hypertension in COPD patient. In the future, treatment of this condition in COPD patients could combine LTOT and specific vasodilators.

Humans↗
PubMed1994

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.

Aged↗
PubMed1994

[Diffuse nodular dissemination of thoracic actinomycosis].

Thoracic actinomycosis is a rare infection but sensitive to penicillin G which is the antibiotic of choice. We report a case of thoracic actinomycosis which was characterised by a relapse, probably linked to antibiotic resistance following treatment with Tetracycline. This relapse presented as diffuse nodular dissemination, of miliary type, of which there are only a few examples in the literature.

Actinomycosis↗
PubMed1994

The pulmonary circulation and the heart in chronic lung disease.

Most studies devoted to the investigation of pulmonary haemodynamics and right ventricular function in chronic lung diseases have concerned patients with chronic obstructive pulmonary disease (COPD). In COPD, pulmonary hypertension is closely linked to the presence of chronic alveolar hypoxia. Pulmonary hypertension is most often mild to moderate (mean pulmonary artery pressure (PAP) in the range 20-35 mmHg) but it may worsen markedly during acute exacerbations of the disease, sleep and exercise. Long-term oxygen therapy is the logical treatment for hypoxic pulmonary hypertension. In time, pulmonary hypertension leads to right ventricular enlargement, which includes right ventricular hypertrophy and dilatation. This is a beneficial adaptation, allowing the right ventricle to cope with an increased afterload and to maintain a normal cardiac output. The right ventricular function, and in particular the right ventricular contractility, are generally preserved in patients with advanced COPD. "True" right ventricular failure can be observed during acute exacerbations of the disease, when worsening of hypoxaemia induces a marked increase in afterload (PAP and pulmonary vascular resistance).

Heart Diseases↗
PubMed1994

[Cystic forms of primary bronchopulmonary cancers. Apropos of a case].

We report a case of primary broncho-pulmonary cancer presenting as a round, fine walled cyst. Based on the observations in this case, and from the data in the literature, we suggest the characteristics of the radiology and scanning which should enable the neoplastic aetiology to be suspected.

Cysts↗