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Biomedical subjects

E Weitzenblum

Publications and source records attributed to E Weitzenblum.

At least 127 records · Page 7Linked to original sources
PubMed1988

[Hypoxia and pulmonary circulation. The importance of hypoxia in pulmonary arterial hypertension of chronic obstructive bronchopneumopathies].

In chronic airflow obstruction (CAO), there are grounds for distinguishing between the effects of acute alveolar hypoxia and those of chronic hypoxia. Acute hypoxia leads, in healthy subjects, to pulmonary vasoconstriction. In patients with CAO, there is however a great variability in the pulmonary vascular response to hypoxia. Chronic hypoxia leads in the long term to structural modifications in the pulmonary vessels (arteriolar muscularization, hypertrophy of the small arterial muscles, and intimal fibrosis), which are similar enough to those seen in residents at high altitude and which lead to an elevation of the pulmonary vascular resistance. These structural changes are potentially reversible but one does not know up to which point they are. This potential reversibility represents one of the justifications of long term oxygen therapy in these patients. The pulmonary arterial hypertension of CAO is generally moderated; it evolves slowly over years and years in the majority of cases; it certainly doesn't merit to be treated at any cost. Up to the present, pulmonary vasodilators have given rather disappointing results. Prolonged oxygen therapy (for greater than 16 hours in 24), which improves in other respects the expectation of life in patients is currently the most logical treatment for pulmonary hypertension in CAO.

Humans↗
PubMed1987

Non-invasive diagnosis of pulmonary hypertension in chronic obstructive pulmonary disease. Comparison of ECG, radiological measurements, echocardiography and myocardial scintigraphy.

The respective value of four non-invasive methods for the diagnosis of pulmonary arterial hypertension (PAH) was investigated in 63 COPD patients, using right heart catheterization as the reference method: 22 patients had no resting PAH (pulmonary artery mean pressure (PAP) less than or equal to 20 mmHg); 26 patients had mild PAH (PAP = 21-30 mmHg); and 15 patients had moderate to severe PAH (PAP greater than 30 mmHg). The specificity of ECG was 86% and the sensitivity 51% (only 38% in mild PAH). The specificity of radiological measurements was 63% and the sensitivity 46% (38% in mild PAH). Echocardiography (echo) had the best results with a specificity of 75% and a sensitivity of 78% (73% in mild PAH), but reliable echo measurements were available in only 52 out of 63 patients. Myocardial scintigraphy had a specificity of 68% and a sensitivity of 66% (58% in mild PAH). A stepwise regression analysis (including one echo, one ECG, one radiological and one functional variable) explained only 43% of the variance of PAP (multiple r = 0.66). These results suggest that no individual method is sufficiently reliable for predicting the presence of PAH, and particularly mild PAH, but the combination of echo + myocardial scintigraphy allows the prediction of PAH with a good probability. The precise level of PAH cannot be estimated, even when using multiple regression equations.

Adult↗
PubMed1987

[M-mode echocardiography in the diagnosis of pulmonary arterial hypertension in chronic respiratory disorders].

Right heart catheterisation (reference method) and M-mode echocardiography were performed in 90 patients with chronic respiratory failure (73 BPCO-chronic airflow obstruction and 17 non-BPCO). The aim of this study was to assess the place of echo-cardiography in the diagnosis and assessment of pulmonary arterial hypertension (HTAP) and/or right ventricular hypertrophy (HVD). The results are somewhat deceptive; first as reliable measurements were impossible in 20% of cases (due to airways distension), then because the sensibility of the method is only 75% (only 62.2% in the group with moderate HTAP with a mean pulmonary artery pressure (PAP) between 21 and 30 mmHg, where as the specificity was satisfactory (87.5%). The best coefficient of linear correlation was observed between the PAP and the end-diastolic diameter of the right ventricle (DTDVD) (r = 0.52; p less than 0.001). Such a correlation does not allow for a prediction of an exact level of PAP in individual cases. The combination of 3 non-invasive methods (ECG, Echo-cardiography and myocardial scintigraphy) allows for an excellent overall sensibility (91.7%) but to the detriment of the specificity (66.6% only).

Adult↗
PubMed1986

Effects on the rabbit carotid body of stimulation by almitrine, natural high altitude, and experimental normobaric hypoxia.

Rabbits were given intraperitoneal injections of almitrine in ascending doses for 5 weeks. They were compared with a control group and with a group of rabbits which had been exposed from birth to the natural hypobaric hypoxia found at Cerro de Pasco (433 m) in the Peruvian Andes. A further group of animals was placed in an experimental normobaric chamber for either 3 or 6 months to subject them to the same degree of hypoxia as that occurring in Cerro. The carotid bodies of the rabbits in all these groups were processed for light and electron microscopy, and examined both qualitatively and quantitatively. The carotid bodies in the group given almitrine showed no changes in their size or in the population of their glomic cells when compared with controls. In contrast, the carotid bodies of Peruvian rabbits were greatly enlarged with a disproportionate increase in the population of the light variant of chief cell. Rabbits from the hypoxic chamber also had enlarged carotid bodies but those killed after 3 months showed an increase in the dark variant of chief cell, whereas after 6 months this cell was reduced in number. There was also intense cytoplasmic vacuolation. Election microscopy confirmed these changes and revealed that dark cells had larger, more pleomorphic granules than the light variant. Vacuolation of the granules in light cells was most pronounced in Peruvian rabbits, but was uncommon in animals exposed to hypoxia for 3 months. We suggest that the dark cell responds to the early stages of hypoxia but later matures into the light variant of chief cell.

Almitrine↗
PubMed1986

Three-month follow-up of arterial blood gas determinations in candidates for long-term oxygen therapy. A multicentric study.

One hundred seventeen patients with severe chronic obstructive pulmonary disease whose PaO2 in a stable clinical state ranged from 41 to 59 mmHg, were included in a multicentric controlled study on the effects of long-term O2 therapy (LTO), and the results of the 3-month probationary period are given here. Arterial blood gases were checked every month in order to assess the stability of hypoxemia. Time 0 represented the beginning and T3 the end of the probationary period. Patients whose PaO2 at T3 was still between 41 and 59 mmHg could be accepted for the long-term study (Group A), whereas patients whose PaO2 had increased over 59 mmHg were excluded (Group B). Only 77 patients could be followed up regularly from T0 to T3 (40 patients were lost to follow-up, missed some visits, or suffered from acute exacerbations of the disease) and 23 of them had a PaO2 at T3 that exceeded 59 mmHg (Group B), allowing the inclusion of 54 patients (Group A) in the long-term study. Patients in Groups A and B did not differ with regard to pulmonary volumes, PaCO2 at T0 or a past history of right heart failure. Arterial O2 tension at T0 was slightly and significantly (p less than 0.02) lower in Group A (51.3 +/- 5.5 mmHg) than in Group B (54.5 +/- 3.8 mmHg), but there was an important overlapping of individual results from one group to another.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗
PubMed1986

Evolution and prognosis of pulmonary hypertension in chronic obstructive pulmonary diseases.

The prognostic value of the presence and degree of pulmonary arterial hypertension (PAH) in chronic obstructive pulmonary diseases (COPD) has been well established by recent studies including the European WHO multicentric study where 591 COPD patients have been included. The level of pulmonary artery mean pressure (PAP) is one of the best predictors of mortality in these patients along with FEV1 and arterial blood gases. The natural history of the course of PAP in COPD was relatively obscure until recent years. The first studies in that field were performed in 1968 but included small numbers of patients. In consideration of the data of three studies published in 1977 to 1979 which concern a relatively homogeneous group of 163 patients with severe COPD, it appears that changes in PAP after an average follow-up period of four years are rather small from 21.4 to 23.6 mm Hg (0.5 to 0.6 mm Hg/year). These results have been confirmed by a very recent study of our group including 93 COPD patients followed-up for five to twelve years (mean = 90 months): the yearly increase in PAP was of only 0.5 mm Hg. Long-term oxygen therapy (LTO) for greater than or equal to 15 h/day rarely normalizes PAP, but can reverse the progression of PAH, particularly in those patients who exhibit a marked worsening of PAH due to a progressive deterioration of arterial blood gases. Very recent studies have clearly indicated that LTO had beneficial hemodynamic effects in a high percentage of COPD patients with PAH.

Exercise Test↗
PubMed1985

Long-term oxygen therapy can reverse the progression of pulmonary hypertension in patients with chronic obstructive pulmonary disease.

Sixteen patients with severe chronic obstructive pulmonary disease (COPD) (average values at the onset of O2 therapy: FEV1, 891 +/- 284 ml; PaO2, 50.2 +/- 6.6 mmHg; PaCO2, 51.0 +/- 6.4 mmHg) underwent 3 consecutive right heart catheterizations. The first was performed 47 +/- 28 months (T0) before the onset of long-term O2 therapy (LTO2). The second was performed just before the onset of LTO2 (T1). The third was performed after 31 +/- 19 months of LTO2 (T2). Oxygen therapy (15 to 18 h/day) was prescribed on the basis of usual criteria. From T0 to T1, PaO2 decreased from 59.3 +/- 9.4 to 50.2 +/- 6.6 mmHg, and mean pulmonary arterial pressure (Ppa) worsened from 23.3 +/- 6.8 to 28.0 +/- 7.4 mmHg (p less than 0.005). From T1 to T2, PaO2 was stable, whereas Ppa decreased from 28.0 +/- 7.4 to 23.9 +/- 6.6 mmHg (p less than 0.05). Pulmonary hypertension improved in 12 of the 16 patients. Before the onset of LTO2 (from T0 to T1), there was a yearly increase in Ppa of 1.47 +/- 2.3 mmHg, whereas during LTO2 a yearly decrease of 2.15 +/- 4.4 mmHg was observed, and the difference between these 2 values was highly significant. The changes in Ppa either from T0 to T1 or from T1 to T2 were not associated with concomitant changes in cardiac output or pulmonary capillary wedge pressure but were related to changes in pulmonary vascular resistance. These results suggest that LTO2 for 15 to 18 h/day can reverse the progression of pulmonary hypertension in a high percentage of patients with severe COPD, but that normalization of Ppa is rarely observed.

Aged↗
PubMed1985

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.

Female↗
PubMed1985

[Sleep and nocturnal desaturation of patients with chronic obstructive bronchopneumopathies. Effects of almitrine bismesylate administered orally].

In order to verify the effect of almitrine bismesylate on episodes of nocturnal oxygen desaturation, 10 patients suffering from chronic obstructive pulmonary disease had polygraphic EEG night sleep recordings with simultaneous measurement of O2 saturation. The subjects presented during nocturnal sleep a quantity of desaturation of at least 2,400 sec. X p. cent (this quantity being represented by the surface of the SaO2 curve under the desaturation level defined as the waking SaO2 less 4 p. cent) and had been included in a matched experimental protocol, double blind, almitrine bismesylate versus placebo. After administration of either placebo or almitrine bismesylate for 14 days (100 mg per day in two doses) a control night sleep recording was performed. The effect of treatment was assessed using an analysis of variance for 2 or 3 factors, completed by a Student t test in case of significant interaction between the factors. It appears that almitrine bismesylate produces: a non significant decrease in total sleep, slow wave sleep and REM sleep time; a significantly earlier awakening (p less than 0.05); a significant reduction of the total duration of desaturation episodes (p less than 0.05) without any correlation with the variations of total sleep time; a non significant decrease in the quantity of desaturation; a significant increase in PaO2 (p less than 0.001) and in SaO2 (p less than 0.01) measured two hours after the awakening. However there was no evidence of any significant change in mean SaO2 and lowest SaO2 during the night. Finally the variability of the effect of almitrine bismesylate during day or night time remains unexplained.

Administration, Oral↗
PubMed1985

[Noninvasive diagnosis of pulmonary arterial hypertension in chronic respiratory insufficiency].

A precise assessment of pulmonary arterial hypertension (HTAP) in chronic lung disorders is not possible without right heart catheterisation. In spite of technological advances (floating catheters with or without balloons) the examination remains invasive, at least to a certain degree, in addition it is not currently practiced in respiratory function laboratories or in services specialising in thoracic medicine. The diagnosis of HTAP is important when considering both the prognosis and the therapeutic approach notably in chronic airflow obstruction (BPCO) and thus the interest in non-invasive diagnostic methods for HTAP. Do current methods offer such a diagnosis? It is this question that the authors endeavour to answer in analysing the possibilities of the principle methods available, from the most standard (eg ECG, chest radiographs) to the most recent (right heart echo-cardiography, myocardial scintigraphy, isotopic measurement of the right heart function). The reference factor is usually the mean pulmonary artery pressure at rest (PAP) supplied by right heart catheterisation. The ideas of sensibility and specificity of a method are defined and the importance of the correlation between the numerical results obtained by a given method and right heart catheterisation is emphasized: only a very strong correlation could assure the possibility of a correct prediction of the level of PAP. Individually no current methods allow such a prediction in a satisfactory manner. Right heart echo-cardiography is "a priori" the most tempting, but it is unfortunately difficult to accomplish in patients with BPCO. Bidimensional echo-cardiography and the Doppler have given very promising results, which need to be confirmed in patients with BPCO. By combining the results of several methods (eg. ECG, radiological measurements, echocardiography) to those of respiratory function (FEV1, PaO2, PaCO2) one can predict in a satisfactory manner the existence (or the absence) of HTAP but not the precise level of the PAP. An approach of this kind may help to limit the indications for right heart catheterisation which remains irreplaceable for the precise knowledge of pulmonary hemodynamic parameters.

Blood Pressure↗
PubMed1984

[Sleep apnea syndromes. Treatment with continuous positive pressure by the nasal route].

Nine patients with severe, predominantly obstructive sleep apnoea syndromes were treated during one night by continuous positive pressure under polygraphic monitoring. Three patients did not tolerate the treatment for either mechanical reasons (2 cases) or ventilatory reasons (1 case). In the remaining 6 patients, continuous positive pressure resulted in reorganization of sleep and disappearance of obstructive and central apnoeic episodes. This effect was incomplete at low pressure (2 cm H2O) and complete at pressures of 6 to 10 cm H2O. The fact that continuous positive pressure was effective against both obstructive and central apnoea suggests that its mode of action is not purely mechanical but involves the central ventilatory control, probably by a reflex mechanism. In view of its effectiveness, continuous positive pressure appears to be the treatment of choice for sleep apnoea syndromes.

Aged↗
PubMed1984

Relationship between pulmonary artery mean pressure and the vertical gradient of perfusion in chronic respiratory diseases.

The relationship between mean pulmonary artery pressure (PPA) and the regional distribution of perfusion, investigated with 133Xe, was studied in 67 patients with chronic respiratory diseases, including 57 patients with chronic obstructive pulmonary disease. The vertical gradient of perfusion, assessed by the ratio upper/lower perfusion (RQ), was considered as normal when RQ was less than or equal to 0.85. Patients were divided into three groups: no pulmonary hypertension, mild hypertension, moderate to severe hypertension. RQ was normal in the majority of patients, even in the group with PPA greater than 30 mm Hg. The average values of RQ did not significantly differ from one group to another. There was no correlation between PPA or pulmonary vascular resistance and RQ. These results suggest that the vertical gradient of perfusion is generally conserved and that the distribution of perfusion cannot provide any reliable prediction of pulmonary hypertension in chronic obstructive pulmonary disease.

Adult↗