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A study of lung volumes offers an overall index of thoracic mobility. The techniques of magnetometry and respiratory plethysmography by induction allow studies of thoracic wall movements to be separated into two compartments by measuring thoracic and abdominal movements. These techniques enable a quantitative evaluation of thoraco-abdominal incoordination seen notably in patients with chronic airflow obstruction and in cases of respiratory muscle fatigue. Similar information is obtained by measuring variations in inspiratory pleural and abdominal pressure, using oesophageal and gastric balloons. The maximal force of respiratory muscles is an important index of the functional reserve at a patient's disposal and may be assessed by measuring maximal inspiratory and expiratory pressures at the mouth against an occlusion. Diaphragmatic force is assessed by the maximal trans-diaphragmatic pressure. Respiratory muscle fatigue appears when their contraction is sustained above a certain threshold of tension and duration. This phenomenon may be detected by a diminution of maximal pressures. For example, the fatigue of inspiratory muscles is accompanied by a fall of maximal inspiratory and trans-diaphragmatic pressures. The fatigue process can also be detected early by changes in the pattern of the diaphragmatic electromyogram. The principles and limitations of different techniques of assessment of respiratory muscle fatigue are analysed. The use of one or several of these techniques accompanied by an awareness of the clinical signs of respiratory muscle fatigue ought to enable an early detection of this condition.
Rev Mal Respir 1986
PMID:[Technics for the functional evaluation of the thoracic cage]. 353 51

The clinical and electrophysiological features and the natural history of median intra-His block with a normal resting electrocardiogram were studied: 11 patients had a fixed split H1-H2 potential with a spontaneous or induced block between H1 and H2. The patients (5 men and 6 women) were aged 17 to 70 years (average 53 years). Associated pathology included 2 cases of aortic stenosis (1 severe), 1 case of ischaemic heart disease (effort angina), 1 case of mitral valve prolapse and 2 cases of hypertension. The presenting symptoms were syncope (4 cases), dizziness (2 cases), effort angina (1 case) and tiredness (3 cases); 1 patient was asymptomatic. Holter monitoring (24 hours) was performed in 8 patients and s-owed paroxysmal conduction defects in 6 cases; 4 Mobitz II 2nd degree AV block, 1 3rd degree AV block with narrow QRS complexes and 1 case of blocked atrial extrasystoles at coupling intervals longer than 480 ms and sinus cycle lengths of over 800 ms. Exercise testing by bicycle ergometry (4 patients) was normal in 1 case and revealed Mobitz II 2nd degree AV block in 3 cases. Baseline electrophysiological studies showed an A-H1 interval ranging from 60 to 100 ms (average 78 ms), a H1-H2 interval of 20 to 40 ms (average 31 ms) and a H2-V interval of 30 to 50 ms (average 32 ms). Block between H1 and H2 was observed: "spontaneously" during electrophysiological investigation in 6 cases, after IV atropine in 1 case, during overdrive atrial pacing at rates slower than 150/min in 7 cases, after atrial extrastimulus with a functional intra-His refractory period of over 420 ms in 7 cases, after ajmaline in 3 of the 4 cases in which this test was performed. A cardiac pacemaker was implanted in 10 patients in whom the initial symptoms have all regressed; the remaining patient considered to be "epileptic" had another syncopal attack under therapy and was finally paced. This series demonstrates that the diagnosis of median intra-His block depends on precise electrophysiological criteria and should be looked for even when the presenting symptoms are atypical; some of our patients complained only of tiredness. The value of Holter monitoring and careful endocavitary investigation is emphasised. Median intra-His block should be distinguished from longitudinal and functional His bundle dissociation.
Arch Mal Coeur Vaiss 1985 Jul
PMID:[Clinical and electrophysiological aspects of median intra-His bundle block with normal electrocardiogram at rest]. 392 29

A controlled multicentre trial was organised to compare the effects of 20 mg Nifedipine tablets (N) and 2,5 mg Indapamide tablets (I) during a 4 months' treatment period after a placebo period, in 59 patients with moderate essential hypertension (n = 59). The results of blood pressure measurements of 18 patients treated by nifedipine (1 tablet twice daily) and 22 patients treated by indapamide (1 tablet every morning) were compared. The systolic blood pressure, after 10 minutes recumbency, fell from 165 +/- 10 mmHg to 148 +/- 13 mmHg (p less than 0.01), and the diastolic pressure from 104 +/- 6 mmHg to 86 +/- 7 mmHg (p less than 0.01) in the patients treated with nifedipine. In the indapamide group, the SBP fell from 164 +/- 13 mmHg to 152 +/- 15 mmHg (p less than 0.01) and the DBP from 100 +/- 4 mmHg to 87 +/- 6 mmHg (p less than 0.01). There were no significant changes of heart rate with either drug; plasma creatinine, potassium and uric acid concentrations were also unchanged. There was a higher incidence of headaches and tiredness in the nifedipine group, whilst patients treated with indapamide complained more often of muscular cramps. Flushing was observed in nearly a quarter of the patients in both groups. These results confirm that both nifedipine and indapamide induce significant and persistant falls in systolic and diastolic blood pressure. Although the fall was greater with nifedipine than with indapamide, the difference was not statistically significant. The tolerance was satisfactory in both groups of patients.(ABSTRACT TRUNCATED AT 250 WORDS)
Arch Mal Coeur Vaiss 1985 Nov
PMID:[Comparative effects of nifedipine and indapamide in the treatment of arterial hypertension]. 393 9

The recent renewed interest in respiratory analeptic action in chronic respiratory failure raises the problem of the site of action and nature of these drugs. They lead to a direct or reflex increase in central nervous activity, which in consequence increases respiratory muscle activity. Indeed, patients with respiratory failure develop pressures two or three times greater than normal subjects to achieve adequate ventilation. During acute exacerbations the pressures generated are five or six times as large. This increase in pressure may risk precipitating fatigue. In general the anomalies of blood gases seem much more related to changes in ventilation-perfusion relationships than to global hypoventilation. Finally, a large increase in the force of muscular contraction may only have a minor effect on ventilation, given the alinear nature of the dynamic compliance curve. An increase of central respiratory activity may thus be ineffective and possibly even dangerous. In the overall assessment of drug considered as an analeptic one always ought to consider the possible non-analeptic actions on the bronchial calibre, the force of the respiratory muscles and the ventilation-perfusion relationships. Thus, it is possible that the therapeutic effects of certain analeptic drugs may be due to actions other than those of respiratory stimulation.
Rev Fr Mal Respir 1981
PMID:[The place of respiratory analeptics in chronic respiratory failure (author's transl)]. 611 48

The acute decompensation of chronic obstructive respiratory failure is characterised by a deterioration of the respiratory mechanics which leads to a reduction of maximum ventilatory output, the respiratory muscles are placed at a mechanical disadvantage and in attempting to compensate are vulnerable to muscle fatigue. A large part of ventilation is wasted in ventilatory dead space. Total ventilation is normal but tidal volume is shallow and respiratory rate rapid. This type of breathing is partially responsible for the large dead space effect. Respiratory centre activity is greatly increased. The prescription of bronchodilators is debatable because there is a risk of increasing the dead space effect. The hypoxic and hypercapnic stimuli have a weak and roughly similar effect on ventilatory control, but the effect of pure oxygen on PaCO2 is due to factors other than those relating to respiratory centre activity.
Rev Fr Mal Respir 1983
PMID:[Physiopathology of acute decompensation in chronic obstructive respiratory insufficiency]. 642 25

Aseptic osteonecrosis is observed in 25% of cases after renal transplantation. This etiological variety of osteonecrosis is unusual in that it is frequently bilateral and has multiple localisations. Apart from the classical radiological signs, attention in attracted by isolated images of osteocondensation in the metaphyses and/or the diaphyses suggesting massive bony infarction and the appearances of fatigue fractures observed frequently (14%). In 43% of cases, the obvious necrosis was proceeded by early bone pain, around the 7 th day, during massive administration of corticosteroids in the prevention or cure of graft resection. This finding suggested to us that the best time to observe ischemia of the bone or marrow is very early and led us to undertake an experimental study in the rabbit. Two series of New Zealand White rabbits were treated with massive doses of corticosteroid and sacrificed between the 3rd and the 21st day. The treated animals presented an early peak of hyperlipemia from the 7th day onwards, and diffuse lesions of hepatic and renal steatosis. Fat emboli associated with appearances of parietal thrombosis were observed in most cases. In the same animals, there were also appearances of stage I or stage II necrosis. Referring to the description of bone marrow necrosis in stages by Arlet and Ficat, there was observed in all the series, a frequency of marrow lesions of all stages much higher in treated animals (16 out of 20) than in controls. Only one lesion of stage I was observed in controls; the difference was highly significant. (0,000001 < p < 0,00001). If one only considers necroses of stage II and III (10/20 in the treated group nil in controls) the frequency was still significant p < 0.001. The preliminary results of the fixation of tetracycline are reported.
Rev Rhum Mal Osteoartic 1980 Dec
PMID:[Cortisone-induced osteonecrosis: knowledge acquired from observations in man and comparison with the results of animal experimentation]. 700 46

The object of therapeutic trials in cardiac failure is to improve the quality of life by controlling the principal symptoms which are dyspnoea and tiredness on effort and to improve survival. A critical review of therapeutic trials in cardiac failure must examine whether these two objectives have been attained and if they are attained simultaneously. In some cases, there is symptomatic improvement but with decreased life expectancy whereas in others, survival is prolonged without adequate control of symptoms. A critical analysis should examine the pertinence of these criteria of efficacy, and confirm that the problem of survival has been assessed, that reliable data has been provided, that the study population is representative of the real population of the patients to be treated, and finally, that the experimental protocol is realistic, i.e. a prospective study with analysis of intention to treat.
Arch Mal Coeur Vaiss 1994 Dec
PMID:[Reading of the trials in cardiac insufficiency; therapeutic studies (phases II B and III)]. 778 38

Chronic eosinophilic pneumonia (CEP) was described by Carrington in 1969. It is twice as common in women as it is in men and is probably most common at middle age. Symptoms usually associated fever, weight loss, fatigue and dyspnoea. Extra-respiratory manifestations are rare but may involve many organs. Classical radiological findings are diffuse alveolar infiltrates, with a peripheral predominance which explains the classic description of a "negative of pulmonary edema". Peripheral blood eosinophilia is present in 90%. The inflammatory syndrome with an eosinophilic alveolitis is constant. Pulmonary function tests show a restrictive pattern with depressed DLCO and hypoxemia. In atypical cases, proof of diagnosis is supported by lung biopsies that show intra alveolar and interstitial accumulation of eosinophils in peripheral air spaces. Areas of bronchiolitis obliterans are also frequently seen. In some atypical forms of chronic eosinophilic pneumonia, other disorders have to be discussed, like bronchiolitis obliterans with an organizing pneumonia or cryptogenetic organizing pneumonia and even tuberculosis. After corticosteroid therapy, the resolution occurs very rapidly but relapses are frequent. Steroid-dependence is seen in 20 to 30% of patients.
Rev Mal Respir 1993
PMID:[Chronic eosinophilic pneumonia or Carrington's disease]. 812 16

The silicone implant controversy wavers between reassuring epidemiological studies and about 300 case reports of patients developing a definite or incomplete/atypical connective tissue disease (CTD) after receiving a silicone gel-filled breast implant (SBI). Since Hashimoto's thyroiditis (HT) is rarely reported in this context, we report here two new cases of HT associated with a history of bilateral cosmetic SBIs. The first patient was a 45-year-old white woman who had SBIs in 1976. In 1991 she developed HT, evolving to thyroid deficiency which was compensated with levothyroxine treatment. In addition, the patient complained of fatigue, arthralgia, morning stiffness and developed a sicca syndrome necessitating artificial tears. The 1995 evaluation disclosed the presence of antinuclear antibodies at a titre of 1/640, and high level anti-thyroid microsomal antibodies (1/256,000). Gamma globulins rose to 22.6%. Thyroid ultrasonography showed an enlarged thyroid gland with a diffusely hypoechogenic pattern. The implants were painful, and in 1996 they were removed. Microscope examination of the fibrous capsule surrounding the prostheses showed extremely dense connective tissue with fibrosis. The second patient was a 55-year-old white woman who had SBIs in 1984. In 1995, she developed HT with clinical pain and tenderness of the thyroid gland, with mild hyperthyroidism and positive antithyroglobulin antibodies, and was given corticosteroid treatment for 5 months. In 1996, the implants were again painful and the patient developed positive antinuclear antibodies with a titre of 1/200. Ultrasonography showed a heterogeneous thyroid gland, and implant removal was advised. Hashimoto's thyroiditis is recognized as a subset of chronic auto-immune thyroiditis, and its association with SBI is rare. In these 2 observations, an association without relation is possible, but a future survey of similar cases seems warranted.
J Mal Vasc 1997 Jul
PMID:[Hashimoto's thyroiditis and silicone breast implants: 2 cases]. 930 36

Results of radiofrequency ablation of the atrioventricular junction on functional capacity and left ventricular systolic function were assessed in 8 patients (aged 68 +/- 12 years) with refractory atrial fibrillation and severe left ventricular dysfunction, the mean ejection fraction being 31 +/- 11% (range: 20-48%). A clinical, echocardiographic and angioscintigraphic follow-up was performed 24 hours (basal), 3 and 6 months after the procedure. During follow-up, all patients reported the disappearance of palpitations and tiredness, a significant and early regression of effort dyspnoea from average NYHA Class 3.4 +/- 0.7 to 2.2 +/- 0.4 (M3), (p < 0.01), a decrease in end diastolic echocardiographic dimensions (from 57 +/- 10 to 52 +/- 9 mm (M3); p < 0.05) resulting in an increase in fractional shortening from 26 +/- 7% to 34 +/- 6%; p < 0.05. The isotopic EF increased from 31 +/- 11% to 42 +/- 12% (M3) (p < 0.01), and attained 48 +/- 12% (M6). This study shows that controlling the frequency and regularity of cardiac rhythm by ablation of the atrioventricular junction in patients with refractory AF and left ventricular dysfunction results in functional and haemodynamic improvement, especially when there is no apparent underlying cardiac disease. This suggests that this method should be proposed in all patients with refractory atrial fibrillation and left ventricular dysfunction.
Arch Mal Coeur Vaiss 1997 Sep
PMID:[Results of radiofrequency ablation of the atrioventricular junction in patients with refractory atrial arrhythmia and severe impairment of the left ventricular systolic function]. 948 72


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