[Improvement of cardiovascular performance during exertion by beta-blockers in mitral stenosis].
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Biomedical subjects
Publications and source records attributed to M Tartulier.
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Forty-eight patients (25 M, 23 F) age range 25 to 83 years were admitted for treatment of deep vein thrombosis (DVT) of lower limbs confirmed by phlebocavography. Lesions were sural in 6 cases (Gr. 1), subcrural in 28 (Gr. 2) and supracrural in 13 (Gr. 3). Rheoplethysmography with venous occlusion (ORP) was performed and repeated every four months until (possible) recovery of normal emptying parameters (EI). Mean observation period was 25 +/- 8 months. In group 1, ORP indices were always restored to normal values within 4 months. In groups 2 and 3, normal values of IDV were observed in 23/38 patients within a median period of 10 months. Actuarial analysis of changes in EI values showed normalization in 65% of patients within 12 to 16 months with lack of significant differences between values for groups 2 and 3. Beyond this period of time any recovery of normal emptying indices is more aleatory, the residual obstructive syndrome appearing to be established definitely. Antivitamin K therapy (AVK) was instituted in 44 patients, and discontinuation was a function of normalization of EI. Good long-term results (clinical and ORP) were noted in 26/28 cases: one patient had recurrence of DVT with regional extension of thrombus and another a thrombosis on a Mobin-Uddin filter. Restoration of normal EI values during the 16 months following onset of DVT of lower limbs constitutes a valuable index for cessation of AVK therapy. After this period, recovery from the obstructive syndrome is more aleatory and decision to continue therapy must be based on other criteria.
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177 mitral valve replacements with the St Jude Medical prosthesis (SJM) were carried out from March 1979 to December 1983. 45 of these patients (22 men and 23 women) underwent right heart catheterisation 6 or 8 months after surgery. These patients were operated for pure mitral stenosis in 24 cases, mitral regurgitation in 10 cases and mixed mitral disease in 24 cases. There was associated aortic valve disease in 26 patients and valve replacement with a Björk prosthesis was carried out in 19 cases. Tricuspid valvuloplasty was performed in 6 patients. 37 patients were at Stage III or IV of the NYHA classification before surgery; one year later, only 1 patient remained at Stage III, 4 patients were at Stage II and 38 at Stage I. 2 patients died in the first postoperative year of extracardiac causes. Resting pulmonary capillary pressure (Pw) fell from 18 +/- 7 mmHg to 9 +/- 4 mmHg after surgery (p less than 0.001); cardiac index rose from 2.21 +/- 0.45 to 2.59 +/- 0.49 1/min/m2 (p less than 0.001). A capillary arteriolar obstruction observed in 16 patients before surgery was only found in 9 of these patients after surgery. The changes in pulmonary pressures and cardiac output during exercise were studied in 22 patients. Pw rose from 7.6 +/- 1.5 mmHg to 20 +/- 4 mmHg; cardiac index increased from 2.62 +/- 0.19 to 5.46 +/- 0.72 1/min/m2. When compared with theoretical results in a normal subject, pulmonary artery pressures were abnormally high in 13 subjects (59 p. 100), reflecting a stenosing effect of the prosthesis, unmasked by exercise.(ABSTRACT TRUNCATED AT 250 WORDS)
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The differences between lung transfer factor values measured in supine and standing positions were correlated with pulmonary artery pressures in 61 patients with chronic obstructive lung disease and in 34 patients with recurrent pulmonary embolism. No significant correlation was found. The postural change of transfer factor cannot be used as a noninvasive indicator of pulmonary artery pressure in these diseases.
Despite all precautions taken by cardiac surgeons to eliminate air remaining in the cardiac cavities and pulmonary veins at the end of cardiopulmonary bypass, many micro bubbles probably remain and pass into the systemic circulation with a risk of deteriorations of cerebral or myocardial function. Over the last four years we have used ultrasound to try to prevent the risk of preoperative gas microemboli: the machine is equipped with a detector (a quartz oscillator coupled to a piezoelectric transducer emitting a continuous beam of ultrasound at a frequency of 5 Mhz) which allows the following variables to be determined: the time interval from the onset of detection, the total quantity of bubbles (arbitrary units) in the examined regions, the quantity of bubbles detected over a given time interval which can be adjusted from 15 to 120 seconds. The passage of bubbles is also indicated by light and sound alarms. The smallest diameter of bubbles which can be detected is about 10 mu. There are periaortic probes adaptable to the calibre of the ascending aorta, transcutaneous probes for carotid artery detection and a left ventricular probe. In a preliminary series of 74 valve replacements in adults, this apparatus was used immediately after terminating cardiopulmonary bypass after we had thought that the cardiac cavities had been satisfactorily purged of air, and whilst active aspiration was continued in the ascending aorta distal to the periaortic probe: the total quantity of bubbles detected varied from less than 50 to more than 2000 AU, over a variable period of time which may exceed 20 min after termination of cardiopulmonary bypass. The total quantity of bubbles recorded after mitral valve (582 +/- 154 AU) or combined mitral and aortic valve replacement (685 +/- 167 AU) was generally greater than after isolated aortic valve replacement (335 +/- 126 AU). Therefore, after cardiopulmonary bypass, and despite all efforts at purging the air, we showed that numbers of microbubbles were ejected into the ascending aorta for a variable period of time: only some of them were eliminated by active aspiration through a trocar placed distal to the periaortic probe. The right coronary ostium was poorly protected against microbubbles because of its anatomical situation (6 cases in this series). We therefore established a protocol for the use of this apparatus to aid the purging of the cardiac cavities and pulmonary veins before stopping cardiopulmonary bypass: the manoeuvres, guided by the ultrasound probes, are performed before the left ventricle is allowed to eject blood into the ascending aorta.(ABSTRACT TRUNCATED AT 400 WORDS)
Forty six patients aged 25 to 67 years (average : 52 years) underwent measurement of pulmonary arterial pressure (PAP), systemic pressure and cardiac output (Fick) at rest and during exercise in the recumbent position 12 +/- 3 weeks after uncomplicated myocardial infarction; the results were then compared with those of coronary angiography and right anterior oblique monoplane left ventriculography. The site of infarction was anterior in 18 cases and postero-diaphragmatic in 28 cases; it was non-transmural in 4 cases. Twenty patients (43%) had multivessel disease; this was equally common in anterior and inferior wall infarction. Regional wall abnormalities of 3 or more segments were observed in 14 cases. Mean PAP increased from 12,3 +/- 4,6 Torr at rest to 27,8 +/- 10,5 Torr on exercise. In 17 patients (Group A) PAP was normal at rest and during exercise (10 +/- 2 Torr and 18 +/- 3 Torr respectively); 25 patients (Group B) had normal resting PAP (12 +/- 3 Torr) but an abnormal rise on exercise (32 +/- 8 Torr); in 4 patients (Group C) PAP was abnormal at rest (24 +/- 4 Torr) and on exercise (44 +/- 7 Torr). The increase in PAP on exercise was inversely correlated to the ejection fraction (p less than 0.001) and related to the extent of left ventricular hypokinesia (p less than 0.001). Patients in Group A had higher ejection fractions (p less than 0.05), dp/dt/p index (p less than 0.01) and left ventricular compliance (p less than 0.01), lower resting (p less than 0.01) and exercise (p less than 0.05) systemic pressures and small regional wall abnormalities (p less than 0.01) than patients in Group B.(ABSTRACT TRUNCATED AT 250 WORDS)
Recurrent pulmonary embolism sometimes (3% of hospital autopsies) determines a progressive obstruction of the pulmonary vascular bed, which in turn causes pulmonary arterial hypertension and in time right ventricular hypertrophy and failure. The first stages of this process are characterized by slight pulmonary arterial hypertension at rest and by few and deceiving symptoms which make the diagnosis very difficult. Regarding anatomy, in most cases recurrent thromboembolism obstructs one of the main branches of the pulmonary artery. At the beginning pulmonary embolism usually manifests itself in a spontaneous and atypical manner: paroxysmal dyspnea, tachycardia, lateral chest pain, mild hemoptysis and recurrent fever. The clinical signs of peripheral thrombophlebitis are not very frequent. The chest roentgenogram supplies diagnostic information in 20% of cases, the electrocardiogram in 10%. Very important is the contribution of the analysis of arterial blood gases: hyperventilation, moderate hypoxia associated with shunting, hypocapnia with a widened difference between alveolar and arterial CO2. Pulmonary perfusion scintiphotography shows vast unperfused areas, different to the "plexogenic" appearance in primitive pulmonary arterial hypertension, in about 50% of cases. Pulmonary angiography discloses the exact site and extension of the obstruction in 80-90% of cases. On catheterization pulmonary arterial hypertension results to be inconstant and may appear only during stress. Regarding the evolution of pulmonary embolism, the forms associated with pulmonary arterial hypertension may last several years, although recurrent embolism may shorten its course. When the stage of right ventricular hypertrophy is reached, the evolution is generally rapid (from 1 to 4 years).(ABSTRACT TRUNCATED AT 250 WORDS)
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Molsidomine was administered sub-lingually to two groups of five patients. One group had normal left ventricular function and the other had abnormal left ventricular function. Molsidomine was found to induce a decrease in the left ventricular filling pressure and volume and an increase in ventricular distensibility. It helps reduce the pre-load on the ventricle and parietal rigidity. It also reduces systemic blood pressure and resistance as well as the parietal pressure and the total systolic load opposing ejection. It helps reduce the post-load and the metabolic requirements of the myocardium. It does not have any depressant action on the myocardium, even when the ventricular function was initially abnormal. The action of the molecule is apparent between the 20th and the 30th minute and is maximal at the 40th minute, which was the limit of the experiment. The tolerance of the product was excellent in these ten subjects.
Haemodynamic studies were made on 31 patients with labile hypertension at rest and during exercise. Plasma renin activity (PRA) was measured in 8 of them. Five haemodynamic types could be recognised and they could be arranged into two groups. The first was characterised by an increase of calculated peripheral resistance, sometimes permanent, sometimes revealed by effort, sometimes in relation to an increased cardiac output; this would appear to predict the development of permanent hypertension. The second group was characterised by normal systemic resistances, adapted to the cardiac output which was either normal or increased; the significance of labile hypertension in these cases was uncertain; from the haemodynamic studies one was unable to distinguish a transient emotive hypertension from potential permanent hypertension. The PRA was raised in the supine position and greatly increased by an orthostatic posture in the 8 patients tested, suggesting therefore an underlying neuro-adrenergic mechanism. In some patients with labile hypertension the haemodynamic tests were normal at rest and during effort. Others had different responses, which may be the result of varieties of hyper-sympathetic activity, either pure or predominantly beta-adrenergic (increased cardiac output, peripheral resistance adapted to the output) or combined beta and alpha (increased cardiac output with raised peripheral resistance) or mainly alpha-adrenergic (normal cardiac output, increased peripheral resistance).
Plasma renin activity (PRA) was increased and highly sensitive to stimulation in eight cases of labile hypertension (HT), which were also studied haemodynamically. This increase in PRA would appear to result from neuro-adrenergic hyperactivity. The haemodynamic were characterised by a diversity which may be explained on the basis of differentiated sympathetic hyperactivity: exclusive or predominant beta-adrenergic activity causing a hyperkinetic cardiac state with moderate HT adapted to the increased cardiac output; A simultaneous alpha- and beta-adrenergic activity resulting in cardiac hyperkinesis with a relative or potential increase in peripheral resistance; isolated or predominant alpha-adrenergic hyperactivity causing a potential increase in peripheral resistance revealed or increased by effort, in the presence of a normal cardiac output. In certain cases of labile HT however, despite an increased PRA, haemodynamic findings were normal at rest and with effort, at the time of catheterisation.
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