Search PubMed⌕ Search

Biomedical subjects

M Brochier

Publications and source records attributed to M Brochier.

At least 37 records · Page 2Linked to original sources
PubMed1987

[Role of urokinase in the acute phase of myocardial infarction].

The prourokinase-urokinase system physiologically contributes to fibrinolysis activation. It is therefore rational to envisage the use of urokinase in thrombotic diseases, and notably in the acute phase of myocardial infarction (MI) where coronary thrombosis is virtually constant. The main studies on this subject were published in 1975 and in 1985, thus reflecting the changes in therapeutic concepts that have occurred during these 10 years. The older studies concerned patients who were admitted within the first 12 hours of MI and had no early angiographic examination; the results were evaluated indirectly on clinical and enzymatic criteria and on the regression of electrical signs of myocardial suffering. The more recent studies concern patients who are treated at an early stage, often within the first 3 hours of the accident, on the basis of experimental data which favoured early coronary reperfusion as a means of protecting the myocardium; in these studies coronary arteriography is performed immediately after the thrombolytic treatment; computer-assisted studies of the left ventricular function are also carried out, so that the results of thrombolysis are expressed in terms of coronary patency and improvement in segmental kinetics. The results of these different sets of studies have proved to be similar with time. Urokinase, notably when injected intravenously, has a beneficial effect in the acute phase of MI when compared to the conventional treatment. The coronary reperfusion obtained with urokinase is favourable to the myocardium, and the sooner it occurs the better. This benefit is demonstrated by clinical, electrical, enzymatic and angiographic data. Thus, despite its cost, urokinase remains useful in the treatment of MI, notably because it is well tolerated.(ABSTRACT TRUNCATED AT 250 WORDS)

Fibrinolysis↗
PubMed1987

[Primary leiomyosarcoma of the pulmonary artery. Apropos of a case].

A case of leiomyosarcoma of the pulmonary artery in a 64-year old man without previous cardiovascular disease is reported. The clinical picture, which comprised episodes of paroxysmal dyspnoea associated with acute cor pulmonale, suggested pulmonary embolism. Radioisotope perfusion study and pulmonary angiography seemed to confirm this diagnosis, but no improvement was obtained with a prolonged thrombolytic treatment. The presence of a median mass at CT led to exploratory thoracotomy and to the finding of a tumour in the pulmonary artery, which turned out to be a leiomyosarcoma. The disease rapidly took an unfavourable course. Comparison of this case with data from the literature showed that primary tumours of the pulmonary artery are extremely rare, that they are diagnosed with difficulty and often at a late stage and that their prognosis is usually very sombre.

Humans↗
PubMed1987

[Cardiovascular involvement in acromegaly. Apropos of 3 cases].

The authors report 3 cases of acromegaly diagnosed while the patients were in hospital for cardiovascular disease: arterial hypertension in two and hypertrophic myocardiopathy in all three. Coronary arteriography was normal in the 3 patients. The exercise-induced dyspnoea observed in these 3 cases was unexplained by right and left cardiac catheterization results (normal pressures, normal or increased cardiac index). It was most probably related to the myocardial hypertrophy and to abnormalities in diastolic function demonstrated by radioisotopic methods in patients 2 and 3. The degree of myocardial hypertrophy present in these 3 patients seemed to correlate with the size of the pituitary adenoma and the plasma level of growth hormone rather than with the duration or degree of arterial hypertension. After excision of the pituitary adenoma hypertension persisted in 1 case, due to associated adrenal gland hyperplasia, and subsided in the other cases. Abnormalities of diastolic function and dyspnoea are gradually regressing but left ventricular hypertrophy has not significantly decreased after 6 post-operative months.

Acromegaly↗
PubMed1987

[New thrombolytic agents in myocardial infarction].

Fibrinolysis is a physiological process which aims at dissolving intravascular thrombi and is mediated by activation of plasminogen to plasmin. Streptokinase (SK) and urokinase (UK) are non-specific plasminogen activators. They have proved effective as thrombolytic agents, but their use is limited by the risk of haemorrhages due to systemic fibrinogenolysis. More fibrin-specific drugs have recently been developed. One is a tissue plasminogen activator (t-PA), the other is a urokinase precursor (pro-UK), also called single chain urokinase plasminogen activator (scu-PA). Genetic engineering techniques have resulted in the large-scale production of a "recombinant t-PA" (rt-PA) and a "recombinant scu-PA" (r scu-PA) for therapeutic use, notably in acute myocardial infarction. In vitro, these two drugs exhibit a thrombolytic activity that is equal to, or greater than that of SK or UK. In vivo, their fibrinogenolytic effect is less pronounced, and their thrombolytic effect greater than those of SK or UK. "Acyl-enzymes" have more recently emerged. These are inactive acylated SK-plasminogen complexes which progressively become effective in plasma after deacylation. So far, the most extensively studied of these complexes is BRL 26921 (anisoylated plasminogen streptokinase activator complex, or APSAC) which is administered by bolus intravenous injection. It is more thrombolytic than SK but produces systemic fibrinogenolysis to an equivalent degree. Injected intravenously (by infusion or bolus) during the first hours of a coronary infarction these three new thrombolytic agents have proved effective in promoting coronary reperfusion, with an early coronary patency rate of 70-75%.(ABSTRACT TRUNCATED AT 250 WORDS)

Anistreplase↗
PubMed1987

[Diagnosis of primary hyperaldosteronism. Apropos of 3 cases].

Primary hyperaldosteronism (HA1) represent a rare etiology of arterial hypertension (less than 1%). It concerns, most of the time, aldosterone-producing adenomas or bilateral adrenal hyperplasias although intermediate forms have been reported. The diagnosis of HA1 is based on simple examinations, especially systematic measurement of kaliemia in every hypertensive patient with a normal sodium diet before treatment. The elevation of aldosterone blood levels associated with a low plasma renin activity confirms the autonomous nature of the hormonal secretion which is dissociated from the renin-angiotensin system. Study of the ratio aldosterone blood level/ARP and the captopril test are particularly useful in borderline cases. Once the diagnosis of HA1 is made, a topographic analysis may be undertaken; tomodensitometry and adrenal scintigraphy are currently the examinations of choice in the diagnosis of adrenal tumors. Due to biological, morphological and topographic factors, aldosterone-producing adenomas may be identified with a great deal of certainty: surgical excision ensures a cure in a large majority of cases. The treatment of bilateral hyperplasias remains medical.

Adenoma↗
PubMed1987

[Analysis of segmental kinetics of the left ventricle after intravenous administration of urokinase in the acute phase of myocardial infarction].

From 1982 to 1984 included, 31 patients under 70 years of age were admitted during the first three hours of a primary myocardial infarction (MI) and are the subject of a randomized prospective study. 16 patients are treated with 5,000 U of heparin given in intravenous bolus, followed with 150,000 IU of urokinase (UK) in intravenous bolus, then 12,000 IU of UK/min for 90 min or a total dose of 1,230,000 IU. 15 patients are treated with heparin alone (intravenous bolus of 5,000 U). Repeated titrations of creatine phosphokinase (CPK) and the coagulation parameters are performed during the first 24 hours. A coronary angiography with ventriculography (RAO 30 degrees) is performed on the 1st day (D1) and the 3rd week (W3). Study of the left ventricular kinetics (LV) is carried out according to the Stanford method. At D1, the rate of coronary patency is 56 p cent (n = 9) in the UK (A) group and 53 p. cent (n = 8) in the control group B (heparin alone). The percentage of late re-thrombosis is 0 p. cent in group A and 12.5 p. cent in group B (heparin alone). 1 patient died in each group. The CPK peak is less high in case of coronary patency in group A than in case of thrombosis (1,444 +/- 413 vs 1,710 +/- 120 U -heparin alone) and occurs earlier (16 +/- 2 h vs 21 +/- 1 h). In group A a significant decrease of fibrinogen (p. 0.01) as well as plasminogen and alpha-2-antiplasmins (p less than 0.001), is noted. No severe haemorrhagic complications nor sustained rhythm disorders are noted.(ABSTRACT TRUNCATED AT 250 WORDS)

Female↗
PubMed1986

[Therapeutic value of a combination of trimetazidine with a calcium inhibitor in the treatment of chronic coronary insufficiency].

This double-blind, placebo-controlled study sought to examine the short-term benefit of adding 60 mg of trimetazidine to the daily therapeutic regimen of 29 male patients with coronary insufficiency who had persistent ST depression on exercise tolerance test (greater than or equal to 1 mm), despite treatment with nifedipine 40 mg per day. As compared with the placebo group, after only 14 days, the patients treated with trimetazidine showed statistically significant increases in the maximum workload level attained before ST depression occurred (31% versus - 6%; P = 0.009), the total work performed (31% versus 2%; P = 0.024) and a significant decrease in the systolic tension time (double product)/workload ratio (-5% versus +11%; P = 0.005). Throughout the study the clinical acceptability was excellent, with no side effects attributable to trimetazidine being recorded. This study shows that the addition of trimetazidine to a calcium antagonist brings a valuable improvement in therapeutic results.

Chronic Disease↗
PubMed1986

[Regional blood flow in congestive cardiac failure and inhibition of angiotensin converting enzyme].

In congestive cardiac failure myocardial deficiency is accompanied by neurohormonal dysfunction with reflex stimulation of the sympathetic nervous system and the renin-angiotensin-aldosterone system (RAAS). These two systems act synergistically, resulting in peripheral vasoconstriction with increased vascular resistance and therefore greater demand on left ventricular haemodynamics. The role of the RAAS is better understood when angiotensin-converting enzyme inhibitors (ACEI) are used. The vasodilatation produced by these inhibitors mostly affects those vascular beds that depend on the vasopressor effect of angiotensin II, and primarily the renal vascular system: glomerular filtration is improved, and sodium excretion is increased. The RAAS has little influence on the other regional blood flows, so that the administration of ACEI is not followed by cutaneous, muscular or visceral vasodilatation. However, the cerebral blood flow remains normal or even increases despite the fall in systemic arterial pressure, and the coronary output is preserved. Angiotensin-converting enzyme inhibitors produce a strong, though selective, vasodilatation without reflex tachycardia, benefiting primarily the kidneys. The resulting increase in sodium excretion contributes to the long-term effect of ACEI in the treatment of congestive cardiac failure.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1986

[Treatment of acute pulmonary embolism with urokinase compared with the combination plasminogen-urokinase. Apropos of 67 cases].

Sixty-seven patients with recent acute pulmonary embolism (within 5 days) and an angiographic deficit of over 30% were included in a randomised study designed to compare the efficacy of the associations of urokinase-heparin (Group I) and lysyl-plasminogen-urokinase-heparin (Group II). Plasminogen was administered as an intravenous bolus of 150 microkatal units at the beginning of the urokinase infusion, the dosage of which was set at 2 700 000 IU over 24 hours. Both groups received anticoagulant doses of heparin. The efficacy of treatment was judged by early revascularisation on pulmonary angiography performed during the 24 hours after the end of treatment and by changes in the parameters of fibrinolysis and its inhibitors. The clinical features of the two groups were comparable but the angiographic changes were more pronounced in Group I (deficit: 68.5 +/- 10.4% vs 62.3 +/- 10.9%, p less than 0.02). Treatment had to be stopped before the 24th hour in 4 cases (3 early deaths and 1 severe haemorrhage). The average revascularisation was 30.5 +/- 6.8% in Group I and 38.3 +/- 31.1% in Group II (NS). The alpha-2-antiplasmins were lower (NS) in Group II as were the fibrinogen levels (p less than 0.01 at the 12th and 24th hour) whilst the plasminogen levels and surface of fibrin plateaux were higher (p less than 0.01 at the 6th hour and p less than 0.05 at the 12th hour, respectively). These results show that moderate doses of urokinase associated with heparin are effective in the treatment of acute pulmonary embolism.(ABSTRACT TRUNCATED AT 250 WORDS)

Acute Disease↗
PubMed1986

[Bilateral coronary-pulmonary fistula and tritruncal stenotic coronary atheroma. Apropos of a new case with review of the literature].

In a 62 years old patient suffering from stenocardia and paroxysms of atrial fibrillation, coronary angiography disclosed two coronary-pulmonary fistulas associated with a tritruncal stenotic coronary atheroma. During the operation consisting of a double aortocoronary shunt and closing the anomalous pulmonary ostium, a control coronary angiography confirmed the shunt permeability and showed the absence of opacifications at the passage of the fistulas. In the immediate postoperative period the recurrence of paroxysmal atrial fibrillation was no longer accompanied by stenocardia which did not reappear one year after operation. This observation illustrates the fact that coronary-pulmonary fistulas may aggravate a fortuitously associated coronary insufficiency.

Angina Pectoris↗
PubMed1986

[Arteriovenous fistula disclosing a renal cancer. Apropos of a case].

The authors report the case of a 49 year old woman who presented with congestive cardiac failure and hypertension. Clinical examination revealed a high output state and an abdominal mass with a continuous murmur which angiography showed to be a very vascular right renal tumour with a large and early venous return. Catheter studies confirmed the increased cardiac output (cardiac index 5.37 l/mn/m2), an increase in right heart and mean pulmonary capillary pressures (28 mmHg), decreased peripheral arterial resistances and a left-to-right shunt effect at the level of the suprarenal inferior vena cava (+ 3.8 volumes of oxygen per 100 ml). After radical right nephrectomy, the cardiac failure and hypertension regressed and the haemodynamic parameters returned to normal.

Arteriovenous Fistula↗
PubMed1985

[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Apropos of 39 cases].

Episodic mitral regurgitation due to ischaemia of one or both papillary muscles was studied in a review of 39 cases with complementary investigations and compared with previously reported data. The condition occurred after myocardial infarction in 69 p. 100 of cases (usually after inferior infarction: 54 p. 100) associated with ischaemia of the controlateral territory; there was no history of myocardial infarction in 31 p. 100 of cases. The patients were usually elderly (73 years), often hypertensive (77 p. 100) and diabetic (62 p. 100). The clinical syndrome was that of severe anginal pain, mitral regurgitation and left ventricular failure which was critical in some cases. The ECG showed typical ST depression (4.1 +/- 1.6 mm) especially in the antero-lateral leads; left bundle branch block (28 p. 100) with left axis deviation (18 p. 100), sometimes associated with changes of chronic infarction (64 p. 100) was also recorded. Mitral regurgitation and left ventricular failure regressed almost completely in typical cases between attacks, whilst the ECG showed slight residual sub-endocardial ischaemia (ST depression of 1.5 +/- 0.4 mm) in 30 cases and/or subepicardial ischaemia observed in the anterolateral leads in 13 cases. Phonomechanographic recordings (n = 32) showed moderate mitral regurgitation (1-2/6), usually parasystolic (47 p. 100) or early and mid systolic (36 p. 100) in 87.5 p. 100 of cases between attacks, aggravated by handgrip exercise and improved by trinitrin administration. Echocardiography (n = 27) only showed mitral valve changes in 2 patients (increased density of the papillary muscle in 1 case and prolapse of the anterior leaflet in 1 case); however, segmental wall hypokinetic (51 p. 100) or dyskinetic (15 p. 100) motion, was common with increased left ventricular end diastolic dimensions (mean 56.3 +/- 8.0 mm) and decreased fractional shortening (mean 0.30 +/- 0.07) (67 p. 100). Left atrial dimensions were increased (mean 39.7 +/- 6.4 mm) in 52 p. 100 of patients. Thallium 201 myocardial scintigraphy (n = 32) showed hypofixation in 57 (36 p. 100) and a lacuna in 23 (14 p. 100) of the 160 segments analysed. Left ventricular angioscintigraphy (n = 27; 135 segments) showed hypokinesia in 72 segments (53 p. 100); 2.7 segments per patient), akinesia in 19 segments (15 p. 100; 0.7 segment per patient) and dyskinesia in 2 segments (1.5 p. 100); 0.1 segment per patient). The global ejection fraction was 46 +/- 13 p. 100. Coronary angiography (n = 8) showed significant diffuse atherosclerosis.(ABSTRACT TRUNCATED AT 400 WORDS)

Aged↗
PubMed1985

[Paroxysmal mitral insufficiency caused by ischemic dysfunction of the papillary muscles. Hemodynamic and angiographic study of 18 cases. Pathogenic hypotheses].

18 of 39 cases of ischaemic papillary muscle dysfunction reported elsewhere underwent cardiac catheterisation and angiography. Fifteen patients had previous myocardial infarction. The average age of the patients was less than in the overall series (69 vs 73 years) but the incidence of infarction and the degree of cardiac disease were greater. The absence of catheter data in the other patients is explained by their older age (76.4 years) and the longer period of recruitment. Their results and outcome of medical or surgical treatment are reported. The pathogenesis of the syndrome is reconsidered in the perspective of paroxysmal forms. A protocol for investigation is suggested to guide the therapeutic options. Right heart catheterisation at rest (n = 16), on exercise (n = 12), under vasodilator therapy (n = 6) and during angiography (n = 2) does not show a specific profile. These investigations only provide haemodynamic data related to therapy but they are essential for the interpretation of ventriculography. Ventriculography (n = 8) demonstrated 4 cases of mitral regurgitation (2 major and 2 minor), a reduced EF (0.47 +/- 0.17), asynergy of 36.1 p. 100 of segments analysed, predominantly in the inferior and lateral zones. Coronary angiography showed triple vessel disease in 6 cases, double vessel disease in 1 case and 1 stenosis of the left main coronary artery. Stenosis was commonest on the left circumflex (87.5 p. 100) and right coronary arteries (87.5 p. 100) but also frequently involved the left anterior descending artery (75 p. 100). Of the 12 patients treated medically, 8 died (66.6 p. 100) and the survivors remain symptomatic (33.3 p. 100), half with and half without attacks. After surgery (n = 8) comprising coronary bypass surgery (n = 6) or mitral valve replacement (n = 2), patients were asymptomatic. 1 patient died of cancer. These paroxysmal forms of mitral regurgitation may be explained by the association of aggravating, reversible ischaemic or haemodynamic factors to organic mitral lesions. Mitral valve replacement is justified when dysfunction becomes permanent and coronary bypass surgery is advocated whenever possible. The indications for surgery can only be taken into account after complete haemodynamic and angiographic investigation. A protocol for the interpretation of these investigations is suggested.

Aged↗