Search PubMed⌕ Search

Biomedical subjects

M Galinier

Publications and source records attributed to M Galinier.

At least 73 records · Page 4Linked to original sources
PubMed1994

Relationship between arterial blood pressure disturbances and alpha adrenoceptor density.

To investigate the influence of blood pressure disturbances on human platelet alpha 2-adrenoceptor density, we studied 7 normotensive Parkinsonians with orthostatic hypotension and 23 mild essential hypertensive patients. Plasma catecholamine levels were measured by HPLC and alpha 2-adrenoceptor number and affinity determined by [3H]-yohimbine binding. Alpha-adrenergic reactivity was investigated by blood pressure response to noradrenaline infusion in Parkinsonians and by adrenaline-induced platelet aggregation in hypertensive patients. In Parkinsonians with orthostatic hypotension, in comparison with Parkinsonians without orthostatic hypotension and normotensive control subjects age and sex matched, noradrenaline plasma levels were significantly lower (62 +/- 11, 195 +/- 14 and 219 +/- 13 pg. ml-1 respectively, p < 0.05), platelet alpha 2-adrenoceptor number was significantly higher (313 +/- 52, 168 +/- 9 and 174 +/- 4 fmol.mg-1 protein respectively, p < 0.05) and the noradrenaline dose required for a 25 mm Hg increase of systolic blood pressure significantly lower (0.19 +/- 0.03, 0.86 +/- 0.11 and 0.68 +/- 0.10 microgram.Kg-1 respectively, p < 0.05). In hypertensive patients, in comparison with normotensive control subjects age and sex matched, plasma noradrenaline levels remained unchanged (306 +/- 68 vs 246 +/- 28 pg.ml-1) whereas both platelet alpha 2-adrenoceptor number (137 +/- 15 vs 177 +/- 15 fmol.mg-1 protein, p < 0.05) and velocity of adrenaline-induced platelet aggregation were significantly decreased. These results indicate that platelet alpha 2-adrenoceptor density is related to blood pressure values. In Parkinsonians with orthostatic hypotension, the up-regulation of alpha 2-adrenoceptors was induced by the decrease of endogenous catecholamines. In contrast, in essential hypertension a down-regulation of alpha 2-adrenoceptors was observed in spite of no significant increase of catecholamine levels. These results suggest that only sustained abnormal plasma noradrenaline levels could allow the development of alpha 2-adrenoceptor regulatory mechanisms.

Aged↗
PubMed1994

[Changes in myocardial beta adrenergic receptors in left ventricular hypertrophy caused by barometric and volumetric overloads].

While most prior studies examined late stages of heart failure, we determined initial changes of beta-adrenergic receptors (beta-AR) during left ventricular chronic volume and pressure overload. We investigated right auricular (RA) and left ventricular (LV) beta-AR density (Bmax, fmoles/mg protein) and beta 1-AR percentage in two groups of patients undergoing valve replacement without LV systolic dysfunction (LV ejection fraction > or = 60%), with normal plasma catecholamine levels and echocardiography LV hypertrophy. These results were compared with the values of a control group, composed by 8 patients with mitral stenosis and 5 cardiac transplant donors, and the values of 5 patients undergoing heart transplantation because of end-stage idiopathic dilated cardiomyopathy. These results show that, before alteration of LV systolic function occurs, left ventricular chronic overload induces a selective down-regulation of LV beta 1-AR compensated by an increase in beta 2-AR. These variations may be due to LV hypertrophy induced by volume or pressure overload.

Catecholamines↗
PubMed1994

[Inferior wall myocardial infarction and atrioventricular block; angiography and prognosis].

This study was based on 42 cases of 2nd or 3rd degree atrioventricular block out of 292 cases of inferior wall myocardial infarction. The criteria of selection were monitoring in the intensive care unit during the acute phase, selective coronary angiography in the first 48 hours to 5 days, and regular clinical follow-up during the first year after infarction. The conduction defect was either immediately recorded on the first ECG, delayed (between the 12th and 24th hour) or late (after the 3rd day). These 42 inferior wall infarcts with atrioventricular block (incomplete in 14 and complete in 28 cases) differed from inferior infarction without block by: - the severity of the clinical signs during the acute phase (35% with cardiac failure, 19% with cardiogenic shock); - the severity of the coronary lesions (71.4% with triple vessel disease in infarction with atrioventricular block compared with 32% in those without block, p < 0.02); - the prevalence of the association of > 70% stenosis of the right coronary and left anterior descending arteries; - the alteration of left ventricular function (53% patients with atrioventricular block had ejection fraction of under 30%); - the severity of these infarcts was not related to the atrioventricular block which regressed in 95% of cases but to the severity of the coronary disease, the left ventricular dysfunction and the advanced age of the patients (72.3 +/- 8 years).

Aged↗
PubMed1994

[Prognosis of silent myocardial ischemia].

Asymptomatic or silent myocardial ischemia (SI) is frequent in coronary heart disease and its prognostic value is controversial. The aim of our study is to compare coronary atherosclerosis, left ventricular function and clinical out come of 110 patients with S.I. (A group) and 210 patients with stable angina (B group). The 320 patients were submitted: to symptom limited exercise stress-test with permanent electrocardiographic control by a Case 12-15 digitalized system with ST segment depression interpretation. A test was considered positive for ischemia if there was ST depression of > 1 mv in magnitude from baseline, persisting for 0.08 sec or exercise angina and ischemia: to selective coronarography by Seldinger technic, with left ventricular cineangiography in 2 incidences. A significant coronary stenosis was defined as > 50% reduction of luminal diameter; to medical treatment with betablockers (87.5% of patients), calcium inhibitors (12.5%), aspirin (90%) and nitrates; to regular medical surveillance. During the follow-up (42.4 +/- 5 months in mean) the number of deaths, myocardial infarctions, heart failure, unstable angina and revascularizations were analyzed. Patients of A group with S.I. had a high percentage of risks factors (diabetes mellitus 55%, nicotinism 85%, dyslipidemia 22.5%) and history of previous myocardial infarction in 33% of cases. There are not significant differences between severity and extension of coronary disease, or ventricular dysfunction in patients of A group or B. The percentages of deaths (2.10 versus 3%), acute myocardial infarctions (9.5 versus 8.5%), heart failures (2.72 versus 3%), surgical indications (14.7 versus 15.7%) are not significantly different between the 2 groups. In A group, 34% of patients were treated by angioplasty versus 40% of patients in group B (p < 0.02). S.I. has a bad prognostic and the clinical out come of coronary heart disease is not dependent of presence of angina during exercise testing and daily activities.

Aged↗
PubMed1993

[Beta-adrenergic receptivity and left ventricular hypertrophy caused by pressure overload in man].

The effect of left ventricular chronic pressure overload on right atrial (RA) and left ventricular (LV) myocardial beta-adrenoceptor (beta-AR) density and subtypes ([I125] cyanopindolol binding), adenylate cyclase activity (AC) and ADP-pertussis toxin ribosylated proteins was investigated in 13 patients with aortic stenosis (AO) and compared with the results obtained in 10 patients with mitral stenosis (MI) taken as controls. None of the patients included had any impairement of systolic function or increased plasma catecholamine levels. The total number of beta-AR in RA (62 +/- 6 vs 77 +/- 12 fmoles/mg prot) and LV (39 +/- 7 vs 32 +/- 2 fmoles/mg prot) was similar in AO and in MI. The percentage of beta 1-AR was significantly lower in LV from AO (35 +/- 11 vs 73 +/- 5% in MI) but identical in RA (79 +/- 5 vs 73 +/- 8%). The basal activity of AC was similar in membranes from patients with AO (19 +/- 4 and 22 +/- 5 pmol.mg-1 prot in RA and LV) and in controls (21 +/- 6 and 27 +/- 3 pmol.mg-1 prot in RA and LV). Isoprenaline-induced stimulation of AC was significantly lower in LV membranes from patients with AO (7 +/- 6 vs 45 +/- 6% in MI) but remained identical in RA membranes (51 +/- 18 vs 36 +/- 18% in MI). The quantification of ADP-pertussis toxin ribosylated proteins indicated a lower substrate concentration in myocardial membranes from patients with AO when compared with controls.(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1993

[Therapeutic choices in silent ischemia].

Silent or painless myocardial ischaemia is a common presentation of coronary insufficiency. Repeated episodes lead to anatomical and functional myocardial changes and are associated with the risk of ischemic cardiomyopathy, infarction, arrhythmias and sudden death. The physiopathology is complex and involves transient changes in coronary flow secondary to abnormalities of coronary vasomotricity. It is commonly observed in association with symptomatic angina, in unstable angina and after acute myocardial infarction. In all cases, appropriate treatment is required, the aim being to decrease and suppress not only pain but also ischaemia. Treatment is guided by the ischemic episodes. "Isolated" silent myocardial ischaemia as the only sign of coronary insufficiency justifies accurate evaluation of the coronary status, risk factors and a therapeutic trial, followed by systematic coronary angiography if the ischaemia persists. Silent myocardial ischaemia has modified classical therapeutic attitudes in which the choice of treatment is based on the severity of functional impairment. Priority should now be given to treating the severity of the ischaemia and of the anatomical lesions.

Decision Making↗
PubMed1993

[Action of converting enzyme inhibitors on myocardial ischemia and reperfusion injuries].

During myocardial ischaemia, either in chronic coronary insufficiency or the acute phase of myocardial infarction, the renin-angiotensin system is activated which, by its deleterious cardiac effects, aggravates the ischaemia. Angiotensin Converting Enzyme (ACE) inhibitors, by their indirect effects (improved conditions of left ventricular load, negative inotropism, attenuation of catecholaminergic stimulation), reduce myocardial oxygen consumption, and by their direct coronary vasodilator effect reduce myocardial ischaemia. In addition, by attenuating the formation of oxygen-free radicals, by participating in the inactivation of some of them and protecting the lysosomal membranes, they combat reperfusion injury. In the animal model of acute myocardial infarction, they reduce myocardial infarct size and the prevalence of reperfusion arrhythmias. In the clinical situation, their effects on the ischemic response to effort in anginal patients remain controversial, appear to be more marked in abnormalities of the coronary micro-circulation especially in syndrome X and in hypertensive heart disease. In ischemic heart disease, long-term treatment may be beneficial by their trophic coronary and myocardial effects and two large scale trials report a decrease in the recurrence of myocardial infarction with ACE inhibitors. In the acute phase of myocardial infarction if their possible actions on reducing the infarct size and reperfusion arrhythmias require further confirmation, they do limit expansion of the infarct and decrease early left ventricular dilatation. However, the appreciation of tolerance is variable and the timing of their introduction remains controversial.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed1992

Myocardial hypertrophy, cardiac beta-adrenoceptors and adenylate cyclase activity during sinoaortic denervation in dogs.

1. The long-term effects of sinoaortic denervation on the development of left ventricular hypertrophy (assessed by the measurement of the ratio (R): heart weight/total body weight and LVT: left ventricular thickness), myocardial beta-adrenergic receptivity (measured by [125I]-cyanopindolol binding and adenylate cyclase activity) and plasma catecholamine levels (measured by h.p.l.c.) were investigated in three groups of dogs: normotensive controls (group 1), dogs made hypertensive by sinoaortic denervation and evaluated 1 (group 2) and 18 months (group 3) later. 2. Noradrenaline (NA) and adrenaline (A) plasma levels were 461 +/- 54 and 85 +/- 45 pg ml-1 in controls, 861 +/- 185 and 191 +/- 23 pg ml-1 in group 2 (P less than 0.05). They were normal in group 3 (426 +/- 132 and 110 +/- 16 pg ml-1). 3. R and LVT values were significantly (P less than 0.05) higher in sinoaortic denervated dogs (R = 7.7 +/- 0.1 and 7.8 +/- 0.2; LVT = 13.6 +/- 1.3 and 14.2 +/- 0.9 mm in groups 2 and 3 respectively) than in normotensive dogs (group 1: R = 6.7 +/- 0.1, LVT = 9.3 +/- 0.8 mm). 4. In group 1, the total number of beta-adrenoceptors (Bmax) was 37 +/- 11 and 29 +/- 6 fmol mg-1 protein in the left ventricle (LV) and right auricle (RA) respectively. In group 2, Bmax was significantly lower (10 +/- 3 in LV and 13 +/- 2 fmol mg-1 protein in RA, P less than 0.05) than in group 1. There was no difference between group 1 and group 3 (37 +/- 3 fmol mg-1 prot in LV and 31 +/- 3 fmol mg-1 protein in RA). 5. The percentage of beta 1-adrenoceptors was 82 +/- 4 in LV and 75 +/- 5 in RA in group 1. It was significantly lower (P less than 0.05) in groups 2 (LV: 33 +/- 6 and RA: 33 +/- 5) and 3 (LV: 59 +/- 3 and RA: 55 +/- 4). 6. Basal values of adenylate cyclase activity in LV significantly decreased after sinoaortic denervation.7. These data show that sinoaortic denervation is associated with left ventricular hypertrophy which appears early (1 month) and persists until 18 months despite the normalization of plasma catecholamine levels. The total number of myocardial beta-adrenoceptors is closely related to catecholamine levels but a selective decrease in beta 1-adrenoceptors is observed during cardiac hypertrophy. The fall in basal adenylate cyclase activity suggests that cardiac hypertrophy is associated with an impairment of transmembrane signalling.

Adenylyl Cyclases↗
PubMed1992

[Beta adrenergic receptors and experimental left ventricular hypertrophy].

The effects of sinoaortic denervation (SAD) on the development of left ventricular hypertrophy (R: heart weight/total body weight; LVT : left ventricular thickness), myocardial beta-adrenergic receptivity ([125I]CYP binding; adenylate cyclase activity) and plasma catecholamine levels (HPLC) were investigated in both normotensive (group 1) and hypertensive dogs evaluated (group 2) 1 and 18 months (group 3) after SAD. Noradrenaline (NA) and adrenaline (A) plasma levels were 461 +/- 54 and 85 +/- 45 pg/ml in controls, 861 +/- 185 and 191 +/- 23 pg/ml in group 2 (P < 0.05) and were normal in group 3 (426 +/- 132 and 110 +/- 16 pg/ml). R and LVT values were higher (p < 0.05) in SAD dogs (R = 7.7 +/- 0.1 and 7.8 +/- 0.2; LVT = 13.6 +/- 1.3 and 14.2 +/- 0.9 mm in groups 2 and 3 respectively) than in group 1 (R = 6.7 +/- 0.1, LVT = 9.3 +/- 0.8 mm). In group 1, the total number of beta-adrenoceptors (beta-AR) was 37 +/- 11 and 29 +/- 6 fmol/mg prot in left ventricule (LV) and right auricle (RA) respectively. Bmax was significantly lower in group 2 (LV: 10 +/- 3; RA: 13 +/- 2 fmol/mg prot, p < 0.05) than in group 1 but was normal in group 3 (LV: 37 +/- 3 and RA: 31 +/- 3 fmol/mg prot).(ABSTRACT TRUNCATED AT 250 WORDS)

Adenylyl Cyclases↗
PubMed1992

[Myocardial beta-adrenergic receptors and left ventricular hypertrophy induced by pressure overload in man].

In experimental models, the characteristics of beta-adrenoceptors in left ventricular hypertrophy (LVH) due to pressure overload remain controversial and no data are still available in man. We investigated right auricular (RA) and left ventricular (LV) beta-adrenoceptors characteristics (125 I cyanopindolol binding) in two groups of patients undergoing valve replacement without heart failure (LV ejection fraction > 55%). Height patients with mitral stenosis (mean age: 64 +/- 4 years) and without LVH (LV mass index < 120 g/m2) constituted the control group and 13 patients with aortic stenosis (mean age: 66 +/- 4 years) and LVH (LV mass index > 150 g/m2) the study group. The results are: [table: see text] These results show that, in man, LVH due to pressure overload does not induce variation of total number beta-adrenoceptors, but is associated with a selective decrease in left ventricular beta 1-adrenoceptors.

Aged↗
PubMed1992

[Hypertensive cardiopathy and ventricular late potentials].

Ventricular arrhythmias occur with increased frequency in hypertensive patients with left ventricular hypertrophy (LVH). The aim of this work is to study the incidence of ventricular late potentials (LP) and their relation to ventricular arrhythmias in 148 hypertensive patients, 87 men and 55 women, without evidence of a coronaropathy. For each patient we carried out a signal-averaged electrocardiography, an echocardiogram to determine the LV mass index (LVMI) and the LV end-diastolic dimension (EDD), and 24 hours Holter monitoring to record ventricular arrhythmias filed according to Lown's classification. LP were considered present if the root-mean-square voltage during the last 40 ms of the QRS was: < 20 uV in absence of bundle branch block, or < or = 17 uV in presence of bundle branch block. [table: see text] The frequency of LP appears exceptional in hypertensive patients without LVH (5%) and remains uncommon in patients with concentric LVH (13%). The incidence of LP is only frequent at the end stage of hypertensive cardiopathy with eccentric LVH (48%). The severity of ventricular arrhythmias is only correlated to the presence of LP in patients with concentric LVH (p < 0.02).

Action Potentials↗
PubMed1992

[Ambulatory blood pressure monitoring and left ventricular hypertrophy: correlations and trial of predictive value].

The purpose of the study is to make a selection of patients with left ventricular hypertrophy from Ambulatory Blood Pressure Monitoring (ABPM) values. We studied 39 patients, 23 men and 16 women, without treatment. These patients had systolic pressure > 140 mmHg and/or diastolic pressure > 90. With ABPM we measured mean systolic (MS) and diastolic (MD) pressure during the day (D) and the night (N), the percentages of systolic values (%S) > 160 mmHg and of diastolic values (%D) > 95 mmHg. With echocardiography we measured left ventricular mass index (LVMI: Devereux) and with pulsed Doppler peak of early (E) and late (A) ventricular filling and the ration A/E. We found the same amount of correlations between ABPM and echocardiographic parameters as other authors. [table: see text] The study of LVMI found a difference between groups when MD were > 140/90 (*) and A was significantly greater in patients with MSD > 140 (*). LVMI was greater in patients with MDD > 80 (*) and A was greater in patients with MSN > 120 (*). Predictive value of MSD > 140: 53% specificity: 79%. Predictive value of MSN > 120: 80% specificity: 45.8%. We concluded that the correlations between ABPM and echocardiographic disturbances are not very strong, but significant. If the predictive value of MSF is low, his specificity is rather high and conversely MSN has a good predictive value for selection of hypertrophic patients.

Adult↗
PubMed1991

[Idiopathic chylopericardium. Apropos of a new case. Review of the literature].

The authors report a new case of primary chylopericardium in an asymptomatic 26 year old male. In view of the negativity of the complementary etiological investigations a surgical subxiphoid window was performed and this confirmed the diagnosis. After failure of isolated evacuatory drainage, the patient was cured by pericardectomy. The anatomo-clinical, biochemical and diagnostic features of this condition are described based on a review of the other cases of primary chylopericardium reported in the literature. Surgical pericardectomy seems to be the only effective long term treatment.

Adult↗
PubMed1991

[In which type of hypertension should ventricular hyperexcitability be suspected?].

The aim of the present study was to determine when a search for ventricular arrhythmias, by ambulatory electrocardiographic monitoring, is necessary in hypertensive patients. An electrocardiogram, an echocardiogram and a 24 hour Holter monitoring were recorded in 88 patients with essential hypertension. According to the results of electrocardiogram patients were subdivided into 4 groups: normal electrocardiogram, isolated left auricular hypertrophy (LAH), isolated left ventricular hypertrophy (LVH) and major ST-T wave changes. According to the degree of septal thickness (ST), patients were classed in 4 groups. [table; see text] For hypertensive patients with normal electrocardiogram, Holter monitoring is not necessary; in fact practically no complex arrhythmias is found in this group. On the contrary, for hypertensive subjects with ST-T waves changes, this investigation seems very interesting, nearly 75% of them present high-grade ventricular arrhythmias. For the patients with electrocardiographic isolated LAH or LVH, the realisation of an echocardiography permits to separate the subjects with mild LVH (ST less than 12 mm) where Holter monitoring is not necessary (81% Lown O-I) and the patients with mean or severe LVH (ST greater than or equal to 12 mm) where this investigation seems very interesting, nearly 65% of them present high-grade ventricular arrhythmias.

Adult↗
PubMed1991

[Left ventricular hypertrophy and myocardial ischemia (coronary atherosclerosis excluded)].

The diagnosis of myocardial ischemia due to coronary artery disease in the presence of left ventricular hypertrophy associated with chest pain and ST-T wave changes is difficult. Resting and exercise ST changes are not specific and even stress or dipyridamole Thallium scintigraphy may give erroneous results. In fact, the changes of myocardial perfusion induced by left ventricular hypertrophy reflect a reduction of coronary vasodilator reserve and the increased coronary vascular resistance explains the angina with normal coronary arteries observed in these patients. The reduction of coronary reserve is the result of complex and controversial processes: increased vascular compression, reduction of capillary density: hypertrophy of the arteriolar media or simply changes in coronary vasomotricity. Understanding these abnormalities implies appropriate antihypertensive treatment: lowering the blood pressure, reducing the myocardial hypertrophy and improving subendocardial perfusion.

Cardiomegaly↗
PubMed1991

[Coronary endoprosthesis. Short- and mid-term results].

Mechanical stenting of the coronary wall by an endoprosthesis is a method of treating and preventing the 2 major complications of balloon angioplasty: acute occlusion by dissection and secondary restenosis. Forty-four self expanding stents were implanted in 42 patients presenting with post-angioplasty restenosis (35 cases), stenosis of an aortocoronary bypass graft (4 cases) or symptomatic post-angioplasty coronary dissection (3 cases). The primary results featured a high early occlusion rate of the endoprosthesis (28.5%, 12 cases). Better patient selection to include patients with stable angina and coronary arteries with a diameter greater than 3 millimeters, and the administration of an association of platelet antiaggregant therapy with heparin and oral anticoagulants has led to an improvement in these results. The early occlusion rate in the first 23 patients implanted without these selection criteria was 43% (10 cases) whereas it was only 10.5% (2 cases) in the last 19 selected patients who were prescribed effective medical therapy. The medium term results of the 27 patients implanted without complications at 6 months showed restenosis in 5 cases and reocclusion (asymptomatic) in 1 case (22.2% at control angiography at the 6th month). Restenosis was only observed in cases in which the endoprosthesis did not completely cover the coronary lesion (3 out of 3 cases) or when the endoprosthesis was implanted in a saphenous vein graft (2 out of 4 cases) and the only case of reocclusion occurred on a stent implanted in a coronary artery responsible for previous myocardial infarction. In the 21 patients in whom the stenosis had been totally covered by the stent there were no cases of restenosis.(ABSTRACT TRUNCATED AT 250 WORDS)

Adult↗