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M Galinier

Publications and source records attributed to M Galinier.

At least 19 recordsLinked to original sources
PubMed2007

NMR and cDNA array analysis prior to heart failure reveals an increase of unsaturated lipids, a glutamine/glutamate ratio decrease and a specific transcriptome adaptation in obese rat heart.

Obesity is a risk factor for heart failure through a set of hemodynamic and hormonal adaptations, but its contribution at the molecular level is not clearly known. Therefore, we investigated the kinetic cardiac transcriptome and metabolome in the Spontaneous Hypertensive Heart Failure (SHHF) rat. The SHHF rat is devoid of leptin signaling when homozygous for a mutation of the leptin receptor (ObR) gene. The ObR-/- SHHF rat is obese at 4 months of age and prone to heart failure after 14 months whereas its lean counterpart ObR-/+ is prone to heart failure after 16 months. We used a set of rat pangenomic high-density macroarrays to monitor left ventricle cardiac transcriptome regulation in 4- and 10-month-old, lean and obese animals. Comparative analysis of left ventricle of 4- and 10-month-old lean rat revealed 222 differentially expressed genes while 4- and 10-month-old obese rats showed 293 differentially expressed genes. (1)H NMR analysis of the metabolome of left ventricular extracts displayed a global decrease of metabolites, except for taurine, and lipid concentration. This may be attributed to gene expression regulation and likely increased extracellular mass. The glutamine to glutamate ratio was significantly lower in the obese group. The relative unsaturation of lipids increased in the obese heart; in particular, omega-3 lipid concentration was higher in the 10-month-old obese heart. Overall, several specific kinetic molecular patterns act as a prelude to heart failure in the leptin signaling deficient SHHF obese rat.

Adaptation, Biological↗
PubMed2006

[Cardiac asystole during acute anterior myocardial infarction: a consequence of endocardiac reflexes].

The authors report a case of paroxysmal, complete atrioventricular block during an anterior acute myocardial infarction, leading to asystolia. The different possible physiopathological mechanisms are discussed, suggesting a paroxysmal nodal conduction defect, secondary to transient parasympathetic stimulation, triggered by a Bezold-Jarish type of cardiac reflex. This reflex is frequently involved in various pathologic situations or diagnostic procedures, usual in cardiology. Although it is frequently observed in inferior myocardial infarction, it can occur during an anterior acute myocardial infarction.

Aged↗
PubMed2006

Heart failure with preserved systolic function: a diagnostic algorithm for a pragmatic definition.

Heart failure is a major health problem which often concerns the elderly. Prevalence of heart failure with preserved systolic function is increasing and varies from 40 to 50%. In the literature, and in the large epidemiological studies, it is commonly designed with the term of "diastolic heart failure", even if a precise analysis of diastolic function is not performed. A diagnostic algorithm is proposed in order to better define the concept of heart failure with preserved systolic function. It consists of seven steps from symptoms and clinical signs to the echocardiographic analysis of diastolic function, in order to confirm the definition of heart failure with preserved systolic function.

Algorithms↗
PubMed2005

[Long-term follow-up after primary angioplasty: is stenting beneficial?].

BACKGROUND: Primary stenting leads to a better short-term outcome than balloon angioplasty for acute myocardial infarction in randomised trials. However few data are available about the long-term outcome of primary stenting in acute myocardial infarction (AMI). OBJECTIVES: The aim of this study was to compare the three-year outcome after primary stenting versus balloon angioplasty in patients with acute myocardial infarction. METHODS: We conducted a retrospective study including 157 patients with AMI in a single center. Patients underwent balloon angioplasty (N = 48) or primary stenting (N = 109) within six hours after the onset of chest pain. We looked at the outcome during three years focusing on global mortality, major adverse cardiac events (MACE), reinterventions and target vessel revascularization (TVR). RESULTS: The two groups are similar for their baseline characteristics. No difference was noted for in-patient mortality in the balloon angioplasty group and the primary stenting group (2.1 vs 2.8%; P = ns). The three-year mortality was not significantly different in the two groups. Regarding MACE (27.8 vs 31.7; P = 0.95), reinterventions (20.4 vs 24.7%; P = 0.98) and TVR (18.6 vs 17.8%; P = 0.69), both groups were statistically not different. CONCLUSION: In the long-term patients treated with stent placement have similar rates of MACE, reinterventions or TVR than patients undergoing balloon angioplasty. If few studies noted a benefit in short-term outcomes, primary stenting doesn't improve the prognosis of acute myocardial infarction on long-term follow-up, which is dependent on atherosclerosis.

Adult↗
PubMed2005

Insulin downregulates M(2)-muscarinic receptors in adult rat atrial cardiomyocytes: a link between obesity and cardiovascular complications.

OBJECTIVE: To determine whether decreased cardiac parasympathetic activity observed in obesity is due to insulin-induced alterations in cardiac M(2)-muscarinic receptors and/or adenylyl cyclase activity. DESIGN AND METHODS: After incubation with increasing concentrations of insulin, adult rat atrial cardiomyocytes were assayed for M(2)-muscarinic receptor binding density and affinity, and for M(2)R mRNA expression using RT-PCR analysis. Forskolin-stimulated adenylyl cyclase activity and its inhibition by carbachol were also assayed, as was endothelial nitric oxide synthase mRNA expression. The effects of insulin on M(2)-muscarinic receptor density and mRNA expression levels were analyzed using the insulin signaling inhibitors rapamycin, wortmanin and PD 098059. RESULTS: Insulin induces a concentration- and time-dependent decrease in expression of the M(2)R mRNA, and in [(3)H]N-methylscopolamine binding by the receptor. These effects on the M(2)R mRNA levels and on [(3)H]N-methylscopolamine binding were prevented by PD 98059, but not by wortmanin or rapamycin. Basal and forskolin-induced cAMP production did not differ, but the inhibition of forskolin-simulated enzyme activity by carbachol was blunted by insulin. No change in the mRNA levels for endothelial nitric oxide synthase was observed. CONCLUSION: In rat atrial cardiomyocytes, insulin markedly alters both the M(2)-muscarinic receptor density, and its mRNA expression through transcriptional regulation and adenylyl cyclase activity. These data suggest that the obesity-associated decrease in cardiac parasympathetic tone may be related to hyperinsulinemia, which could directly contribute to cardiovascular morbidity in obese patients.

Adenylyl Cyclases↗
PubMed2005

[Obesity and cardiac failure].

Obesity alone is the cause of 11% of cases of cardiac failure in men and 14% of cases in women in the United States. The frequency of obesity continues to rise in our country, 41% of our compatriots being obese or overweight. It is expected that obesity will become an important cause of cardiac failure in the coming years. The Framingham study showed that, after correction for other risk factors, for every point increase in body mass index, the increase in risk of developing cardiac failure was 5% in men and 7% in women. There are three physiopathological mechanisms to explain the adverse effects of obesity on left ventricular function: an increase in ventricular preload secondary to increased plasma volume induced by the high fatty mass; an increase in left ventricular afterload due to the common association of hypertension generated by activation of the sympathetic nervous system by hyperinsulinism; and systolic and diastolic dysfunction due to changes in the myocardial genome and coronary artery disease induced by risk factors of atherosclerosis aggravated by obesity. The adipocyte also secretes a number of hormones which act directly or indirectly on the myocardium: angiotensin II, leptin, resistin, adrenomedulin, cytokines. These haemodynamic and hormonal changes profoundly modify the genetic expression of the myocardium in obesity, favourising hypertrophy of the myocyte and the development of interstitial fibrosis. Whether it be eccentric in the absence of hypertension or concentric when hypertension is associated with obesity, left ventricular hypertrophy, although normalising left ventricular wall stress, has adverse consequences causing abnormal relaxation and decreased left ventricular compliance. Therefore, in obese patients, two forms of cardiac failure may be observed. The more common is due to diastolic dysfunction, obesity being one of the principal causes of cardiac failure with preserved systolic function. Cardiac failure due to systolic dysfunction is less common and may be observed in cases with inappropriate left ventricular hypertrophy which does not normalise abnormal left ventricular wall stress leading to cardiomyopathy, and in cases with associated coronary artery disease. Whatever the underlying mechanism, the diagnosis of cardiac failure is made more difficult by obesity. From the prognostic point of view, in the global population of patients with cardiac failure, obesity improves survival because it counteracts the adverse effect of cachexia; however, obesity increases the risk of sudden death. In fact, obesity is associated with dynamic change in QT interval. In cases of cardiac failure secondary to obesity-related cardiomyopathy, loss of weight leads to an improved functional status and a reduction of left ventricular remodelling and an increase of the ejection fraction.

Cardiomyopathy, Dilated↗
PubMed2005

[Identification of viable myocardium in ischemic heart disease with severe left ventricular contractile dysfunction: comparison of myocardial scintigraphy with 99mTc-sestamabi and with 201-thallium].

The aim of this study was to compare quantitatively uptake of 99mTc-Sestamibi at rest and that of late redistribution of 201Tl in the same patients with severe ischaemic left ventricular dysfunction, and to correlate the uptake of the tracer to regional ventricular dysfunction studied by ECG grated 99Tc-Sestamini. A double isotope myocardial scintigraphy, 201 Thallium at rest/redistribution and 99Tc-Sestamibi at rest and on exercise, was performed in 28 patients with severe postinfarction ischaemic cardiomyopathy (EF= 29 +/- 4%). Quantitative analysis for each patient and each isotope were performed with respect to the number of hits expressed in percentage of the activity of a normal zone in 17 circumferential profiles distributed in 4 zones, that is to say in 476 segments. A score allowed counting of viable and non-viable segments and evaluation of contractile function of the 17 segments with respect to wall motion and systolic thickening. Total concordance of global uptake of the two isotopes was observed in 430 of the 476 segments (90.3%) (r= 0.814, p< 0.0001), but the 99mTc-Sestamibi uptake was less than 201 Th (71 +/- 23% vs 73 +/- 21%, p= 0.0001). With respect to left ventricular wall motion, uptake of 99mTc-Sestamibi was greater than that of 201Tl in normal or hypokinetic segments but less in akinetic and dyskinetic segments. The difference between the two isotopes was most marked in segments with very severe contractile dysfunction. The authors conclude that the uptake of 99mTc-Sestamibi is correlated with that of late distribution of 201Tl when left ventricular contraction is not too poor and should no longer be considered as only a marker of perfusion but can also be useful in the investigation of myocardial viability.

Aged↗
PubMed2005

[Cardiac cellular therapy: from cells to the first clinical uses].

Despite the improvement in revascularisation techniques, coronary artery disease remains the principal aetiology of cardiac failure in developed countries. The therapeutic management of cardiac failure has been improved over recent years, yet cardiac failure is still associated with significant morbidity and mortality. As cardiac transplantation lacks donors, techniques that allow myocardial regeneration represent an attractive alternative. To date, several types of cells are under study and are suitable for implantation into infarcted myocardium (myoblasts, medullary stem cells...). Following good preclinical study results, the first human cell therapy trials, using the intramyocardial route, have begun, in the course of aorto-coronary bypass surgery in patients with chronic ischaemic cardiopathy and little altered left ventricular function, and then in those with ventricular dysfunction. Different modes of administration of these cell therapy products are under study and could be envisaged in clinical situations such as just after infarction in order to improve ventricular remodelling with an intracoronary injection technique. As for every new treatment, there are numerous problems to resolve, from understanding the relevant mechanisms of cellular transplantation, to the secondary effects that it could entail. Nevertheless, cardiac cellular transplantation is expanding rapidly and with the evolution of techniques it allows a glimpse of a new field of treatment for cardiac failure.

Cell Transplantation↗
PubMed2005

[Prescriptions following acute coronary syndrome].

Each year in France, 150,000 to 180,000 new patients are the subject of prescriptions following acute coronary syndrome with or without ST segment elevation. There are two targets of the treatment, atherosclerosis, a diffuse, evolving trouble which, in this situation, is coming out of an unstable phase, and the myocardium, which has often been revascularised and has suffered deterioration of its contractile and electrophysiological characteristics to a greater or lesser extent. Prescriptions, based on proven factors and always centred on hygiene and dietary advice and the use of a combination of statins and aspirin, are adapted to suit the atherosclerotic and myocardial risk assessed for the individual patient. The prescription starts off the secondary preventive phase. It marks the first stage of the follow up, which is inevitable though of variable duration, for a disease which may evolve. It is the first step in the accompaniment of an attentive, informed patient whose confidence has been restored and who must now avoid falling into the double trap of not taking the treatment sufficiently seriously or of obsessively over-reacting.

Angina, Unstable↗
PubMed2005

[Evaluation of therapeutic strategies for myocardial infarction: the ESTIM Midi-Pyrénées survey].

UNLABELLED: The aim of the ESTIM Midi-Pyrénées survey was to monitor the management of acute coronary syndrome with ST segment elevation by cardiologists and emergency departments in the Midi-Pyrénées region. Over a period of 2 years between June 2001 and June 2003, 1287 patients presenting with acute coronary syndrome within the first 24 hours were recruited prospectively. The initial management of these patients was undertaken either by a mobile medical team in the pre-hospital phase, or in a hospital emergency department, non-interventional cardiology department or an interventional cardiology department in 51.8%, 28.8%, 9.6% et 9.9% of cases respectively. Depending on these four modes of initial management, the median time for initial management was 1h30, 2h45, 4h30 et 4h respectively. Emergency coronary reperfusion was proposed in 89.6% of cases. Of the patients in whom reperfusion was attempted within the first 12 hours, 33.7% underwent pre-hospital thrombolysis (median delay of 1h48), 35.8% underwent thrombolysis in hospital (median delay 3h), and 30.4% underwent primary angioplasty (median delay 4h40). Thrombolysis was followed by angioplasty in 80% of cases. A combined approach with thrombolysis and angioplasty was applied in 41% of patients. At one month the rate of major cardiac events, death, and/or subsequent myocardial infarction was 12%. Multivariate analysis revealed that the only significant adverse prognostic features were: not offering reperfusion [Odds ratio (OR) 4, confidence interval (CI) 2.3-3.7] and age [OR 3.8, CI 2.3-6.2]. The method of reperfusion did not influence the subsequent outcome in this regional survey. CONCLUSION: pre-hospital management allows early revascularisation. In our region there was no significant prognostic difference between pre-hospital thrombolysis and primary angioplasty. It shows that the logistic and therapeutic potentials of prehospital care are not being sufficiently exploited.

Adult↗
PubMed2004

[Prognosis scores to help revascularization for ischemic heart failure].

AIMS: Patients suffering from coronary heart disease with ventricular systolic dysfunction present a bad prognosis and should be potentially revascularized. Up to now, surgery appeared to be the most feasible revascularization technique for such patients. Aims of this study were to assess the influence of different treatments (surgery, angioplasty or exclusively medical treatment) on clinical outcome and to establish a prognostic score practitioners to select the most appropriate therapy adapted to their patient profiles. METHOD: From 1995 to 2000, 492 patients were included in this cohort: 365 in the angioplasty group, 96 in the surgical group and 31 in the medical group. Kaplan Meier curves were made with a multivariate analysis to determine the significant predictive factors of mortality and major adverse cardiac events. RESULTS: After a mean follow-up of 32 +/- 19 months, there was no statistical difference in mortality rate between the groups. However, the survival rate without MACE is higher in the surgical group, intermediate in the angioplasty group and lower in the medical group. Using the significant predictive factors of MACE in multivariate analysis, a prognostic score has been established in order to discriminate three categories of severity. For each category, angioplasty was compared with surgery in terms of the event-free-survival rate. For the two extreme categories (severe and non-severe), both treatments were equal. For the intermediate category, surgery obtained greater results. CONCLUSION: This prognostic score could help physicians in choosing the appropriate revascularization technique to treat patients with severe ischemic heart failure.

Aged↗
PubMed2003

Pre-hospital fibrinolysis followed by angioplasty or primary angioplasty in acute myocardial infarction: the long-term clinical outcome.

BACKGROUND: Randomized trials comparing primary angioplasty and in-hospital fibrinolysis in acute myocardial infarction (AMI) have shown an advantage for primary angioplasty. The long-term follow-up of pre-hospital fibrinolysis followed by elective or rescue coronary angioplasty versus primary angioplasty is not well established after acute myocardial infarction. This study sought to assess the long-term clinical outcome of patients with AMI having either received pre-hospital fibrinolysis optimized by coronary angioplasty or primary angioplasty. METHODS: We conducted a retrospective analysis involving 318 patients who either underwent primary angioplasty ( n = 157) or received pre-hospital fibrinolysis followed by an angioplasty (rescue or elective) ( n = 161) within 6 hours of the onset of chest pain. RESULTS: The groups were similar regarding their baseline characteristics except for the ages. No difference was noted for in-hospital mortality (primary PTCA group: 2.48%, combined group: 2.54%; p = ns) with no increased risk of hemorrhage. The 3-year mortality was not significantly different in the two groups (9.7% vs. 4.9%; p = 0.15). Regarding major adverse cardiac events (29.5% vs. 37.5%; p = 0.23), reintervention (22.5% vs. 23.2%; p = 0.99) or target lesion revascularization (16.1% vs. 14.7%; p = 0.68), the groups were statistically similar. CONCLUSION: These data from real-life practice emphasize the safety and similar benefits on the long-term clinical outcome of AMI patients having undergone either pre-hospital fibrinolysis followed by angioplasty or primary angioplasty.

Aged↗
PubMed2002

[Holter EKG for the hypertensive heart disease].

During chronic mechanical overload induced by hypertension, left ventricular hypertrophy predisposes to atrial and ventricular arrhythmias. Atrial arrhythmias, mainly atrial fibrillation, decrease cardiac output and increase the risk of embolism whereas ventricular arrhythmias remain the major cause of sudden death. In hypertensive patients, Holter EKG recordings frequently detect atrial or ventricular premature beats and more rarely atrial or ventricular tachycardia. In these patients, the presence of non-sustained ventricular tachycardia is considered as an independent predictor of mortality. Moreover, this non invasive method through the assessment of heart rate variability allows the study of the autonomic control of the heart, known to modulate occurrence of arrhythmias.

Atrial Fibrillation↗
PubMed2002

[Prognostic value of the assessment of ischemic status at admission to the coronary care unit after pre-hospital thrombolysis].

The object of this study was to assess and analyse TIMI (Thrombolysis in Myocardial Infarction) grade and secondary major cardiac events of patients with acute myocardial infarction benefiting from pre-hospital thrombolysis according to their predefined clinical and electrical "ischaemic status" (Active, Inactive, Intermediate) on admission to the coronary care unit and at the end of thrombolysis (90th minute). This single centre study was undertaken from March 1994 to August 1999 on 161 patients treated by thrombolysis by the emergency ambulance service for acute myocardial infarction (< or = 6 hours). The mean age was 56.2 +/- 11.3 years with 8.7% of women. On admission to the coronary care unit. 30.8% were classified as Inactive and 51.6% as Active. At the end of thrombolysis, 62.3% were classified as Inactive and 27.7% as Active. Nearly 93% of TIMI 3 flow was observed in Inactive patients at the 90th minute and 76.7% of TIMI < or = 2 flow in Active patients (p < 0.0001). Global hospital mortality was 2.48% but it was zero in the Inactive group at the end of thrombolysis. With an average follow-up of 26.9 +/- 15.8 months, the incidence of major cardiac events was 34.1%, including 16.1% of revascularisation of the target lesion. In multivariate analysis, predictive factors for TIMI < or = 2 at the end of thrombolysis included persistent pain, the number of leads with ST elevation and the absence of regression of ST elevation on admission to the coronary care unit. The only predictive factor for secondary major cardiac events was persistent ST elevation at the 90th minute of thrombolysis.

Aged↗
PubMed2002

[Effects of bradykinin in the cardiovascular effects of angiotensin-converting enzyme inhibitors].

The role of bradykinin in the cardiovascular effects of angiotensin converting enzyme inhibitors remains difficult to establish. On their haemodynamic effects, bradykinin acts during their acute administration, participating in their vasodilatation action, while during their chronic administration they act slightly or not at all. On their trophic effects, the action of the tissue kallikrein-kinin system, suggested by the results of animal experimentation, is yet to be demonstrated in man. For their effects on cardiovascular morbidity and mortality the role of bradykinin remains under discussion. Nevertheless, besides ACE inhibitors, the other therapeutic agents which increase the levels of bradykinin, such as neutral endopeptidase inhibitors, have a significant field of development in the course of cardiovascular pathologies.

Angiotensin-Converting Enzyme Inhibitors↗
PubMed2002

[Revascularization of acute myocardial infarction. Doing better and doing more].

Effectiveness, safety, moderation, complementary, network, consensus, strategy and evaluation are the key words in the therapeutic management of acute myocardial infarction. They focus the development of pharmacological and interventional tools of recanalisation, and the decisions for those who use them. In order to cover a condition for which the patient and doctor alike choose neither time nor place, they lead to linking methods and disciplines together for a united approach. They take account of practice in order to adapt scientific data to the realities of exercise, to justify the given means, and to propose clear, realistic and useful management guidelines to first contact doctors. They deliver the best to the greatest number of patients.

Exercise↗
PubMed2001

[Atherosclerosis--the role of nitric oxide].

ATHEROSCLEROSIS: Currently regarded as a multifactorial disease, atherosclerosis involves several factor including: oxidized LDL, endothelial cells, macrophages, immune cells, vascular smooth muscle cells. The endothelium appears to play a key role through the production of vasomotor, antiaggregate and leukocyte antiadhesion molecules. NITRIC OXIDE: NO is one of the most important mediators of endothelial antiatherothrombotic functions. Loss of endothelial production, called "endothelial dysfunction", i.e. loss of endothelial vasorelaxing, antiaggregate and leukocyte antiadhesion properties, could lead to increased fatty streak formation and acute arterial events (thrombus formation, vascular spasm). ANIMAL EXPERIMENTS: Although animal models strongly suggest a major role for NO in the pathophysiology of atherosclerosis, human studies with nitrates have been disappointing to date. The local effect of NO is probably closely adapted to local conditions. Therefore, massive delivery of NO as is achieved with nitrates could not repair endothelial dysfunction.

Animals↗