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O Piot

Publications and source records attributed to O Piot.

At least 19 recordsLinked to original sources
PubMed2005

Changes in adsorption and permeability of mitoxantrone on plasma membrane of BCRP/MXR resistant cells.

A selective analysis of adsorbed mitoxantrone (MTX) was performed by surface-enhanced Raman scattering (SERS) at the range of cellular membrane. Disruption of the membrane fluidity was carried out to appraise changes in membrane adsorption of MTX and drug uptake in sensitive (HCT-116 S) and resistant BCRP/MXR (HCT-116 R) cells. Based on spectral MTX modifications, micro-SERS spectroscopy discriminated clearly drug adsorption phenomena on plasma membrane from drug in solution. A 3-fold higher SERS intensity of MTX for HCT-116 R was observed concluding to a higher drug adsorption on resistant membrane. The increase of membrane fluidity with benzyl alcohol (BA) or chloroform (CF) resulted in a 3-fold decrease of MTX adsorption on HCT-116 R, exclusively. BA and CF improved intracellular accumulation of MTX (e.g., 823 and 191 pmol MTX/10(6) HCT-116 R incubated with or without BA). At 4 degrees C, drug accumulation measurements showed a decrease of MTX permeability in resistant membrane (42 pmol MTX/10(6) cells), restored with fluidizers (e.g., 342 pmol MTX/10(6) cells with BA). Fluorescence confocal microscopy involved an exclusive MTX emission around the plasma membrane of resistant cells whereas fluidizers increased the intracellular uptake of MTX in both cell lines at the same time with less drug emission around the plasma membrane. Changes of the membrane structure of resistant cells should modify both drug adsorption and membrane permeation.

ATP Binding Cassette Transporter, Subfamily G, Mem↗
PubMed2004

[The choice of pacing sites: should we change our practice?].

For the past 45 years the sites used for elective pacing have been the apex of the right ventricle and the right atrium. Although the initial objective of pacing was the "simple" correction of a conduction disorder, a more recent evolution has been to achieve a favourable haemodynamic effect, considering left ventricular filling and synchronisation of ventricular contraction as essential. Demonstration of the benefit in terms of survival brought about by pacing in atrioventricular block has not required large trials. However, it is possible that this improvement in morbidity and mortality is in part offset by the altered haemodynamics due to pacing at the right ventricular apex. At the atrial level, the prevention of AF is the holy grail of atrial pacing, but is far from being attained, perhaps because the physiopathological bases are not clear and have not really been demonstrated, casting doubt on the final objective. The choice of pacing site is essential in this context, as much in the atrium as in the ventricle. The current problem regarding this choice is the same as for all medical treatment, where the risk/benefit ratio is evaluated: if the usual sites are potentially deleterious, is it possible to continue using them or is it necessary to change implantation practices, and what level of proof is needed?

Atrial Fibrillation↗
PubMed2003

[External electrical cardioversion of atrial arrhythmia: predictive criteria of success].

AIM: Supraventricular arrhythmia is a major public health problem because of its prevalence and clinical consequences. The first step of the treatment usually consists in restoring sinusal rhythm. The aim of this study is to evaluate results and predictive factors of success of electrical cardioversion. METHODS: We studied a series of 143 consecutive electric cardioversion preformed in 131 French patients. RESULTS: The rate of successful direct current cardioversion was 91.2%. Negative predictive factors are the height body mass index and the age of arrhythmia. Atrial flutter is a predictive factor of success. These results agree with published results. Our study highlights the interest of some nonantiarrhythmic drugs received by the patient during the period before the direct current cardioversion. Thus, a spironolactone treatment appears to be a new predictive factor of the success of electrical cardioversion (success in patients treated with spironolactone: 100% vs 89% without, P = 0.04). CONCLUSIONS: Our results agree with usual predictive factors of the success of cardioversion. Nevertheless, a new approach is that of the positive effect of spironolactone on cardioversion. A prospective randomized study is necessary to confirm this result.

Adult↗
PubMed2003

[Electrophysiologic remodeling and drug treatment of atrial fibrillation].

Since 1995, a number of studies have established and detailed the mechanisms of electrical and structural atrial remodeling induced by atrial fibrillation. Atrial remodeling involves many cellular components, from ionic channels to connexins. The determination of these mechanisms may help to define a new therapeutic targets of atrial fibrillation, a frequent arrhythmia that remains difficult to treat. Atrial remodeling prevention may lead to limit the evolution of the arrhythmia (early recurrences after reduction, AF secondary to atrial tachycardia, permanent AF, decrease in atrial contractility, sinus dysfunction). Except amiodarone, the usual antiarrhythmic drugs have no effect on atrial remodeling. Calcium channel inhibitors prevent early remodeling but have no effect on prolonged remodeling. Digoxin increases remodeling. Angiotensin II receptor inhibitors have been shown to prevent early AF recurrence after reduction and are very promising in such a direction. Other methods such as the one of antioxidant therapy seem to be promising and could define soon a new antiarrhythmic therapeutic class, the antiremodeling drugs.

Atrial Fibrillation↗
PubMed2003

[Predictive criteria of early recurrence of atrial arrhythmia after reduction by electrical cardioversion].

The management of atrial arrhythmias aims not only to restore sinus rhythm but also to maintain it. Ten to thirty per cent of patients have early recurrence of atrial arrhythmias, the treatment of which remains empiric. The aim of this study was to define factors predictive of early recurrence of atrial arrhythmias and the consequences on the length of hospital stay. A series of 131 patients who underwent reduction of atrial arrhythmias by electrical cardioversion was studied retrospectively. A recurrence within 24 hours was observed in 12.2% of the patients. These recurrences significantly increased the length of hospital stay (6.8+/-6.3 versus 3.6+/-3.8 days, p=0.005). This study confirms two previously reported results with respect to more long-term recurrences. In the "early recurrence" group, the duration of the atrial arrhythmia was longer (p=0.003) and there were fewer treatments with amiodarone (p=0.03). In addition, original results were obtained. In the "early recurrence" group, the patients were more often treated with furosemide (p=0.02), class Ic antiarrhythmics (p=0.007) or anaesthetised with thiopental (p=0.002) than patients without early recurrences. Experimental data explain these results. However, they require confirmation by a prospective randomised trial.

Adult↗
PubMed2001

[Arrhythmic cardiomyopathy].

Arrhythmic cardiomyopathy (ACM) is a clinical entity which can be reproduced in experimental models and which corresponds to all myocardial changes induced by chronic tachycardia. It may affect the atria and/or ventricles and, in this case, occur with all types of arrhythmia. Arrhythmia complicating a cardiomyopathy is the differential diagnosis of ventricular ACM. Nevertheless, the potential deleterious haemodynamic changes of any chronic arrhythmia may aggravate pre-existing ventricular dysfunction and, therefore, should always be considered. The development of ACM is usually progressive and depends on the heart rate, but there may also be a myocardial predisposition in certain cases. ACM is an association of haemodynamic, electrophysiological, metabolic and histological changes. Regression, which is the rule, starts in the first days following control of the ventricular rhythm but continues clinically over several months. The physiopathological mechanisms of ACM are multiple and include essentially abnormal cellular calcium concentrations. The treatment is optimally the restoration and maintenance of sinus rhythm, or at least control of the ventricular rate. Because of its curative effects, selective radiofrequency ablation of the arrhythmogenic substrate is the treatment of choice when this is localised. In chronic atrial fibrillation, when sinus rhythm cannot be maintained, the control of the ventricular response at rest and on exercise depends on pharmacological treatment, and, when ineffective, on radiofrequency modification of atrioventricular conduction with optimisation of the pacing mode.

Arrhythmias, Cardiac↗
PubMed2000

Temporal and geographical trends in indications for implantation of cardiac defibrillators in Europe 1993-1998. Medtronic ICD System Investigators.

Despite the demonstrated efficacy of implantable cardioverter defibrillators (ICDs) in reducing sudden and total mortality in selected populations, their implantation rates vary greatly between countries. The aim of our study was to analyze temporal and geographical trends in ICD implantations in countries with similar health related expenditure in Western Europe. A total of 2,257 patients from ten European evaluation studies of Medtronic defibrillators and defibrillation electrodes, conducted between 1993 and 1998, representing 12 countries, was included in this analysis. Rates of implantation and clinical characteristics were compared between countries and years of implantation. Rates of implantation differed greatly between Western European countries and did not correlate with indices of health related expenditure (i.e., number of patients per physician and number of patients per hospital bed). However, there was a strong and statistically significant negative correlation between the use of amiodarone and the rates of implantation (r = -0.66, P = 0.02). Temporal trends showed a significant increase in the age of the patients receiving an ICD between 1993 and 1998 (57 +/- 14 vs 61 +/- 12 years, mean +/- SD, P < 0.001). There was also a temporal trend towards an increased incidence of coronary artery disease and a significant decrease in the incidence of cardiomyopathy. There was a temporal increase in implantations in patients with a history of ventricular tachycardia. Despite a general scientific agreement that ICDs are a first line treatment for patients at high risk of sudden cardiac death, their acceptance remains low in several developed countries. This low acceptance may not be entirely related to budget constraint but may also be related to their perceived efficacy by physicians and health authorities.

Amiodarone↗
PubMed2000

[Electrophysiological remodeling induced by atrial fibrillation. An experimental curiosity or major factor in atrial fibrillation in man?].

Atrial fibrillation usually progresses from a paroxysmal to a permanent arrhythmia, even in the absence of underlying cardiac disease. The treatment is more difficult when the arrhythmia is chronic. This progression may be explained by the aggravation of underlying cardiac disease with time. Another explanation is that the arrhythmia induces functional and structural changes of the atrial tissues (remodelling) which promote the perpetuation of the arrhythmia and which make treatment less effective. Although the electrophysiological changes predisposing to atrial fibrillation have been known for over 15 years, it was only in 1995 that experimental studies showed the presence of atrial electrophysiological remodelling induced by the arrhythmia. This process of long term adaptation of the atrial myocytes to the tachycardia comprises marked changes of the parameters which sustain the arrhythmia: changes in refractory period (decreased duration, inadaptation to the heart rate, increased dispersion), reduced conduction speed and sinus dysfunction. Atrial remodelling also affects the contractile function by the structural changes. The calcium currents play a major role in its development. This mechanism has not yet been completely defined in the clinical setting and its importance in sustaining the arrhythmia has not been clearly evaluated. Atrial fibrillation remains one of the most difficult arrhythmias to treat. A better understanding of cellular mechanisms of remodelling could open up new therapeutic approaches to limit the natural history of the arrhythmia with progression to chronicity and structural changes responsible for the degradation of atrial contractility.

Atrial Fibrillation↗
PubMed2000

[Heart rate and mortality: review of the literature].

A great number of studies focussed on a wide variety of subjects have been concerned with the subject of morbi-mortality and the effect of heart rate. These studies show that there is a connection between high heart rate and arterial hypertension, and a significant coronary, cardiovascular, non-cardiovascular and overall mortality risk. Two explanations are possible for this. The increase in heart rate together with associated sympathetic hyperactivity can be considered a cardiovascular risk factor: or it could be viewed as an independent risk factor, associated with an increase in mechanical constraints.

Cardiovascular Diseases↗
PubMed1999

Blood pressure response to the first 36 hours of heart failure therapy with perindopril versus captopril. French General Hospitals National College of Cardiologists.

An open randomized hospital study conducted in 169 centers in France compared the blood pressure response to the first 36 h of treatment with perindopril (PER), 2 mg once daily, with that to captopril (CAP), 6.25 mg t.i.d., in 725 patients (mean age, 70 years; men, 67%) with echocardiographic left ventricular systolic dysfunction (fractional shortening, < or = 28%) due to ischemia (56.7%) or hypertension (34.5%) and a systolic blood pressure (SBP) > or = 120 mm Hg. Each dose of CAP induced a sharp and rapid decrease in blood pressure (maximum, 1.5-2 h); with PER, the decrease was gradual (maximum, 6 h) and variation was less marked. However, at 36 h, the decrease in blood pressure versus baseline was similar on both treatments. Over the 36-h period, there were 22 (3%) dropouts due to marked orthostatic hypotension (SBP, <90 mm Hg), and they were fewer with PER than with CAP: 16 cases in the CAP group versus six in the PER group (p = 0.036). At 36 h, heart rate was lower with CAP than with PER: 75.2 versus 77.5 beats/min, respectively (p = 0.039). As initial therapy for stabilized left ventricular systolic dysfunction, the first dose of PER (2 mg) induced a significantly smaller decrease in blood pressure than the first dose of CAP (6.25 mg); dropouts due to orthostatic hypotension were also significantly fewer with PER than with CAP.

Aged↗
PubMed1998

Effects of a selective A1-adenosine receptor agonist on heart rate and heart rate variability during permanent atrial fibrillation.

BACKGROUND: Mean heart rate and irregularity of the rate, i.e., heart rate variability (HRV), are two aspects of heart rate during atrial fibrillation (AF). An important goal of AF therapy is to control mean heart rate during exercise; the determinants of HRV during AF remain poorly known although its prognostic value has been established. OBJECTIVES: To investigate the effects of a stable, long-acting, selective A1-adenosine receptor agonist, SDZ WAG994, on heart rate during exercise and on HRV. METHODS: In a multicenter, double-blind, randomized, placebo-controlled, parallel group study, patients with permanent AF performed a symptom-limited exercise test and underwent 24-hour ECG monitoring on day 1 during treatment with placebo, and on day 2 during treatment with either placebo or 2 mg SDZWAG994 orally. Changes in mean heart rate during exercise and changes in HRV indices between day 1 and day 2 were compared between the two groups. RESULTS: Thirty-two patients (64 +/- 8 years; 81% male; 25% in NYHA Class II; 38% with no structural heart disease) were included in the study. During active treatments, heart rate remained unchanged at rest and increased significantly during exercise. A significant daytime increase in short-term HRV indices (DpNN50 = 4.5% P = 0.01; DrMSSD = 6% P = 0.03; DSDNN Index = 6% P = 0.02) occurred during active treatment. CONCLUSIONS: Selective A1-adenosine receptor agonism with SDZ/WAG994 limits the increase in mean heart rate during exercise in patients with AF. In addition, this agonist selectively increases short-term HRV indices, suggesting that pNN50, rMSSD, and SDNN reflect vagal influences during AF.

Adenosine↗
PubMed1998

[Management of arrhythmias in patients with heart failure].

Cardiac failure is a common cause of arrhythmia. Many factors predispose to the genesis of arrhythmias in these patients. A number of non-invasive methods allow stratification of the risk of arrhythmia in cardiac failure. Approximately half the deaths of these patients are due to arrhythmia. Unfortunately, most of the investigations for risk evaluation have a high negative predictive value but a lower positive predictive value. The treatment of supraventricular arrhythmias, mainly atrial fibrillation, is complex in cardiac failure. Class I antiarrhythmics are contraindicated. The only remaining options are Class II, especially Sotalol, and Class III drugs, especially Amiodarone. In some cases, non-pharmacological methods such as ablation, pacing or an implantable atrial defibrillator must be considered. The treatment of ventricular arrhythmias is also difficult. In this indication, Class I antiarrhythmic agents must also be avoided. Non-sustained ventricular tachycardia may be treated by betablockers or amiodarone. The use of an implantable defibrillator is increasingly recommended after the results of several controlled large scale trials. The indication is obvious in patients resuscitated from sudden death and these devices are also beneficial in sustained ventricular tachycardia in patients with cardiac failure. Many studies are currently under way to determine the value of this therapeutic modality in indications now considered to be "prophylactic".

Adrenergic beta-Antagonists↗