Biomedical subjects

C Piot

Publications and source records attributed to C Piot.

At least 19 recordsLinked to original sources

PubMed2006

Myocardial perfusion imaging and cardiac events in a cohort of asymptomatic patients with diabetes living in southern France.

AIMS: To assess the association between abnormal stress myocardial perfusion imaging (MPI) and cardiac events (CE) in asymptomatic patients with diabetes and with > or = 1 additional risk factor. Predictors of abnormal stress MPI were also evaluated. METHODS: Four hundred and forty-seven consecutive patients who underwent stress MPI were prospectively followed for 2.1 [0.5-4.1] years for the subsequent occurrence of hard CE (myocardial infarction and sudden or coronary death) and soft CE (unstable angina and ischaemic heart failure requiring hospitalization). Re-vascularization procedures performed as a result of the screening protocol were not included in the analysis. RESULTS: Follow-up was successful in 419 of 447 patients (94%), of whom 71 had abnormal MPI at baseline. Medical therapy was intensified in all subjects and especially in those with abnormal MPI. Twenty-three patients with abnormal MPI underwent a re-vascularization procedure. CEs occurred in 14 patients, including six of 71 patients (8.5%) with abnormal MPI and eight of 348 patients (2.3%) with normal MPI (P < 0.005). Only two patients developed a hard CE and 12 a soft CE. In multivariate analysis, abnormal MPI was the strongest predictor for CEs [odds ratio (OR) (95% CI) = 5.6 (1.7-18.5)]. Low-density lipoprotein cholesterol > or = 3.35 mmol/l [OR (95% CI) = 7.3; 1.5-34.7] and age > median [OR (95% CI) = 6.0 (1.2-28.6)] were additional independent predictors for CE. The independent predictors for abnormal MPI were male gender, plasma triglycerides > or = 1.70 mmol/l, creatinine clearance < 60 ml/min and HbA1c > 8%, with male gender the strongest [OR (95% CI) = 4.0 (1.8-8.8)]. CONCLUSIONS: Asymptomatic patients with diabetes in this study had a very low hard cardiac event rate over an intermediate period. This could be explained by the effects of intervention or by the low event rate in the background population. Randomized studies of cardiac heart disease screening are required in asymptomatic subjects with diabetes to determine the effectiveness of this intervention.

Aged↗

PubMed2006

[Surgery of ventricular tachycardia in post-infarction left ventricular aneurysm].

The treatment of post-infarction ventricular tachycardias with antiarrhythmic drug therapy, implantable automatic defibrillators, radiofrequency ablation, also includes different surgical procedures such as endocardial resection of the infarct scar, encircling endocardial ventriculotomy and endocardial cryoablation or thermoexclusion by laser. These procedures may be extensive or limited, guided or not by preoperative mapping. The aim of this review of the literature is to update our knowledge of these different surgical techniques and to define their indications.

Cryosurgery↗

PubMed2004

[Does symptomatic stable coronary artery disease still exist in France?].

In spite of the continuous growth of myocardial revascularisation techniques, stable angina remains an important clinical burden. In France, and based upon estimates from the European Society of Cardiology and from diverse epidemiological sources, 2 million people are likely to have stable angina. Though primary and secondary prevention are improving, this figure is likely to increase further, in particular because of the constant aging of the population (20% of patients more than 80 years of age have angina), but also because of the epidemics proportions that diabetes mellitus and obesity take.

Adolescent↗

PubMed2003

[Mechanisms of action of antiarrhythmics in cardioversion of atrial fibrillation and atrial flutter].

The mechanisms of action of antiarrhythmic drugs at atrial level are multiple. Antiarrhythmics may act at three levels in the prevention of paroxysmal atrial fibrillation: on the arrhythmogenic atrial substrate, the initiating extrasystoles including those of the pulmonary veins, and in the modulation of the autonomic nervous system. However, there are many modes of initiation which are not well understood so that the preventive role of the antiarrhythmic drugs remains imprecise. Cardioversion of persistent atrial fibrillation has been better analysed in healthy hearts: Class I antiarrhythmics in particular, despite their depressive effects on the conduction which are potentially arrhythmogenic, are beneficial by decreasing the number of reentry circuits, prolonging the atrial refractory period on short cycles and, paradoxically, by increasing the period of excitability in AF. All have a preferential action on anisotropic conduction, especially at the pivotal point of reentry. On the other hand, their role in electrophysiological remodelling in the prevention of immediate recurrences and in pathological atria, remains poorly understood. As for atrial flutter, despite many clinical and experimental studies with antiarrhythmics, the current predominant role of radiofrequency ablation greatly limits the value of these pharmacological studies.

Anti-Arrhythmia Agents↗

PubMed2003

[Arrhythmogenic effects of non cardiovascular drugs].

Among the unwanted effects of drugs, arrhythmogenic effects are particularly fearsome. Although rare they are serious, and responsible for syncope or sudden death, often linked with torsades de pointe on established long QT. For non cardiovascular drugs, detection is difficult because patients do not undergo systematic cardiological surveillance. Nevertheless understanding the risk, identification of predisposing factors, and consideration of the contra-indications are the rules of prescription, which are even more indispensable when the pathology being treated is benign. In effect, the implicated drugs are mainly anti-histamines, antibiotics, neuroleptics and antidepressants. The pharmaceutical companies, regulatory agencies, and pharmacological surveillance services must recognise the greatest possible risk of a drug, thanks to pre-clinical data, experimental electrophysiology both in vivo (measurement of the QT interval) and in vitro (action potential duration) or even in the elementary channel (essentially analysis of the iKr current). Correlated with clinical data (QT changes, pharmacokinetic interactions), a risk/benefit profile can therefore be established, which is even more demanding when the pathology is benign or when alternative drugs are available.

Arrhythmias, Cardiac↗

PubMed2002

[Continuous nodal reciprocal rhythm and Steinert's disease: treatment by double chamber stimulation. A case report].

We report a case of continuous supraventricular tachycardia in a patient affected by Steinert's myotonic dystrophy. The investigation of this tachycardia showed that there was a "slow-fast" common nodal re-entry, rendered continuous by the existence of significant conduction defects in the fast pathway and the slow anterograde pathway. Implantation of a double chamber cardiac stimulator, necessary for conduction defects present in the basal state in this patient allowed, with the evolution of the conduction defects, the complete eradication of reciprocal rhythm entry, without resorting to ablation.

Electroencephalography↗

PubMed2001

Routine measurements of left and right ventricular output by gated blood pool emission tomography in comparison with thermodilution measurements: a preliminary study.

The aim of this preliminary study was to evaluate the accuracy of left and right ventricular output computed from a semi-automatic processing of tomographic radionuclide ventriculography data (TRVG) in comparison with the conventional thermodilution method. Twenty patients with various heart diseases were prospectively included in the study. Thermodilution and TRVG acquisitions were carried out on the same day for all patients. Analysis of gated blood pool slices was performed using a watershed-based segmentation algorithm. Right and left ventricular output measured by TRVG correlated well with the measurements obtained with thermodilution (r = 0.94 and 0.91 with SEE = 0.38 and 0.46 l/min, respectively, P < 0.001). The limits of agreement for TRVG and thermodilution measurements were -0.78-1.20 l/min for the left ventricle and -0.34-1.16 l/min for the right ventricle. No significant difference was found between the results of TRVG and thermodilution with respect to left ventricular output (P = 0.09). A small but significant difference was found between right ventricular output measured by TRVG and both left ventricular output measured by TRVG (mean difference = 0.17 l/min, P = 0.04) and thermodilution-derived cardiac output (mean difference = 0.41 l/min, P = 0.0001). It is concluded that the watershed-based semi-automatic segmentation of TRVG slices provides non-invasive measurements of right and left ventricular output and stroke volumes at equilibrium, in routine clinical settings. Further studies are necessary to check whether the accuracy of these measurements is good enough to permit correct assessment of intracardiac shunts.

Adult↗

PubMed2001

[Electrocardiographic alternans].

A simple ECG curiosity or a precursor of serious arrhythmia, associated with pericardial effusion or a sign of inotropic alteration, the phenomenon of electrical alternans has intrigued clinicians and research workers in its multiple facets, mechanical and electrical, consequences on PR interval, QRS complex or ventricular repolarisation. As a consequence, the causal mechanisms are very different, but these last few years, a predominant role of calcium flux, especially intracellular, has been demonstrated. Recently, clinical interest in this phenomenon has been revived with the demonstration of micro-alternans of repolarisation, apparently a new marker for the risk of sudden death.

Arrhythmias, Cardiac↗

PubMed2001

[Results of coronary artery surgery in octogenarians].

Over an 11 year period from January 1990 to December 2000, 3282 patients underwent isolated or combined surgical myocardial revascularisation. In this group, 42 were aged 80 or over (maximum 87 years), 1.3% of the total patient population. The mean age of this subgroup was 81.8 +/- 1.75 years) with a male predominance (61.9%). All patients were autonomous and considered to be in good general and psychological health. Preoperative coronary angiography showed 33.3% of left main stem lesions either alone or associated with a right coronary lesion. The ejection fraction was over 50% in 78.6% of cases. Saphenous vein grafts were used in all but 5 patients who also had left internal mammary artery grafts. Thirteen patients (31%) underwent combined valvular surgery (11 aortic and 2 mitral valve) and 2 patients underwent combined vascular surgery. Three patients were operated as an emergency. A total of 5 patients died in the first 30 postoperative days, a hospital mortality of 11.9%. There were 2 postoperative hemiplegias and 2 cases of renal failure which were aggravated in the postoperative period. The other patients were discharged from hospital with a satisfactory cardiac and functional status. The global mortality was 14% at 3 years and 18% at 5 years. The main bad prognostic factor for survival was the association of aortic valve surgery. In selected octogenarians in good general and psychological health without severe co-morbid conditions, surgical myocardial revascularisation may be considered with an acceptable operative risk.

Aged↗

PubMed2001

[Metabolic considerations in the treatment of coronary disease in diabetic patients].

Coronary heart disease represents the first cause of death in diabetic patients. The poor outcome of this ischemic disease is multifactorial. The abnormalities in myocardial energy metabolism encountered by the diabetic heart explain both the ischemic severity and the worsening of reperfusion lesions. The metabolic abnormalities in diabetic heart consist in both an impairment of glucose metabolism (diminished glucose uptake, reduced glycolysis, decreased glucose oxidation...) and an increase in fatty acid oxidation. During ischemia, glucose oxidation is reduced and anaerobic glycolysis becomes the main ATP substrate. Lactate accumulate in myocardial cells, inducing both a metabolic acidosis and an intracellular calcium overload. During reperfusion, intracellular homeostasis is restored very slowly in diabetic heart. Several therapeutic approaches are used to correct these metabolic disturbances. Glucose--insulin--potassium infusion in acute myocardial infarction leads to a significant reduction in the mortality relative risk in diabetic patients (ECLA and DIGAMI studies). The benefit is greater in diabetic patients who where non-insulin-treated prior to ischemia followed by myocardial reperfusion therapy. Others more direct pharmacological approaches improve glucose oxidation during myocardial ischaemia and myocardial reperfusion. The reference drug remains trimetazidine for which one of the fundamental mechanism of action was discovered recently. This specific metabolic, non haemodynamic approach, complete the gold-standard treatment of coronary heart disease in diabetic patients (e.g. aspirin, beta-blockers, ACE inhibitors and statins).

Coronary Disease↗

PubMed2000

Facilitation of L-type calcium currents by diastolic depolarization in cardiac cells: impairment in heart failure.

OBJECTIVE: Decay kinetics of the voltage-gated L-type Ca(2+) current (I(CaL)) control the magnitude of Ca(2+) influx during the cardiac action potential. We investigated the influence of changes in diastolic membrane potential on I(CaL) decay kinetics in cardiac cells. METHODS: Cells were isolated enzymatically from rat ventricles, human right atrial appendages obtained during corrective heart surgery and left ventricles from end-stage failing hearts of transplant recipients. The whole-cell patch-clamp technique was used to evoke I(CaL) by a 100-ms depolarizing test pulse to -10 mV. Conditioning potentials between -80 and 0 mV were applied for 5 s prior to the test pulse. RESULTS: Depolarizing the cells between -80 and -50 mV prior to the test pulse slowed the early inactivation of I(CaL) both in rat ventricular and human atrial cells. This slowing resulted in a significant increase of Ca(2+) influx. This type of facilitation was not observed when the sarcoplasmic reticulum (SR) Ca(2+) content was depleted using ryanodine which reduced the rate of inactivation of I(CaL), or when Ba(2+) replaced Ca(2+) as the permeating ion. Facilitation was favored by intracellular cAMP-promoting agents that, in addition to increasing current peak amplitude, enhanced the fast Ca(2+)-dependent inactivation of I(CaL). Facilitation was impaired in atrial and ventricular human failing hearts. CONCLUSION: Decay kinetics of I(CaL) are regulated by the diastolic membrane potential in rat and human cardiomyocytes. This regulation, which associates slowing of I(CaL) inactivation with reduced SR Ca(2+) release and underlies facilitation of Ca(2+) channels activity, may have profound physiological relevance for catecholamines enhancement of Ca(2+) influx. It is impaired in failing hearts, possibly due to lowered SR Ca(2+) release.

Adrenergic beta-Agonists↗

PubMed2000

Dietary coconut oil affects more lipoprotein lipase activity than the mitochondria oxidative capacities in muscles of preruminant calves.

The presence of coconut oil in a milk replacer stimulates the growth rate of calves, suggesting a better oxidation of fatty acid in muscles. Because dietary fatty acid composition influences carnitine palmitoyltransferase I (CPT I) activity in rat muscles, this study was designed to examine the effects of a milk replacer containing either tallow (TA) or coconut oil (CO) on fatty acid utilization and oxidation and on the characteristics of intermyofibrillar (IM) and subsarcolemmal (SS) mitochondria in the heart and skeletal muscles of preruminant calves. Feeding CO did not affect palmitate oxidation rate by whole homogenates, but induced higher palmitate oxidation by IM mitochondria (+37%, P < 0.05). CPT I activity did not significantly differ between the two groups of calves. Heart and longissimus thoracis muscle of calves fed CO had higher lipoprotein lipase activity (+27% and 58%, respectively; P < 0.05) but showed no differences in fatty acid binding protein content or activity of oxidative enzymes. Whatever the muscle and the diet, IM mitochondria had higher respiration rates and enzyme activities than those of SS mitochondria (P < 0.05). Furthermore, CPT I activity of the heart was 28-fold less sensitive to malonyl-coenzyme A inhibition in IM mitochondria than in SS mitochondria. In conclusion, dietary CO marginally affected the activity of the two mitochondrial populations and the oxidative activity of muscles in the preruminant calf. In addition, this study showed that differences between IM and SS mitochondria in the heart and muscles were higher in calves than in other species studied so far.

Journal Article↗

PubMed2000

The antiangiogenic factor 16K PRL induces programmed cell death in endothelial cells by caspase activation.

We asked whether the antiangiogenic action of 16K human PRL (hPRL), in addition to blocking mitogen-induced vascular endothelial cell proliferation, involved activation of programmed cell death. Treatment with recombinant 16K hPRL increased DNA fragmentation in cultured bovine brain capillary endothelial (BBE) and human umbilical vein endothelial (HUVE) cells in a time- and dose-dependent fashion, independent of the serum concentration. The activation of apoptosis by 16K hPRL was specific for endothelial cells, and the activity of the peptide could be inhibited by heat denaturation, trypsin digestion, and immunoneutralization, but not by treatment with the endotoxin blocker, polymyxin-B. 16K hPRL-induced apoptosis was correlated with the rapid activation of caspases 1 and 3 and was blocked by pharmacological inhibition of caspase activity. Caspase activation was followed by inactivation of two caspase substrates, poly(ADP-ribose) polymerase (PARP) and the inhibitor of caspase-activated deoxyribonuclease (DNase) (ICAD). Furthermore, 16K hPRL increased the conversion of Bcl-X to its proapoptotic form, suggesting that the Bcl-2 protein family may also be involved in 16K hPRL-induced apoptosis. These findings support the hypothesis that the antiangiogenic action of 16K hPRL includes the activation of programmed cell death of vascular endothelial cells.

Antibodies, Monoclonal↗

PubMed2000

[Electrophysiologic and anatomic atrial remodeling: an atrial rhythmic cardiomyopathy].

In 1995, Wijffels and Alessie, using a curious goat model of atrial fibrillation, introduced the concept of atrial remodelling. The classical atrial substrate (anatomopathological-dilatation and hypokinesis-, and electrophysiological-short refractory periods and decreased conduction-), appeared not only to be one of the causes of atrial fibrillation but also the consequence of atrial fibrillation itself, the mechanism being a vicious circle. In addition to ventricular rhythmic cardiomyopathy, responsible for cardiac failure, the concept of atrial rhythmic cardiomyopathy with the same mechanical and electrophysiological consequences, has developed. These changes, characterised mainly by calcium overload associated with cellular hibernation and differentiation, have not been totally elucidated but have already renewed the physiopathology of atrial fibrillation.

Anti-Arrhythmia Agents↗

PubMed1999

A "dysautonomic" head-up tilt test pattern in elderly patients with neurocardiogenic syncope.

The characteristics of neurocardiogenic syncope (NCS) in elderly patients remain unclear. We compared the hemodynamic profiles of young and older patients with consecutive and positive head-up tilt tests (HUT). Continuous, noninvasive, and reliable monitoring of arterial pressure (AP) and heart rate (HR) was done throughout 46 consecutive positive HUTs of symptomatic patients. The population (12-82 years old) was divided into two groups: younger patients, Y (n = 25, < or = 65 years), and older patients, O (n = 21). Changes in AP and HR after the first minute of tilting, during the stable orthostatic phase and during syncope were compared. Except for systolic pressure, baseline hemodynamic parameters were similar in Y and O. No difference appeared in the mean time elapsed before syncope (19+/-9 vs 22+/-2 min). Asymptomatic hypotension was observed, only in O, 1 minute after tilting, followed by a progressive fall in the mean AP before syncope (0+/-0.9 vs -1+/-0.7 mmHg/min) without HR increase (0.7+/-1 vs 0+/-0.6 beats/min). This pressure slope was strongly related to age (r = 0.54, P < 0.001). Hemodynamic recording during HUT identifies a dysautonomic pattern in elderly patients with NCS and the abnormal AP/HR responses to orthostasis may be a feature specific to this population. Although the central mechanism of NCS is common to all ages, the age-related characteristics of the trigger event may indicate the need for specific management at different ages.

Adolescent↗

PubMed1999

Pharmacological manipulation of Ins(1,4,5)P3 signaling mimics preconditioning in rabbit heart.

Recent evidence revealed biphasic alterations in myocardial concentrations of the second messenger inositol (1,4,5)-trisphosphate [Ins(1,4,5)P3] with ischemic preconditioning (PC), i.e., increase during brief PC ischemia and decrease early during sustained test occlusion. Our aim was to determine whether an agonist and an antagonist of Ins(1,4,5)P(3) signaling (D-myo-inositol-1,4,5-trisphosphate hexasodium salt [D-myo-Ins(1,4, 5)P3] and 2-aminoethoxydiphenyl borate (2-APB), respectively), given such that they mimic this biphasic profile, would mimic infarct size reduction with PC. To test this concept, isolated, buffer-perfused rabbit hearts received no intervention (control), ischemic PC, D-myo-Ins(1,4,5)P3, D-myo-Ins(1,4,5)P(3) + PC, 2-APB, or 2-APB + PC. All hearts then underwent 30-min coronary occlusion and 2 h reflow, and infarct size was delineated by tetrazolium staining. In addition, the effects of D-myo-Ins(1,4,5)P3 and 2-APB on Ins(1,4,5)P3 signaling were evaluated in isolated fura 2-loaded rat cardiomyocytes. Mean infarct size was reduced with PC and in all D-myo-Ins(1,4,5)P3- and 2-APB-treated groups versus control (59 and 42-55%, respectively, vs. 80% of myocardium at risk, P < 0.05). Thus pharmacological manipulation of Ins(1,4,5)P3 signaling mimics the cardioprotection achieved with ischemic PC in rabbit heart.

Animals↗

PubMed1999

[Electrocardiographic aspects of the pathology of the bundle of His].

The ECG appearances of His bundle pathology are very variable and endocavitory recordings are often required to confirm the diagnosis which may be suspected by close analysis of the surface ECG. Truncular AVB is a serious condition as the block is infranodal but with a supraventricular and therefore a narrow QRS complex: it may be median with a double His potential or proximal and distal, which are more difficult to diagnose. Hisian extrasystoles are particularly polymorphic, either overtly, suggesting successively atrial and ventricular extrasystoles, or masked with deceptive pseudo-1st or 2nd degree atrioventricular block. More rarely, hisian tachycardias complicating congenital heart disease in children are observed, particularly in the postoperative period.

Bundle of His↗

PubMed1999

Effects of dietary coconut oil on fatty acid oxidation capacity of the liver, the heart and skeletal muscles in the preruminant calf.

The oxidative capacity of the liver, the heart and skeletal muscles for fatty acids were investigated in preruminant calves fed for 19 d on a milk-replacer containing either coconut oil (CO, rich in 12:0) or tallow (rich in 16:0 and 18:1). Weights of the total body and tissues did not differ significantly between the two groups of animals but plasma glucose and insulin concentrations were lower in the CO group. Feeding on the CO diet induced an 18-fold increase in the hepatic concentration of triacylglycerols. Rates of total and peroxisomal oxidation of [1-14C]laurate, [1-14C]palmitate and [1-14C]oleate were measured in fresh tissue homogenates. Higher rates of total oxidation in liver homogenate and of peroxisomal oxidation in liver, heart and rectus abdominis muscle homogenates were observed with laurate used as substrate. Furthermore, the relative contribution of peroxisomes to total oxidation was 1.9-fold higher in the liver and in the heart with laurate than with oleate or palmitate. Finally, the peroxisomal oxidation rate of oleate was 1.5-fold higher in the hearts of calves fed on the CO diet. Whatever the tissue, citrate synthase (CS, EC 4.1.3.7) and cytochrome c oxidase (COX, EC 1.9.3.1) activities were similar between the two groups of calves but the COX: CS activity ratio was lower in the liver of the CO group. In conclusion, laurate is better catabolized by peroxisomes than long-chain fatty acids, especially in the liver. Elongation of lauric acid after partial oxidation might explain the hepatic triacylglycerol accumulation in calves fed on the CO diet.

Analysis of Variance↗