Search PubMed⌕ Search

Biomedical subjects

T Lavergne

Publications and source records attributed to T Lavergne.

At least 55 records · Page 3Linked to original sources
PubMed1995

[Treatment of obstructive cardiomyopathy by permanent apical ventricular stimulation].

The treatment of obstructive hypertrophic cardiomyopathy is classically based on beta blockers, cardiac calcium channel blockers or amiodarone to improve the symptoms and to decrease the intraventricular gradient. However, this treatment may prove to be insufficient or poorly tolerated. Two chamber cardiac pacing no constitutes an alternative to surgical treatment, as it improves the symptoms and decreases the left intraventricular gradient, by modifying the ventricular activation sequence. In order to be effective, ventricular pacing must be continuous, with a sufficiently short atrioventricular period to allow continuous ventricular preexcitation, while preserving atrial contraction. However, it has yet to be demonstrated that continuous ventricular pacing provides a survival benefit for these patients.

Cardiac Pacing, Artificial↗
PubMed1995

[Changes in heart rate variability after myocardial infarction. Value of Poincareé's diagram].

The variability of the heart rate is reduced after myocardial infarction. It then progressively increases, to return to near normal values after several months. However, these changes in heart rate variability occur at the same time as slowing of the heart rate which makes interpretation difficult. Poincaré's diagram is constructed from a Holter recording plotting each RR interval against the preceding RR interval. The authors have developed a geometric approach to this diagram to evaluate parasympathetic tone for a given heart rate. By measuring the dispersion in height of the Poincaré's diagram, the authors evaluate the shor-term variability for a given RR interval. Two 24 hr Holter recordings were performed in 52 patients at one and two weeks after a myocardial infarction. The dispersion in the height of the Poincaré's diagrams was measured at the 10th, 25th, 50th, 75th and 90th percentiles of the total dispersion. The authors have shown an increase in the short-term variability of the shortest RR intervals (1th, 25th and 50th percentiles) which is not observed in the longer RR intervals (75th and 90th percentiles). In conclusion, theres is an increase in the heart rate variability at the shortest RR intervals. This suggests that the recovery of parasympathic tone after myocardial infarction occurs mainly at the fastest heart rates.

Aged↗
PubMed1994

[Limitations of ventricular late potentials in atrial fibrillation].

It is generally admitted that the chaotic atrial activation in atrial fibrillation makes analysis of ventricular late potentials uninterpretable. However, some workers have contradicted this affirmation. The authors performed signal averaged electrocardiogram in 17 patients with atrial fibrillation before cardioversion for external D.C. shock. The recording was repeated 15 minutes after restoration of sinus rhythm. None of the patients had complete bundle branch block in atrial fibrillation or sinus rhythm. Analysis was made with a band pass filter of 40 Hz and to a final noise level of 0.3 microV. The positivity of late ventricular potentials was confirmed by the presence of at least 2 of the usual 3 criteria: an averaged QRS duration > 120 ms, a RMS 40 < 20 microV and a LAS > 40 ms. The mean duration of the averaged filtered QRS complex was 122 ms in atrial fibrillation and 112 ms in sinus rhythm, a non significant decrease of 9%. The mean value of the RMS 40 was 24 microV before cardioversion versus 29 microV after restoration of sinus rhythm, a significant increase of 19% (p < 0.05). Finally, the mean duration of the LAS in atrial fibrillation was 45 ms, decreasing to 35 ms in sinus rhythm, a significant reduction of 22% (p < 0.05). In atrial fibrillation, 10 patients had ventricular late potentials (2 positive criteria) and 7 had no ventricular late potentials. In sinus rhythm, on the other hand, 6 patients were positive and 11 negative.(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1994

[Radiofrequency catheter ablation: theoretical and technical aspects].

Radiofrequency currents produce circumscribed tissue necrosis by progressive and localised heating. Endocardial application via the percutaneous approach with a specific electrophysiological catheter enables destruction of the anatomical substrate of many cardiac arrhythmias. The technique is well tolerated due to the absence of barometric phenomena and general anaesthesia, and the possibility of modulating the energy delivered, which explains why it has supplanted fulguration in most indications. The technological evolution aims to increase the lesional power and decrease the number of complications. This implies the development of catheters capable of delivering greater currents without the risk of thrombus formation and of generators dependent on electrical or thermal parameters. The low incidence of complications reported by centres using the technique is based on an excellent understanding of the technique, the use of appropriate material, the surveillance of parameters which allow detection of unwanted effects and the respect of a strict operation protocol. In the absence of these precautions, the wide diffusion of this technique, favored by its low cost and relative simplicity, may be associated with an increase in the number of side effects which could be lethal. This cannot be accepted in a technique with such wide indications, including arrhythmias with a usually benign long-term prognosis.

Animals↗
PubMed1994

[Mechanisms of atrial fibrillation: recent advances].

Atrial fibrillation (AF) is due to the presence of multiple reentry pathways. Although this mechanism has been known for some time, new information has recently been acquired about the factors of atrial vulnerability and the conditions of myocardial alteration. There are two main factors of atrial vulnerability: intra-atrial conduction defects and abnormalities of the refractory periods. In addition, the concept of critical mass and the influence of the autonomic nervous system have to be taken into consideration. The abnormalities of the refractory periods liable to increase atrial vulnerability are their shortening, spatial dispersion and poor adaptation to the heart rate. All these changes may be demonstrated at cellular level. The product of the intra-atrial conduction velocity and the duration of the refractory period defines the wave length. The risk of developing reentry pathways increases as the wave length shortens. Moreover, the more the atrium fibrillates, the greater will be the decrease of the refractory periods, atrial fibrillation giving rise to atrial fibrillation. Histological lesions of the atrial tissue may be demonstrated, even in the absence of underlying cardiac disease. They mainly consist of fibrosis, fatty degeneration and myocytic hypertrophy. In the long-term, atrial fibrillation leads to a number of structural abnormalities of the atrial, and sometimes ventricular tissues, progressing to cardiomyopathy in some cases.

Action Potentials↗
PubMed1994

[Interventional cardiology methods in the treatment of ventricular arrhythmia].

Sustained ventricular arrhythmias are the primary cause of sudden death in France. Treatment possibilities have increased in recent years with the development of interventional rhythmology techniques. Thus alongside the classical pharmacological approach, clinicians now have access to more aggressive treatment methods such as implantable pacing-defibrillation systems or endocavitary excision techniques. Implantable defibrillation systems are of proven efficacy in reducing ventricular arrhythmias but their action is merely palliative. Technological advances have simplified their implantation and increased their diagnostic and therapeutic abilities. Their high price is nevertheless one of the factors limiting their wider use in some countries. Endocavitary excision techniques, with a radical curative effects, are used only in cases of sustained monomorphous ventricular tachycardia in the absence of any associated cardiac surgery procedure. Coronary angioplasty is of rhythmological value when the etiopathogenesis of the arrhythmia is of proven ischemic origin. Rather than being competitors, these various methods are complementary, each having specific characteristics forming the basis of particular indications.

Arrhythmias, Cardiac↗
PubMed1993

[Torsades de pointes].

Torsades de pointes are defined and characterised by specific, polymorphic but organised ventricular activation on the surface electrocardiogram. They constitute episodes of rapid tachycardia which are usually short lasting and terminate spontaneously. However, they may recur and persist, leading to syncope or sudden death. They occur typically in cases with abnormalities of ventricular repolarisation with prolongation of the QTU interval and variable deformations of the TU waves. The basal abnormalities may be modest or intermittent. A bigeminy with a long coupling interval and alternating long and short cycles often precede the burst of arrhythmia. Abnormalities of ventricular repolarisation and torsades de pointes may be the result of congenital syndromes (catecholamine-dependent torsades) or acquired factors (pause-dependent torsades) such as paroxysmal bradycardia, drugs which prolong the repolarisation and potassium and magnesium deficiencies. The electrophysiological mechanisms comprise reentry and after depolarisation induced activity genetic factors causing abnormalities of the G-proteins, potassium currents or adrenergic receptors may also play a role. Emergency treatment consists of intravenous magnesium salts, sometimes of betablockers or verapamil for maintenance therapy. The association of a potassium-sparing drug may be useful. Cardiac pacing may be necessary. Left sympathetic denervation or implantation of an automatic defibrillator are exceptional therapeutic options in refractory congenital torsades de pointes.

Death, Sudden, Cardiac↗
PubMed1992

[Percutaneous ablation of atrioventricular junction by radiofrequency current in resistant atrial arrhythmia. Results of a series of 24 patients].

Catheter ablation of the atrioventricular junction may be proposed for the treatment of certain atrial arrhythmias resistant to antiarrhythmic therapy. One of the methods currently being evaluated uses radio-frequency energy which has certain advantages compared with direct current ablation because of the progressive and limited lesions it produces. This technique was used in 24 patients with atrial arrhythmias resistant to antiarrhythmic therapy. The radio-frequency energy was delivered without general anaesthesia with HAT 100 and 200 (OSYPKA) generators in the unipolar mode (average 17.4 watts) for an average period of 22.3 +/- 8 seconds. The catheter (8F USCI suction catheter in the first 18 patients and a 7F Polaris Mansfield, deflectable catheter with a large distal electrode in the remainder) was positioned at the nodo-hisian junction at a point where the two distal electrodes recorded a large atrial deflection and the smallest possible hisian potential. The conduction defects induced during the acute phase generally remain stable in cases of complete atrioventricular block and tend to regress in cases of incomplete atrioventricular block despite initial control of atrioventricular conduction. During follow-up (21 +/- 16 months), 14 patients (58%) remained in complete atrioventricular block, 4 patients (17%) had controlled atrioventricular conduction with an acceptable ventricular rate with associated previously ineffective antiarrhythmic therapy. Radio-frequency ablation was a failure in 6 patients (25%). There were no haemodynamic, rhythmic or ischaemic complications during the acute phase or during follow-up. These results suggest radio-frequency energy is a seductive alternative to direct current ablation for percutaneous modification of atrioventricular conduction in patients with refractory atrial arrhythmias. However, simple modulation of atrioventricular conduction gives aleatory results due to the tendency to regression during follow-up. On the other hand, complete atrioventricular blocks created by radio-frequency energy are generally definitive and are associated with a junctional escape rhythm which is usually stable.

Adult↗
PubMed1991

Wenckebach periods in sinoatrial block: experimental and clinical evidence.

The reality of sinoatrial Wenckebach periods (WP) has been suggested, but not proven, in the literature. We report experimental and clinical data showing WP in sinoatrial blocks. Experimental sinoatrial blocks were induced by superfusion of bepridil (10(-5) M) in 15 preparations of isolated rabbit right atria. Different types of block were observed, including Blumberger I block, i.e., sinoatrial WP. The recordings showed that the typical pattern of Blumberger type IA block and sinoatrial WP may be due to transient acceleration of the sinus rate, without change in the increment. We also observed sinoatrial WP in a 72-year-old patient on direct recordings of the sinus node (SN) electrical activity. In this case, transient acceleration of the sinus rate also seemed to be involved in the genesis of sinoatrial WP. Analysis of these clinical and experimental data showed similarities that may explain the mechanism of the WP. Usually type IA Blumberger block is said to involve a decrease in the sinoatrial increment to explain the atrial sequence (decrease in PP interval followed by a pause shorter than twice the value of the preceding cycle, then a cycle longer than the one preceding the pause). In fact, this pattern can be observed when the acceleration of the higher structure, the SN, induces block within the lower structure, i.e., the atrium.

Action Potentials↗
PubMed1991

Cellular electropharmacology of human atrium: effects of antiarrhythmic drugs.

Human atrial tissue exhibits specific electrophysiological properties such as the presence of plateau shaped action potentials characterized by an initial notch followed by a long lasting plateau. In these cells, the notch and the plateau are due to the activation of transient outward currents Ito and slow inward current Isi. The effects of antiarrhythmic agents on this tissue depend on the morphology of the action potentials. We demonstrated that, in these plateau shaped fibers, action potential duration at 50 and 90% of repolarization was increased by flecainide at the concentration of 5 x 10(-7)M. This increase is due to the effect of the drug on Ito, as shown by experiments with 4 amino-pyridine, a blocker of transient outward currents. We also demonstrated that quinidine at the concentration of 10(-5)M decreased in these cells the action potential duration at 50% of repolarization. This decrease is due to the effects of the drug on Isi, as confirmed by experiments using the patch-clamp technique. These modifications of the repolarization duration were not obtained in triangular action potentials which are observed in young subjects and in patients with chronic atrial fibrillation. In these triangular action potentials both Ito and Isi are inactivated. Since the animal tissues do not exhibit the same electrophysiological inhomogeneity, it is interesting to test the different classes of antiarrhythmic drugs on human atrium. These studies on human tissue, especially on diseased atrium, are closer to clinical situations than those performed on normal animal tissue.

Action Potentials↗
PubMed1990

Cellular electrophysiological effects of flecainide on human atrial fibres.

STUDY OBJECTIVE: The aim of the study was to examine the electrophysiological characteristics of human atrial specimens collected during heart surgery and to investigate the effects of the class I antiarrhythmic agent flecainide on their electrical activity. DESIGN: Atrial specimens were studied using standard microelectrode techniques, with and without superfused flecainide (5 x 10(-7) M) or the transient outward current inhibitor 4-aminopyridine (0.5 mM). EXPERIMENTAL MATERIAL: Atrial fragments 0.5-1.0 cm2 were obtained at operation from 34 patients, mean age 30 years. There was no history of previous atrial arrhythmia in any patient and drug therapy was stopped 24 h before surgery. MEASUREMENTS AND MAIN RESULTS: Two types of transmembrane action potential were identified: (1) triangular shaped potentials (group A, classically found in animal models); (2) potentials with a large plateau preceded by a notch (group B). The effect of flecainide was compared on the the two types of action potential. In both, flecainide lessened the depolarisation rate. In group B, but not in group A, it increased the action potential duration at 50% and 90% repolarisation (APD50, APD90) and the effective refractory period. The notch in group B action potentials is generated by transient outward currents (Ito). Inhibition of these currents, either by increasing the pacing rate or by adding 4-aminopyridine, limited the increase in APD50, APD90, and effective refractory period generated by the presence of flecainide. CONCLUSIONS: The effects of flecainide on the atrial repolarisation process depend on the shape of the action potential. These effects are more marked in cells with a plateau, where Ito is activated.

4-Aminopyridine↗
PubMed1990

Electrophysiologic effects of intravenous nicardipine on sinus node function and conduction in humans.

We conducted an intracardiac study of the electrophysiologic effects and kinetics of intravenous nicardipine (N) in 16 patients with or without impaired cardiac conduction, using a randomized, double-blind, crossover design versus placebo (P). N or P were infused intravenously over 5 min: the dose of N was 9.46 +/- 3.85 mg. Standard electrophysiologic parameters of atrioventricular (AV) conduction and sinus function were measured under basal conditions, between 10 and 25 min, and at 65 min, after beginning the first infusion of N or P, and between 10 and 25 min after beginning the second infusion of N or P. Treatment with N significantly reduced systolic (S) and diastolic (D) blood pressure (BP) at 10 min (35 +/- 19 and 25 +/- 17 mm Hg, respectively). N significantly shortened sinus cycle length (SCL), corrected sinus recovery time (CSNRT), AH interval, AV node (AVN) Wenckebach cycle length, and anterograde and retrograde effective (ERPs) and functional refractory periods (FRPs) of the AVN. Infranodal parameters were unaffected. Mean plasma N concentrations at 10 min were 18.5 +/- 7.7 ng/ml/kg and 5.3 +/- 3 ng/ml/kg at 60 min. Two patients experienced slight adverse effects (anginal pain and nausea); another with sick sinus syndrome developed a sinus pause. We conclude that intravenous N affects nodal, but not His conduction, and that it should be administered with care in the presence of SSS.

Adult↗
PubMed1990

[Localized dilatation of the bronchi. A misunderstood etiology of coronaro-bronchial fistula].

The authors report the case of a coronary to bronchial artery anastomosis secondary to focal bronchiectasis. The diagnosis was made after finding large retroatrial vessels on coronary arteriography. A pulmonary steal syndrome, frequently reported in this condition in the literature, was not present in that particular case. The diagnosis of a coronary to bronchial artery anastomosis should alert the physician to possible underlying cardiac disease (Tetralogy of Fallot, supravalvular aortic stenosis, severe coronary artery disease). A bronchopulmonary etiology (chronic obstructive airways disease, multiple bullae, bronchiectasis) is less commonly found as the presentation is often atypical.

Angiography, Digital Subtraction↗
PubMed1990

[Ventricular tachycardia during theophylline overdose. Apropos of a case of reduction by magnesium chloride].

The authors report a case of ventricular tachycardia (VT) induced by theophylline toxicity in a patient with ischaemic heart disease complicated by left ventricular failure and chronic asthma. Two episodes of VT were reduced by intravenous injection of magnesium chloride. The aggravating role of a moderate magnesium deficiency is suggested by the synergy of hypomagnesemia and theophylline on intracellular calcium fluxes contributing to an accumulation of intracytoplasmic calcium, a situation which has been shown experimentally to generate delayed after depolarisations. The respective roles of the correction of the metabolic deficiency and of the specific antiarrhythmic action related to the calcium blocking effect of magnesium salts at cellular level are discussed.

Drug Overdose↗
PubMed1990

[Physiopathology of the sinus node and sinoatrial conduction].

New information about the pathophysiology of the sinus node and sino-atrial conduction has been published in the last few years. The sinus node consists of cells separated by a network of collagen fibres. This anatomical disparity explains the different electrophysiological characteristics of the node; the morphology of cellular action potentials depends on the site of recording. The dominant and most automatic pacemaker cells are situated in the cephalic region and the latent pacemaker cells in the caudal region. However, synchronisation of these different cellular activities is possible and results in a coherent signal. This complex synchronisation has been the object of several recent papers. The phenomenon of intrasinusal pacemaker shift and the stimuli which induce it have been studied in depth. In general, positive chronotropic stimuli tend to shift the dominant pacemaker towards the cephalic part and negative chronotropic stimuli towards the caudal part of the node. It is possible to assess pacemaker shift clinically and this phenomenon must be taken into consideration when studying sinus node function. Intercellular conduction and especially electrotonic conduction does not play a role in the genesis of the flux, which represents spontaneous cellular automatism, but in its mode of expression, that is to say the sinus rhythm. The pathophysiology of sinoatrial block is complex because it may be situated within and/or around the sinus node. The extrinsic or intrinsic mechanisms of these blocks may be interrelated. Variations in sinus rhythm must be taken into account in the genesis of sinoatrial block; an acceleration in rhythm may block conduction in the perisinusal region. Finally, our knowledge of the ionic fluxes underlying sinus automatism has also improved with individualization of the pacemaker current (if).(ABSTRACT TRUNCATED AT 250 WORDS)

Action Potentials↗
PubMed1990

Evidence of mitochondrial impairment during cardiac allograft rejection.

NADH laser fluorimetry and mitochondrial oxigraphy were used to study myocardial oxidative energy metabolism during cardiac allograft rejection. Heterotopic cardiac transplantation was performed on Lewis rats; allografts (with Fischer rat donors) were compared with isografts (with Lewis rat donors). In vivo and in vitro assays were performed six days after transplantation. Myocardial NADH fluorescence was recorded in vivo from grafted hearts, at baseline; during brief, complete ischemia; and during reperfusion. Oxygen consumption of mitochondria isolated from both native and grafted hearts was determined. Neither baseline levels nor maximum ischemic levels of NADH fluorescence (F0 = k[NADH]) were found to be significantly different between allografts (0.45 +/- 0.05 to 0.87 +/- 0.10) and isografts (0.45 +/- 0.04 to 1.11 +/- 0.05). During recovery, the rate of fluorescence decrease was significantly lower in allografts than in isografts (0.024 +/- 0.001 vs. 0.038 +/- 0.002 delta F0.s-1, P less than 10(-3], indicating a lower rate of NADH reoxidation. In the presence of malate and glutamate substrates, mitochondrial O2 consumption was significantly lower in allografts than in isografts (30 +/- 9 vs. 100 +/- 15 nanoatoms O2. min-1.mg prot-1, P less than 10(-2]. These results indicate that mitochondrial oxidative metabolism was impaired during the rejection process. Such energy production disturbances may contribute to the dysfunction of rejecting hearts.

Animals↗