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Biomedical subjects

A Gressard

Publications and source records attributed to A Gressard.

12 recordsLinked to original sources
PubMed2001

[Cardiovascular effects linked to the use of chloroquine].

The chloroquine is the mainly and most frequently drug used as antimalaric in the world, in spite of the extension of resistance phenomena. Besides, the chloroquine is also commonly indicated in rheumatology and dermatology as a chronic treatment of some connective tissue disease. The chloroquine has three main cardiovascular effect: membrane stabilizer, direct negative inotropic effect and direct arterial vasodilator. Thus, these cardiovascular iatrogenic effects of the chloroquine are important both through their potential frequency and seriousness. Personal clinical cases and medical review enables to identify the main effects, observed either with prophylactic, or curative, or even toxic dosages. The more often, there are some rhythm and conductance disorders, myocardiopathy, even sometimes vasoplegic shocks. A list of the commercial patent medicine including chloroquine enables to be aware, to prevent and to take into account the cardiovascular risks of a treatment newly set or carried on for long years.

Antimalarials↗
PubMed1983

Left bundle branch block with left-axis deviation: an electrophysiologic approach.

In an attempt to explain QRS left-axis deviation (LAD) in left bundle branch block (LBBB), 69 patients with LBBB were studied. The patients were separated into 2 groups. Group A included 60 patients with a QRS axis of +80 degrees to -55 degrees (average -11 degrees) and Group B included 9 patients with a QRS axis of -60 degrees. In all patients, a point was detected on the apex of the right ventricle at which activation was simultaneous with the beginning of ventricular depolarization (V-apex = 0). Ventricular stimulation at this point gave a monomorphic response with a QRS axis of -60 degrees and QS in D2 and D3. Minor conduction aberrations related to the relative refractory period of the His Purkinje network were found during atrial premature beats in 40 patients in Group A (and always as LAD of the QRS axis [average 24.6 degrees]) and in 4 patients in Group B. In Group B, these aberrations were in the form of a disappearance of the r2 wave with a QRS axis similar to that achieved through stimulation of the right ventricle apex. Given this aberration, one may conclude that the left bundle branch plays a role in the depolarization of the left ventricle. Blocking it brings the QRS axis closer to that obtained by stimulation of the point of primary depolarization of the right ventricle. Thus, LBBB must have a monomorphic morphology. If not, the left branch is the location of slowed, but persistent, conduction.

Bundle-Branch Block↗
PubMed1981

[Genesis of auricular fibrillation in the Wolff-Parkinson-White syndrome].

Atrial fibrillation seems to be more common in the absence of associated cardiac disease in the Wolff-Parkinson-White syndrome (WPW) than in subjects of the same age without this condition. The aim of this study was to analyse the electrophysiological mechanism of AF and to establish its relationship to the accessory pathway. The series comprises 14 out of 51 patients with WPW undergoing classical endocavitary investigation associating the recording of cardiac potentials from the His bundle, right atrium (RA), left atrium (LA) via the coronary sinus and atrial and ventricular stimulation techniques. Three mechanisms of inducing AF were analysed : - AF triggered by RA stimulation : either by a premature extra stimulus or overdrive atrial pacing. In all cases, the accessory pathway was right sides. - AF triggered by overdrive ventricular pacing : three cases were left sided accessory pathways in which atrial desynchronisation was localised in the LA. - Conversion of reciprocating tachycardia to AF (9 cases). In 2 cases, this was preceded by a progressive acceleration of the heart rate. Of 3 left sided accessory pathways, the atrial desynchronisation was located in the LA in 2 cases. The factors which facilitate AF in THE WPW syndrome are discussed : increased atrial vulnerability, the role of the rapid return of ventricular excitation to the atria through the accessory pathway. Our observations suggest that the accessory pathway plays a role in the genesis of AF in the WPW syndrome.

Atrial Fibrillation↗
PubMed1981

[Effects of mexiletine in the Wolff-Parkinson-White syndrome].

The effects of intravenous mexiletine were studied by His bundle recordings and programmed stimulation in 7 patients aged from 20 to 40 years old (average age : 32 years), 5 of whom had an overt WPW syndrome (4 type A, and 1 type B), and 2 of whom had concealed pre excitation. All had reciprocating tachycardia. Electrophysiological investigation was performed under basal conditions, and then several times in the hour following intravenous mexiletine (3,5 mg/Kg in 5 minutes) followed by an infusion of 0,07 mg/Kg/min. The following results were obtained : 1. mexiletine did not cause any significant changes in the normal AV conduction pathway; 2. the refractory periods of the atria and ventricles were unaffected by the drug; 3. pre excitation regressed in 2 of the 5 patients with overt WPW. In a third patient, the effective anterograde refractory period of the accessory pathway increased by 210 ms. The retrograde refractory period of the accessory pathways increased in three patients and remained unchanged in the others; 4. there was little change in the ability to induce reciprocating tachycardia by stimulation. However, in two patients, the attacks were shortened, terminating spontaneously within a few seconds. This study shows the electrophysiological basis of the use of mexiletine in the WPW syndrome. Although the results do show some variability, they justify the use of mexiletine in patients with paroxysmal tachycardia in the WPW syndrome.

Adult↗
PubMed1980

[Oral contraceptive and coronary thrombosis. Two clinicopathological cases].

The cases reported are interesting from two points of view: they confirm the thrombotic mechanism of the arteria lesions (coronary amongst others) and the oral contraception pill was the only cardiovascular risk factor, smoking, hyperlipidaemia, hypertension and coronary atherosclerosis having been eliminated. The two young women (31 and 34 years old) presented with severe myocardial infarction and shock, leading to death within hours in one case and within weeks in the other (despite an attempt to resect the infarct and prolonged intraaortic balloon pumping). In both cases multiple thromboses were discovered: coronary, intra cardiac and in the collateral aortic circulation.

Adult↗
PubMed1979

Effects of amiodarone on sinus node in man.

The effects of amiodarone on the sinuatrial node were studied in 24 patients after an intravenous injection of the drug (5 mg/kg). Sinuatrial function was assessed by rapid atrial pacing and premature atrial stimulation. Sinus cycle length did not change significantly, but the corrected sinus node recovery time was prolonged. While there was no significant change in sinuatrial conduction time, prolongation of the non-reset zone in 14 cases, as well as the abolition of the platesu in 2/24 patients, suggested that conduction of the atrial responses to the sinus node might have been depressed.

Aged↗
PubMed1979

[Electrophysiological effects of anti-arrhythmia agents in man. Attempt at classification].

The electrophysiological effects of anti-arrhythmic drugs in man may be classified in three groups: -- Group I: comprising drugs whose characteristic action is on the AV node (beta blockers, verapamil, digitalis) The nodal conduction time (A-H interval) and refractory periods are increased. -- Group II: comprising drugs acting on the His-Purkinje system, the AV nodal conduction staying unchanged. This group has two sub-groups. Sub-group A: these drugs delay the His-Prukinje conduction (increased H-V interval). Examples are quinidine, procainamide, disopyramide, ajmaline, chloro-acetyl-ajmaline. In addition these drugs usually increase the atrial refractory periods and those of accessory pathways. Sub-group B: the His-Purkinje conduction is unchanged but the refractory periods are modified: lengthened (bretylium tosylate) or shortened (diphenylhydantoin, lignocaine, mexiletine). -- Group III: which includes amiodarone and aprindine whose effects are mixed: on the one hand AV nodal depression, and on the other, alteration of the His-Purkinje conduction manifested by an increased H-V internal (aprindine) or refractory periods (amiodarone). These preparations also increase the refractory periods of accessory AV pathways and amiodarone increase the refractory periods of the atria. This type of classification could help towards a more rational clinical approach to the use of anti-arrhythmic drugs.

Anti-Arrhythmia Agents↗
PubMed1979

[Value of an automatic chronometer in epicardial mapping].

The use of a digital display automatic chronometer during epicardial mapping is reported. The epicardial potential recorded by a tripolar electrode is transformed electronically by amplification, filtering, rectifying negative deflections and then summation. The interval between the reference signal (electrical impulse or other cardiac potential) is calculated automatically and displayed at an adjustable rate. The presence of a delay increases the range of application of the apparatus. Epicardial mapping is thus simplified and shortened.

Electrocardiography↗
PubMed1978

[Electrophysiological effects of chloroacetyl ajmaline in Wolff-Parkinson-White syndrome].

The electrophysiological effects of chloro-acetyl-ajmaline in the Wolff-Parkinson-White syndrome have been studied in 7 patients after an intravenous dose of 1.5 mg/kg of the drug. Preexcitation was abolished in 3 cases, while 3 other subjects showed a slight increase in effective refractory period of the abnormal route of excitation (a mean of 13 ms). The possibility of bringing about a reciprocal rhythm was removed in one case out of two. During tachycardia, chloro-acetyl-ajmaline produced significant lengthening of the ventriculo-atrial conduction time (p less than 0.05). These results show the usefulness of chloro-acetyl-ajmaline in the control of the arrhythmias associated with the Wolff-Parkinson-White syndrome.

Adolescent↗
PubMed1978

[Electrophysiological study on mexiletine in man with reference to dose-response relation].

The electrophysiological properties of Mexiletine were investigated by endocavitary His Bundle recording and programmed electrical stimulation of the heart in 30 patients. Differing dosage (2, 2.7 and 3.4 mg/kg) were given intravenously in 3 groups of 10 patients. The effects on the length of the sinus cycle, conduction intervals and cardiac refractory periods were observed and the following results obtained : 1. Sinus rhythm increased at all dosages but this effect was much more pronounced with 3.4 mg/kg dosage (--12.8% +/- 2.81% : : % shortening of sinus cycle with respect to the basal cycle +/- SD, p less than 0.005); 2. Atrioventricular nodal conduction time (A-H interval) decreased, the effect being more marked with the larger dose regimes; 3.His-Pirkinje conduction time (H-V interval) unaltered except in 3 cases where it increased by 5 ms after injection of 2.7 mg/kg; 4. Relative refractory period of His-Parkinje system shortened, this effect also being more pronounced with the larger doses ( --3.75 +/- 0.25% :2.7 mg/kg, p less than 0,001; -- 7 +/- 1.46% 3.4 mg/kg, p less than 0.005). In conclusion, the changes observed in the His-Purkinje system after mexiletine were similar to those of Lignocaine and Diphenylhydantoin. The drug also appears to have a marked vagal inhibitory effect as shown by the acceleration of the sinus rhythm and reduced atrioventricular conduction times.

Adult↗