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Biomedical subjects

J M Davy

Publications and source records attributed to J M Davy.

At least 73 records · Page 4Linked to original sources
PubMed1987

[Cardiac metastases. Clinical arguments of the diagnosis].

The case reported here concerns an 80-year old man without history of coronary disease whose electrocardiogram showed localized and stable repolarization disorders, viz. elevated ST segment with isoelectric point J and negative T wave. This pattern suggested cardiac metastasis after chest examination had revealed a bronchial epidermoid carcinoma. Two-dimensional echocardiography showed that the lateral wall of the left ventricle was thickened, hyperechogenic and akinetic. The secondary cardiac lesions were confirmed at pathological examination. This case has prompted us to discuss the frequency of such secondary tumours of the heart, their mode of dissemination to the myocardium and their clinical and electrocardiographic aspects. It underlines the usefulness of echocardiography for the diagnosis of cardiac tumours.

Aged↗
PubMed1986

Effect of quinidine and bretylium on defibrillation energy requirements.

We examined the effect of bretylium and quinidine on the energy requirements for internal defibrillation in 14 pentobarbital-anesthetized dogs. Bretylium, 6 or 10 mg/kg (n = 6), did not affect the relation between energy and the likelihood of successful defibrillation. The mean energy required to achieve 50% success (E50) or 90% success (E90) in defibrillation was not significantly altered; E50 was 5.3 +/- 1.9 J (X +/- s.d) before and 6.1 +/- 3.5 J after bretylium (n.s.), and E90 was 7.2 +/- 2.1 J before and 8.6 +/- 3.3 J after drug (n.s.). Quinidine was administered in a series of two loading and maintenance infusions to achieve mean plasma concentrations of 2.4 +/- 0.63 and 2.95 +/- 0.88 microgram/ml, respectively (n = 8). No significant effect on defibrillation energy requirement was observed; mean E50 before and after treatment was 6.3 +/- 3.3 J and 6.2 +/- 2.9 J, respectively, and mean E90 was 8.3 +/- 4.4 J and 8.3 +/- 4.1 J, respectively. Similarly, saline administration to control dogs (n = 12) resulted in no change in E50 or E90. At concentrations or doses similar to those in patients with serious arrhythmias, neither quinidine nor bretylium appears to have consistent effects on the energy requirements for internal defibrillation in our dog model.

Animals↗
PubMed1986

Triple antegrade nodal pathway in a patient with supraventricular paroxysmal tachycardia.

A 69-year-old patient is described in whom programmed atrial extrastimulus testing revealed dual discontinuity of atrioventricular nodal conduction suggesting a triple antegrade nodal pathway. In this patient, programmed right ventricular pacing initiated two types of tachycardia due to intranodal reciprocating rhythms. In both cases, antegrade conduction occurred via the slow nodal pathway, and retrograde conduction by the fast and intermediate pathways, respectively. During ventricular extrastimulus testing, a single echo beat was elicited via a third circuit: the intermediate nodal pathway in a retrograde direction, and the fast pathway in an antegrade direction.

Aged↗
PubMed1986

Lidocaine causes a reversible, concentration-dependent increase in defibrillation energy requirements.

To investigate the influence of lidocaine on the energy requirements for internal defibrillation, lidocaine (n = 8) or saline solution (n = 12) was administered by intravenous infusion to 20 pentobarbital-anesthetized dogs, and the likelihood of successful defibrillation was examined at various shock energy levels before and after treatment. After lidocaine administration to a mean steady state concentration of 5.6 +/- 2.7 micrograms/ml, the mean energy required to achieve 50 and 90% success in defibrillation (E50 and E90) increased by 61.1 +/- 34.1% (mean +/- SD, p less than 0.005) and 47.1 +/- 28.6% (p less than 0.005), respectively. The steady state log lidocaine concentration correlated positively with the observed increase in E50 (r = 0.887, p less than 0.01) over a concentration range from 1.95 to 9.8 micrograms/ml. In a related experiment, lidocaine infusion was administered to five dogs and then abruptly discontinued. At energy levels achieving a mean 90.0 +/- 10.0% success in defibrillation before treatment, only 43.3 +/- 23.4% success was achieved after 60 minutes of the lidocaine infusion (p less than 0.01) at a mean plasma concentration of 8.4 +/- 2.1 micrograms/ml. The percent of successful defibrillations returned to baseline value (92.0 +/- 18.0%, p less than 0.01) after drug washout at a time when mean lidocaine concentration had declined to 1.8 +/- 0.5 microgram/ml. Lidocaine causes a reversible, concentration-dependent increase in the energy requirements for successful defibrillation; recommendations to administer lidocaine to patients with ventricular fibrillation resistant to defibrillation may need to be reviewed.

Animals↗
PubMed1986

Effects of encainide and its metabolites on energy requirements for defibrillation.

Encainide, a class IC antiarrhythmic agent, has been associated with proarrhythmic responses of ventricular tachycardia and fibrillation requiring defibrillation in patients. We examined the short-term effects of intravenous encainide and its two major metabolites, O-demethyl-encainide (ODE) and 3-methoxy-ODE (MODE), on the energy requirements for successful defibrillation in 25 pentobarbital-anesthetized, open-chest dogs. Truncated exponential (60% tilt) defibrillation shocks were administered through right atrial spring and left ventricular epicardial patch electrodes identical to those used in man with the automatic implantable defibrillator. At baseline multiple shocks of varying energy were applied to construct curves of percent successful defibrillation as a function of energy (DF curves) for each animal. Encainide, ODE, or MODE was then infused in loading and maintenance doses to achieve QRS widening of 20% to 50%. Saline was administered to animals serving as controls. Determination of the DF curve was repeated, after which the infusion was discontinued. After 1 hr washout period, an additional DF curve was constructed. The data were analyzed by logistic regression, and the energies required for 50% successful defibrillation (E50) were compared. No significant differences existed between the four groups in body or heart weight, extent of QRS widening, or baseline E50 values. After administration of encainide and ODE, the E50 increased by 129 +/- 43% (p less than .001) and 76 +/- 34% (p less than .005), respectively. Return of E50 toward baseline was observed after the washout periods in both groups (p less than .025), demonstrating the reversibility of the drugs' effects.(ABSTRACT TRUNCATED AT 250 WORDS)

Anilides↗
PubMed1986

[Infranodal chronic auriculo-ventricular block in subjects under 50 years of age].

The aetiology and evolution of chronic infranodal atrioventricular block (AVB) of young patients are not well known: are they the first sign of subclinical myocardial disease which can only be diagnosed by long term follow-up or do they represent isolated degenerative disease of the conduction tissue (Lenegre's disease)? Eighteen patients (15 men, 3 women) aged 25 to 49 years (average 41.5 years) were followed up for periods of 2 to 20 years (average 7.33 years) after pacemaker implantation for syncopal AVB. Follow-up was focused on the evolution of the conduction defects and the cardiovascular status. The patients were divided into two groups at the initial assessment: Group I: 15 patients with documented AVB; Group II: 3 patients in whom all basal recordings showed sinus rhythm (SR). Apart from one patient with an early non-ischaemic dilated cardiomyopathy, there was no previous cardiovascular disease. There was no history of ischaemic heart disease, drug effects, infection or inflammation in favour of an acute AVB. Three patients had permanent AVB, either 2nd degree with bundle branch block (N = 2) or 3rd degree block (N = 1). The other 15 patients were in sinus rhythm with bundle branch block: left bundle branch block (LBBB) in 5 cases, right bundle branch block (RBBB) in 3 cases; RBBB with left anterior hemiblock in 5 cases, RBBB and left posterior hemiblock in 2 cases. Paroxysmal AVB was recorded in 12 of these 15 patients on at least one occasion.(ABSTRACT TRUNCATED AT 250 WORDS)

Adams-Stokes Syndrome↗
PubMed1986

Qualitative and quantitative comparison of the cardiac effects of encainide and its three major metabolites in the dog.

We have evaluated the electrophysiologic effect of encainide and its three major metabolites, O-demethyl encainide, 3-methoxy-O-demethyl encainide and N-demethyl encainide in an anesthetized dog model. Our results support previous reports that O-demethyl encainide and 3-methoxy-O-demethyl encainide are both more potent than encainide in the depression of conduction. We also have shown that N-demethyl encainide is of about equal potency to encainide. Whereas the major differences between these compounds is primarily one of potency, there are some qualitative differences. Although O-demethyl encainide did not change the ventricular or atrial effective refractory periods significantly, 3-methoxy-O-demethyl encainide and N-demethyl encainide prolonged both. Encainide increased the atrial effective refractory period but did not produce significant changes in the ventricular refractory period. These data support previous suggestions of an important role for these metabolites as modulators of the clinical efficacy of encainide.

Anilides↗
PubMed1985

Muscarinic cholinergic receptor in the human heart evidenced under physiological conditions by positron emission tomography.

The muscarinic receptor was studied in vivo in the human heart by a noninvasive method, positron emission tomography (PET). The study showed that the binding sites of 11C-labeled methiodide quinuclidinyl benzilate [( 11C]-MQNB), a muscarinic antagonist, were mainly distributed in the ventricular septum (98 pmol/cm3 of heart) and in the left ventricular wall (89 pmol/cm3), while the atria were not visualized. A few minutes after a bolus intravenous injection, the concentration of [11C]MQNB in blood fell to a negligible level (less than 100th of the concentration measured in the ventricular septum). When injected at high specific radioactivity, the concentration of [11C]MQNB in the septum rapidly increased and then remained constant with time. This result was explained by rebinding of the ligand to receptors. It was the major difference observed between the kinetics of binding of [11C]MQNB to receptor sites after intravenous injection in vivo and that of [3H]MQNB to heart homogenates in vitro. The MQNB concentrations in the ventricular septum of different individuals were found to be highest when the heart rate at the time of injection was slow. This result suggests that the antagonist binding site is related to a low-affinity conformational state of the receptor under predominant vagal stimulation. Thus, positron emission tomography might be the ideal method to study the physiologically active form of the muscarinic acetylcholine receptor in man.

Atropine↗
PubMed1984

Kinetics of in vivo binding of antagonist to muscarinic cholinergic receptor in the human heart studied by positron emission tomography.

Positron Emission Tomography (PET) was used to analyse in vivo antagonist binding to human myocardial muscarinic cholinergic receptor. The methiodide salt of the muscarinic antagonist, quinuclidinyl benzilate (MQNB), was labeled with the positron emitter, Carbon-11, and injected intravenously to 8 normal subjects. 11C-MQNB concentration was determined in vivo in the ventricular septum from 40 cross-sectional images acquired at the same transverse level over a period of 70 minutes. In 4 subjects, various amounts of unlabeled atropine were rapidly injected at 20 minutes to study whether atropine competitively inhibited MQNB. The kinetics of binding of 11C-MQNB were not the same in vivo and in vitro. The apparent dissociation rate of 11C-MQNB in vivo was much slower (by 1 to 2 orders of magnitude) than that observed in vitro with 3H-QNB. After atropine injection, 11C-MQNB dissociated from its binding sites at a rate that apparently depended on the amount of atropine present. 11C-MQNB kinetics were analysed with a mathematical model which assumes the existence of a boundary layer containing free ligand in the vicinity of the binding sites. The dissociation rate of the radioligand depends on the probability of its rebinding to a free receptor site.

Atropine↗
PubMed1984

Physiopathology of ventricular tachyarrhythmias.

Ventricular arrhythmias may be the result of three mechanisms: abnormal automaticity, triggered activity complicating early or late after-depolarizations, and reentry by circular pathway or by reflection. These three fundamental mechanisms have been observed in the intact heart in experimental models of myocardial ischemia and digitalis intoxication. In man, the arguments in favor of a given mechanism are indirect and may be determined by their response to stimulation. It may be possible to state the following conclusions: (1) reentry is at the origin of ventricular fibrillation, certain ventricular tachycardias of bundle branch reentry and probably most chronic sustained ventricular tachycardias that are easily inducible; (2) the mechanism of certain other ventricular arrhythmias sustained remains unknown; (3) even when arrhythmias are associated with reentry, the triggering extrasystole can arise from a focal origin.

Action Potentials↗
PubMed1983

[Reciprocating tachycardia and anterograde conduction by a nodoventricular pathway].

Two patients were investigated for paroxysmal regular tachycardia with left bundle branch block centrifugation. A right-sided nodo-ventricular accessory pathway was demonstrated in both cases at electrophysiological investigation with His bundle recording and atrial and ventricular programd pacing techniques. However, the function of this pathway was different in the two cases. In the first case, there were no signs of an accessory pathway on the surface ECG in sinus rhythm but it could be unmasked by simple right atrial pacing at the same rhythm (widening of the QRS and shortening of HV from 40 to 25 ms). The tachycardias could be only initiated by ventricular extrastimulus. They showed major pre-excitation with left sided delay and a 1/1 atrio-ventricular response. There was no His potential before the ventriculogramme which retained the same configuration throughout the attack. The investigations also suggested the presence of a dual nodal pathway with the accessory pathway connected to the slow pathway. In the second case, the presence of an accessory pathway could be suspected from the appearance of the QRS complex in sinus rhythms. Tachycardia was initiated by an atrial extrastimulus with initially a first complex showing slightly more marked pre-excitation and a distinct His potential before the QRS but with a shorter HV interval than in sinus rhythm. Then the reciprocating tachycardia had appearances of major pre-excitation, left-sided delay and a 1/1 atrio-ventricular response. However, in contrast to the first case, all ventricular complexes were preceded by a His potential and the degree of pre-excitation was variable with a HV interval ranging from 0 to 15 ms. These two cases merit attention because of: --their points in common: nodal duality and an accessory pathway which was not atrio-ventricular (decremental conduction) but nodo-right ventricular, conducting well in the anterograde direction but more or less masked in sinus rhythm; the presence of the accessory pathway was clearly visible during reciprocating tachycardia; --the differences: in the first case the nodo-ventricular pathway formed part of the circuit of the reciprocating tachycardia which was antidromic: descending limb, the slow nodal pathway and then the accessory nodo-ventricular pathway; ascending limb, the His bundle and then the rapid nodal pathway. In the second case, the reciprocating tachycardia was entirely intranodal, the accessory pathway not being involved in the circuit but connected to it in parallel with the normal Hisian pathway.

Adult↗
PubMed1982

[Beta adrenergic receptor blockade : a self-limited phenomenon explaining the benignancy of acute poisoning with beta adrenergic inhibitors. Report of a series of 40 patients seen at the Fernand-Widal Toxicology Center, with a 0% mortality rate (author's transl)].

Acute poisoning with beta adrenergic inhibitors is rare although such drugs are widely prescribed. Between 1966 and 1980, 40 cases were recorded at the Fernand-Widal Toxicology Center. 40% of patients were asymptomatic and 25% had sinus bradycardia. 35% of patients had specific toxic signs, either atrioventricular block (20%) or hemodynamic disorders (15%); the latter were seen only when associated heart disease was present or when another cardiotropic agent had been absorbed. No deaths were recorded. This favorable prognosis may result from the self-limited nature of poisoning with beta blocking agents, myocardial function being similar to that which follows denervation. In severe cases, management includes pacing and glucagon.

Acute Disease↗