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Biomedical subjects

P Gallay

Publications and source records attributed to P Gallay.

51 records · Page 3Linked to original sources
PubMed1987

[Myoglobin: an early indicator of myocardial infarction during heart surgery].

Plasma myoglobin was measured in 40 patients before, during and after cardiac surgery under cardiopulmonary bypass, in order to study its value as an indicator of intra-operative myocardial damage. Myoglobin levels rose at cannulation, further increased during the operation and reached a peak 2 hours later; they began to decrease 6 hours after surgery and were back to normal 24 hours later. Myoglobin levels from induction of the anesthetics to the 6th post-operative hour were significantly higher in the 8 patients who developed intra-operative myocardial infarction than in the other patients. Thus, myoglobin is an early indicator of intra-operative myocardial ischaemia. An abnormal rise of myoglobin at induction of the anesthetics characterizes a group of patients at high risk of myocardial infarction during surgery.

Cardiac Surgical Procedures↗
PubMed1987

[Comparative study of auricular stimulation by transesophageal and endocavitary approach for evaluating sinus and atrioventricular node function].

The purpose of this study was to find out whether non-invasive transoesophageal pacing could effectively replace right intra-atrial pacing for the indirect evaluation of sinus node and atrioventricular (AV) node function. In a population of 17 patients the corrected sinus node recovery time (CSRT), the atrio-sinu-atrial conduction time (ASACT) and Wenckebach's point (W) were calculated by intracavitary pacing, then by transoesophageal pacing. There was no significant difference between the two methods in pre-pacing sinus cycle. With right intra-atrial pacing, mean CSRT value was 365 +/- 54 ms (with 5 values greater than 520 ms), mean ASACT value was 229 +/- 29 ms (with 8 values greater than 220 ms), and W occurred at a mean cycle length of 425 +/- 29 ms. With transoesophageal pacing, mean CSRT value was 406 +/- 87 ms (with 5 values greater than 520 ms), mean ASACT value was 222 +/- 17 ms (with 8 values greater than 220 ms), and W occurred at a mean cycle length of 408 +/- 26 ms. The two methods correlated very closely for CSRT and W (r = 0.97) and relatively well for ASACT (r = 0.84). The number of CSRT and ASACT values regarded as prolonged was the same with the two methods; 84% of recorded (i.e. maximal) CSRT values occurred with the same length of pacing cycle. There was no statistically significant difference between the two methods in the calculation of CSRT and ASACT, but W occurred at a slightly shorter cycle (p less than 0.05) with transoesophageal pacing. Thus, transoesophageal pacins is a non-invasive, easy to perform method for indirect exploration of sinus node and AV node function in patients who do not require subnodal conduction studies.

Aged↗
PubMed1985

[Transesophageal stimulation in the treatment of atrial flutter and tachysystole].

Transoesophageal left atrial pacing was used to reduce 102 episodes of ectopic atrial rhythms (79 common flutters and 23 ectopic tachycardias) in 83 patients (64 men, 19 women) aged 33 to 85 years (average 61 years). Overdrive pacing, at a faster rate than that of the spontaneous rhythm, was delivered via a bipolar pacing catheter introduced nasally and positioned behind the atrium under fluoroscopic and/or electrocardiographic control. Long pulse durations (up to 20 ms) were used to capture the atria with intensities of less than 20 mA for better tolerance. The overall results were: a) conversion to sinus rhythm in 60.8 p. 100 of cases (47 p. 100 directly and 13.8 p. 100 after transient atrial fibrillation), b) atrial fibrillation lasting over 24 hours in 7.8 p. 100 of cases, c) failure (31.4 p. 100) due to non-capture or intolerance (20.6 p. 100) or recurrence of the arrhythmia after transient atrial fibrillation (10.8 p. 100). Atrial flutter is more accessible to pacing than tachycardia (restoration of sinus rhythm in 63.3 p. 100 and 52.2 p. 100, respectively). Arrhythmias in the postoperative period of cardiac surgery, and isolated and recent arrhythmias were more easily converted. Prior antiarrhythmic therapy did not seem to improve results. Fifty per cent of failures of oesophageal pacing were converted to sinus rhythm by endocavitary pacing. These results show that atrial flutter or tachycardia may be successfully treated by oesophageal pacing in over 50 p. 100 of cases without having to use other forms of electrotherapy (endocavitary pacing or cardioversion).

Adult↗
PubMed1984

[Auricular flutter after cardiothoracic surgery. Treatment by auricular stimulation using the esophageal approach].

Transoesophageal atrial pacing was used in 10 patients to interrupt post-operative atrial flutter after cardio-thoracic surgery. The method was successful in all cases. The arrhythmia was converted directly into sinus rhythm in 8 patients and into atrial fibrillation followed by spontaneous reversion to sinus rhythm in 2 patients. The results differed according to the underlying disease. Return to sinus rhythm was the rule in all patients who underwent coronary artery bypass grafting and pneumonectomy, whereas transient atrial fibrillation seemed to be more frequent (and should be considered a satisfactory result) in patients with heart valve surgery. Relapses of arrhythmias seemed to be more resistant to transoesophageal stimulation irrespective of the operation performed. The method is non-invasive, easy to carry out and safe in patients receiving digitalis. The risk of ventricular pacing is very low. The burning sensation and chest pain experienced during stimulation are well tolerated. Transoesophageal pacing is as effective as epicardial atrial stimulation and more effective in such patients than temporary transvenous atrial pacing.

Aged↗
PubMed1984

[Effects of lidocaine at the plasma concentrations obtained by peridural injection on atrioventricular conduction disorders].

The aim of this study was to measure plasma concentrations obtained during lidocaine extradural blocks, and to determine whether these concentrations were able to induce high degree AV blocks in patients with impaired AV conduction. In a preliminary study, 12 patients were given an extradural block with an initial bolus of 3.4 mg . kg-1 lidocaine. After repeat injections, the mean total dose was 4.7 mg . kg-1. Plasma lidocaine concentrations were determined over an 8 h period after the first injection. The study itself was carried out in 14 patients with conduction disturbances undergoing His-bundle exploration. After informed consent had been obtained, the patients received an intravenous bolus of lidocaine (1.6 mg . kg-1 over 30 s). After baseline values had been measured. His conduction and lidocaine plasma concentrations were recorded 2, 5, 10, 30 and 60 min after lidocaine injection. In the preliminary study, the peak plasma lidocaine concentration was obtained at the 15th min (1.22 +/- 0.81 microgram . ml-1). In the second series, no clinical disturbance was seen after the i.v. injection of lidocaine. The peak plasma lidocaine concentration was obtained at the 2nd min (3.05 +/- 1.44 micrograms . ml-1). No significant alteration of conduction occurred after intravenous lidocaine. It is therefore possible to conclude that bifascicular AV disturbances do not constitute a contraindication to extradural anaesthesia with lidocaine.

Aged↗
PubMed1984

[Treatment by endocavitary fulguration of recurrent ventricular tachycardia caused by right ventricular dysplasia].

A 27 year old man had recurrent ventricular tachycardia since the age of 16. Different antiarrhythmic drugs were used successively without success (mexiletine, amiodarone, acebutolol, propafenone, sotalol). The diagnosis of VT due to arrhythmogenic right ventricular dysplasia was suggested by the morphology of the tachycardia (left-sided delay), surface ECG appearances (right bundle branch block and potential after the QRS in right precordial leads) and the presence of delayed potentials on right ventricular endocavitary recordings. However, there were no obvious RV changes on echo or angiographic examination. The arrhythmogenic zone was localised in the postero-basal zone of the RV using three electrophysiological criteria: the recording of delayed systolic potential in sinus rhythm which overlapped into diastole during tachycardia, mapping of ventricular depolarisation during VT and results of RV "pacemapping" reproducing the appearances of the spontaneous tachycardia. VT was reproducible on stress testing (non-sustained VT at the beginning of the recovery phase) and on endocavitary stimulation. One 250 joule electric discharge between the endocavitary electrodes and a large dorsal surface electrode prevented any further attacks without antiarrhythmic therapy (follow-up: one year). Control electrophysiological investigation after 4 months showed another potentially arrhythmogenic zone which is quiescent at present.

Adult↗
PubMedDate not supplied

Direct current catheter ablation of an accessory pathway in a recipient with refractory reciprocal tachycardia.

A recurrent reciprocating tachycardia developed in a 45-year-old man 2 years after heart transplantation. Electrocardiograms of both donor and recipient were normal, without patent preexcitation. An electrophysiologic study showed a left-sided Kent bundle with only retrograde conduction property. Because antiarrhythmic therapy was unsuccessful, direct current catheter ablation was performed. Since this procedure the patient remained asymptomatic without antiarrhythmic therapy.

Cardiac Pacing, Artificial↗
PubMedDate not supplied

Characterization and detection of naturally occurring antibodies against IL-1 alpha and IL-1 beta in normal human plasma.

During the development and testing of a radioreceptor assay (RRA) for human IL-1, we have detected and identified the presence of auto-antibodies to IL-1 in normal human plasma (NHP). The RRA is based on the competition between human 125I-labeled rIL-1 alpha and standard or unknown quantities of IL-1 alpha or IL-1 beta for binding to a limited amounts of IL-1 receptor (IL-1R) isolated from the EL4 mouse thymoma cell line. NHP from 20 out of 100 unselected blood donors were found to completely inhibit the binding of 125I-labeled IL-1 alpha to its receptor, suggesting the presence in these NHP samples of either abnormal amounts of IL-1 or of a factor binding to the 125I-labeled IL-1 alpha. Special care was taken to ascertain that the inhibitory factors were antibodies and not soluble IL-1 receptor antagonist. When plasma samples with inhibiting activity were incubated with labeled IL-1 alpha and chromatographed on a Sephadex G200 column, they were found to contain 125I-labeled complexes with an apparent molecular weight of 150-200kD. The IL-1 binding factor could be eliminated from plasma by incubation with protein A-Sepharose, suggesting that it consisted in IgG antibodies directed against IL-1. Furthermore, the antibody nature of the inhibiting factor was confirmed by its binding to purified rIL-1 coupled to Sepharose. Screening of 200 NHP samples by incubation with 100 pg of 125I-labeled IL-1 followed by precipitation with 12% of polyethylene glycol (PEG) confirmed that about 25% of NHP contain detectable IgG antibodies to IL-1 alpha, while only 2% of NHP contain antibodies to IL-1 beta. No correlation between the presence of these anti-IL-1 antibodies and any particular major histocompatibility complex or any pathological conditions was detected. We suggest that all serum samples assayed for IL-1 alpha or IL-1 beta content should be pretested with the PEG precipitation assay described here.

Antibodies↗