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Biomedical subjects

J Lacotte

Publications and source records attributed to J Lacotte.

17 recordsLinked to original sources
PubMed2006

[Survey into cardiac pacing in the Ile-de-France area for the year 2001: evaluation of indications].

UNLABELLED: A survey into the implantation of cardiac pacemakers during 2001 in the Ile-de-France area was carried out by the French National Insurance Medical Service in order to evaluate performance in all centres performing more than 10 primary implantations per year. METHODS AND RESULTS: In 2001, 12 centres out of a total of 49 performed less than 50 primary implantations per year, representing 5% of the total regional activity, which was estimated to be 6414 procedures. The remaining 95% of procedures were spread evenly among 8 high-throughput centres (> 200 primary implantations per year) and 29 medium-throughput centres (50 to 200 primary implantations per year). Indications for pacing were analysed retrospectively by a team of regulatory doctors on a sample of 2176 patients with reference to the ACC/AHA/NASPE guidelines. After examination of the medical records, the indication was ranked as being class I, II or Ill (absence of indication). A valid indication was lacking in 8.2% of cases. Sinus node dysfunction represented 74.6% of the non-indications, and this classification had the predictive factors of asymptomatic dysfunction, and treatment with anti-arrhythmic or bradycardic medication. The proportion of class III interventions was significantly lower in the high-throughput centres (5.8 vs 9.9%, p < 0.05). CONCLUSION: 8.2% of primary pacing procedures were not indicated and resulted principally from asymptomatic sinus node dysfunction.

Aged↗
PubMed2002

[Atrial flutter with 1/1 nodo-ventricular conduction with amiodarone. From physiopathology to diagnosis].

Atrial flutter with 1/1 nodo-ventricular conduction is a classical complication of Vaughan-Williams's Class I antiarrhythmic drugs. The increase of the flutter cycle and weak action of the antiarrhythmic on the atrioventricular node leads to 1/1 conduction of atrial depolarisation to the ventricles. In view of their marked action on the atrioventricular node, this type of pro-arrhythmic effect is very unexpected with Class III antiarrhythmics. The authors report 7 cases of 1/1 atrial flutter with oral amiodarone observed between 1994 and 2001. The patients were 6 men and 1 woman with an average age of 58 +/- 14 years. Four of them had underlying cardiac disease; none were hyperthyroid. The initial arrhythmia was 2/1 atrial flutter (n = 4), 1/1 atrial flutter (n = 2) and atrial fibrillation (n = 1). Treatment was preventive with doses of 400 mg/day associated with carvedilol in one patient and 200 mg/day in another. The other five patients all received loading doses of 9200 +/- 2400 mg over 10 +/- 4 days. The symptoms were palpitations (n = 2) associated in one patient with hypotension, one syncope, one near syncope and one cardiogenic shock. The ventricular cycle of the 1/1 flutter was 287 +/- 33 ms. The QRS duration was 136 +/- 35 ms with ventricular tachycardia-like appearances in 3 cases. An adrenergic trigger factor was noted in 5 patients. One patient required emergency cardioversion. The authors discuss the physiopathology of 1/1 flutter and theoretical diagnostic methods are proposed. In conclusion, amiodarone does not always prevent the occurrence of 1/1 nodo-ventricular conduction in atrial flutter.

Administration, Oral↗
PubMed1997

[Glucocorticoid-induced hypertrophic cardiomyopathy in premature infants: apropos of 4 cases].

BACKGROUND: The steroidal treatment used to prevent bronchopulmonary dysplasia (BD) in the preterm babies may be the cause of several complications, one of them being hypertrophic cardiomyopathy. CASE REPORT: Four infants developed hypertrophic cardiomyopathy during glucocorticoid (dexamethasone and/or betamethasone) treatment for bronchopulmonary dysplasia. In one of them, septal hypertrophy led to left ventricular outflow tract obstruction and congestive heart failure. All four were premature infants born after 2 weeks of gestation and weighing 780 to 1,080 g. The first echocardiographic changes appeared between the 4th and 15th day of the glucocorticoid course when the cumulated dose was respectively 1.82-1.87-3.51 and 3.86 mg/kg. Hypertrophic cardiomyopathy resolved completely between 2 and 4 weeks after cessation of the treatment. CONCLUSION: The glucocorticoid dosage to prevent BD should be reduced to 0.3 mg/kg/j and the myocardial function should be monitored by repeated echocardiograms during the first 15 days of treatment.

Betamethasone↗
PubMed1991

Determination of zolpidem and zopiclone in serum by capillary column gas chromatography.

A gas chromatographic method using a short, high-resolution capillary column connected to a specific thermoionic detector and requiring a simple and short extraction step without evaporation was developed for the rapid and precise determination of two new hypnotics, zolpidem and zopiclone, in serum at concentrations greater than 5 ng/mL. The assay was linear between 5 and 200 ng/mL, with coefficients of intra- and interassay variation less than 5% for both. The method was validated and then used to analyze zolpidem serum concentrations in nine rabbits after oral administration of 0.5 mg/kg and zopiclone serum concentrations in six patients treated orally with a 7.5-g dose.

Animals↗
PubMed1989

Substantial rise in sparteine metabolic ratio during haloperidol treatment.

A sparteine test was carried out in 14 patients suffering from acute schizophrenic psychoses before and 1-2 times during oral haloperidol treatment in doses of 10-40 mg day-1. In patients classified as extensive metabolisers (sparteine MR less than 20 before treatment), haloperidol treatment resulted in a rise in sparteine MR that correlated with the serum-haloperidol concentration both within and between patients. At the highest serum haloperidol concentrations (60-80 nM) an increase in sparteine MR by a factor 15-50 was seen, but no patients were transformed into phenotypically poor metabolisers. The steady state concentration of haloperidol on the initial standard dose of 10 mg day-1 was the same in one patient classified as a sparteine poor metaboliser (MR = 112) as in eleven patients classified as extensive metabolisers (MR:0.22-1.47).

Adult↗
PubMed1989

Quinidine disposition in relation to antipyrine elimination and debrisoquine phenotype in alcoholic patients with and without cirrhosis.

Single dose disposition of oral quinidine (400 mg sulfate) was studied in a control group of subjects (No. = 6) and in hospitalized alcoholic patients involving one group with (No. = 6) and one group without (No. = 11) hepatic cirrhosis. All subjects also underwent an antipyrine and a debrisoquine test. Patients with cirrhosis had a prolonged elimination half-life (29.5 +/- 5.9 h) and low clearance (24 +/- 7 ml.kg-1.h-1) of antipyrine and also a considerably higher debrisoquine metabolic ratio (18.8 +/- 3.3) than the controls, whereas the alcoholics without cirrhosis had metabolic patterns for these two test compounds comparable to those seen in the controls (antipyrine half-life: 8.8 +/- 1.1 h and 9.8 +/- 2.0 h; debrisoquine metabolic ratio: 3.6 +/- 0.7 and 3.8 +/- 1.2 for alcoholics and controls respectively). In patients with cirrhosis the apparent elimination half-life of quinidine was longer (12.8 +/- 1.8 h) whereas after oral administration clearance of quinidine (15.6 +/- 3.5 l.h-1) and quinidine/3-hydroxyquinidine ratio (9.9 +/- 2.1) were not different from controls (quinidine clearance: 13.45 +/- 1.9 l.h-1; quinidine/3-hydroxyquinidine: 10.3 +/- 2.7). A possible change in distribution patterns of quinidine in cirrhotics may explain these findings.

Adult↗
PubMed1987

Treatment of caffeine intoxication by exchange transfusion in a newborn.

The symptoms of acute poisoning after accidental administration of ten times the usually prescribed dosage of caffeine in a premature infant included the following neurological signs: incessant tremors, hypertonia, continuous opisthotonos posture, whining and crying and digestive disturbances. The very high serum caffeine levels, 160 mg/l, determined 66 hours after the first administration was confirmed by the very high cerebrospinal fluid caffeine concentration 115 mg/l. Two exchange transfusions performed at an interval of 16 hours produced a large decrease in serum caffeine levels of approximately 40 mg/l each time, and a similar decrease in the cerebrospinal fluid concentration. The clinical status of the infant improved very rapidly and the child's psychomotor development was normal at 3 months of age.

Acute Disease↗