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Biomedical subjects

J Bardet

Publications and source records attributed to J Bardet.

At least 19 recordsLinked to original sources
PubMed2003

[A new cause of increased troponin levels: junctional tachycardia].

The authors report 4 cases of acute coronary syndromes with increased troponine levels during junctional tachycardia in patients with angiographically normal coronary arteries. ST segment changes during junctional tachycardia have no predictive value for the detection of coronary artery disease. Increased troponine, a marker of myocardial cellular necrosis, is not a sign of coronary lesions. A disequilibrium between the increased metabolic and energetic requirements of the myocardium and decreased perfusion due to the tachycardia could explain this observation. The recommended management of these patients is not to perform coronary angiography initially in the absence of cerebrovascular risk factors, but rather to document myocardial ischaemia by a non-invasive method such as echocardiography or scintigraphy.

Adult↗
PubMed2003

[Symptomatic left ventricular dysfunction and Behçet disease. Report of 2 cases].

Behçet's disease is associated with cardiac complications which may affect all three cardiac layers in 1 to 6% of cases. Although pericardial and coronary disease are the most common, the myocardium may also be affected. The clinical presentation may be left ventricular dysfunction with signs of dilated cardiomyopathy. The cause of the left ventricular dysfunction is usually coronary artery disease but it can also be inflammatory, resulting in a myocarditis with normal coronary arteries. The authors report two cases of Behçet's disease with symptomatic left ventricular dysfunction presenting as dilated cardiomyopathy with normal coronary arteries in one of the cases. Recent echocardiographic studies suggest that the incidence of myocardial disease is underestimated in this pathology: 20 to 35% of patients with Behçet's disease but no cardiac symptoms had left ventricular diastolic dysfunction. A more attentive investigation of left ventricular diastolic function in these patients should enable earlier diagnosis of this complication.

Adult↗
PubMed2002

Improving the prenatal diagnosis of citrullinemia using citrulline/ornithine+arginine ratio in amniotic fluid.

Prenatal diagnosis of citrullinemia is performed using a direct argininosuccinate synthetase (ASS) assay on chorionic villi (CV) and citrulline concentration measurement in early amniotic fluid (AF). Here we report the results of 40 prenatal diagnoses performed using this method, discuss the difficulties encountered in interpreting the results, and propose the use of the citrulline/ornithine+arginine ratio (which is more discriminatory than citrulline concentration alone) when performing prenatal diagnosis of citrullinemia.

Amniocentesis↗
PubMed2002

[Pneumococcal endocarditis in native valves. Three original observations in the adult].

The authors report three observations of acute pneumococcal endocarditis located in the aorta in one case, and mitral in the two other cases, admitted over a period of 4 years. Two of the three patients required surgical correction, with no surgical complications. Follow-up revealed a rare complication of infectious endocarditis linked to rupture of the head of the two anterior mitral pillars associated with an abscess. The severity of pneumococcal endocarditis is emphasised, concurring with the data from the literature. The role of echocardiography in pneumococcal septicaemia is clear; transthoracic examination is justified in every case of septicaemia, and transoesophageal echography complements this examination in case of diagnostic doubt or cardiovascular complication.

Adult↗
PubMed2001

[Comparative incidence of protrusive atheromatous plaques of the thoracic artery in patients with atrial fluter and atrial fibrillation].

Although it has been demonstrated recently that in patients with atrial fibrillation, protrusive atheromatous plaques of the thoracic aorta (thickness 4 mm) and left atrial abnormalities such as thrombosis, spontaneous contrast and low atrial blood flow velocities carry an additional embolic risk, this has not yet been studied in atrial flutter. Out of 2493 patients undergoing transoesophageal echocardiography between September 1993 and December 1997, 271 consecutive patients in atrial flutter (N = 41) or fibrillation (N = 230) for over 48 hours, underwent transoesophageal echocardiography before cardioversion. Patients with atrial flutter were compared with those with atrial fibrillation. Their characteristics were comparable with respect to age (68 +/- 13 and 67 +/- 12 years respectively, p = 0.628), sex ratio (men 66 and 54% respectively, p = 0.212), previous thromboembolic disease (5 and 15% respectively, p = 0.126). The incidence of protrusive aortic atheroma (12 and 11% respectively, p = 0.919), of spontaneous contrast in the thoracic aorta (15 and 14% respectively, p = 0.847) were identical in both groups. The left atrium was significantly smaller (3.1 +/- 0.7 and 6 +/- 3 cm2 respectively, p = 0.001), spontaneous atrial contrast less frequent (17 and 37% respectively, p = 0.024) and the velocities of atrial emptying higher (47 +/- 10 and 30 +/- 10 cm/s respectively, p = 0.030) in patients with flutter compared with atrial fibrillation. There was no difference in left ventricular fractional shortening (30 +/- 10 and 33 +/- 13% respectively, p = 0.630), the presence of rheumatic valvular disease (5 and 12%, p = 0.301), left atrial diameter (43 +/- 7 and 45 +/- 8, p = 0.134), right atrial surface area (16 +/- 4 and 17 +/- 6 cm2, p = 0.384) or in intraatrial thrombosis (2 and 3%, p = 0.888) respectively. These results show a high prevalence of protrusive atheroma of the thoracic aorta both in atrial flutter and in atrial fibrillation, and fewer left atrial abnormalities in patients with flutter.

Aged↗
PubMed2000

Comparison of a new method for the direct and simultaneous assessment of LDL- and HDL-cholesterol with ultracentrifugation and established methods.

BACKGROUND: Automated electrophoresis combined with enzymatic cholesterol staining might improve routine assessment of LDL- and HDL-cholesterol (LDLC and HDLC), as an alternative to the Friedewald equation and precipitation. A new method (Hydrasys; SEBIA) that adapts the cholesterol esterase/cholesterol oxidase reaction within urea-free gels was evaluated. METHODS: Fresh sera from 725 subjects (512 dyslipidemics) were analyzed by electrophoresis, in parallel with sequential ultracentrifugation, beta-quantification, calculation, and precipitation. RESULTS: Electrophoresis was linear up to 4 g/L cholesterol, with a detection limit of 0.042 g/L cholesterol/band. Within-run, between-run, between-batch, and between-operator imprecision (CVs) were 1.6%, 2.0%, 1.5%, and 2.7% for LDLC, and 3.9%, 4.3%, 5.5%, and 4.9% for HDLC, and remained unchanged up to 6.3 g/L plasma triglycerides (TGs). Precision decreased with very low HDLC (<0.25 g/L). Serum storage for 3-7 days at +4 or -80 degrees C did not interfere significantly with the assay. Agreement with beta-quantification was stable for LDLC up to 5.07 g/L (r = 0.94), even at TG concentrations >4 g/L (r = 0.91). Bias (2.88% +/- 12%) and total error (7.84%) were unchanged at TG concentrations up to 18.5 g/L. Electrophoresis predicted National Cholesterol Education Program cut-points with <0.04 g/L error, exactly and appropriately classified 79% and 96% of the subjects, and divided by 2.4 (all subjects) and 5.8 (TGs >1.5 g/L) the percentage of subjects underestimated by calculation. One-half of the patients with TGs >4 g/L had LDLC >1.30 g/L. For HDLC, correlation was better with precipitation (r = 0.87) than ultracentrifugation (r = 0.76). Error (-0.10% +/- 26%) increased when HDLC decreased (<0.35 g/L). Direct assessment of the LDLC/HDLC ratio detected 45% more high-risk subjects than the calculation/precipitation combination. CONCLUSIONS: Electrophoresis provides reliable quantification of LDLC, improving precision, accuracy, and concordance over calculation, particularly with increasing plasma TGs. Implementation of methods to detect low cholesterol concentrations could extend the applications for HDLC assessment.

Adolescent↗
PubMed1998

[Diagnostic strategy in acute myocarditis].

Myocarditis is a focalised or diffuse disease of the myocardium. The principal causal agents are viruses in Europe and North America and a parasite in South America (Chagas' disease). The prevalence of acute myocarditis is variable, related to the periodic cycle of viral epidemics. The diagnosis is difficult to establish because the clinical presentation is variable, ranging from asymptomatic forms to rapidly fatal acute congestive heart failure. The diagnostic tools suffer from lack of sensitivity or specificity. Endomyocardial biopsy, despite its low sensitivity, remains the reference investigation as it provides histological proof of the myocarditis. Myocardial scintigraphy with antimyosin antibodies has the advantage of very good sensitivity but with less specificity. The authors discuss the critical indications and limitations of each investigation.

Biopsy↗
PubMed1996

Gestational age-related reference values for amniotic fluid amino acids: a useful tool for prenatal diagnosis of aminoacidopathies.

In this study we have measured the concentration of 24 amino acids and total homocysteine in amniotic fluids obtained between the tenth and 32nd week of gestation from pregnancies not at risk for metabolic diseases. These results are used as reference values to which are compared values obtained from pregnancies at risk for citrullinaemia, argininosuccinic aciduria, HHH (hyperornithinaemia, hyperammonaemia and homocitrullinaemia) syndrome, cobalamin metabolism disorders (CblC or CblD), and sulphite oxidase deficiency. We discuss the helpfulness of amino acid analysis in amniotic fluid for prenatal diagnosis of aminoacidopathies.

Amino Acid Metabolism, Inborn Errors↗
PubMed1996

Clinical outcome and long-term management of 17 patients with propionic acidaemia.

UNLABELLED: A retrospective study was performed on the clinical outcome and long-term treatment of 17 patients with propionic acidaemia diagnosed during the last 20 years in our hospital. The study group consisted of 12 patients with early onset type of disease and 5 patients with late onset. Seven (41%) patients died, five with early onset and two with late onset. The deceased early onset patients had a median survival of 0.4 years while the deceased late onset patients died at the age of 2.8 and 4 years respectively. Median age of the living early onset patients was 5.2 (1-9.25) years, the late onset patients were 4, 7 and 23 years old. Patients were all treated with natural protein restriction and in most cases carnitine and metronidazole were added. The early onset patients were almost all treated with daily home tube feeding. The mean natural protein intake of early onset patients (6.3 +/- 1.5 g/day) was significantly lower than the natural protein intake of late onset patients (17.6 +/- 5.3 g/day). Supplemental protein intake was higher in early onset patients. The general neurological outcome of our study group was satisfactory with a better outcome for early onset patients. As to growth, many patients showed a failure to thrive, this was particularly for height. The strong protein restriction during the first years of life probably contributed to this. CONCLUSION: The prognosis for patients with propionic acidaemia appeared to be satisfactory in terms of survival and outcome characteristics such as neurological and mental development. Despite these results the authors feel that the prognosis and quality of life of these patients might be improved with liver transplantation or possibly somatic gene therapy in the future.

Adolescent↗
PubMed1995

A scheme for the interpretation of primary and secondary disturbances of plasma and urinary amino acid profiles. A possible way to an expert system.

A general scheme for the interpretation of primary and secondary abnormalities of plasma and urine amino acid concentrations is described. The key steps of this scheme are: analytical assessment of the measurements, comparison of results obtained with the reference values expressed in absolute and/or relative concentrations and identification of abnormally increased ninhydrin-positive compounds. The interpretation of results takes account of the various abnormalities induced by drugs or diet. The origins of these abnormalities are ordered by their frequency. A part of the proposed scheme is now computerized as the first step in the development of an expert system.

Amino Acid Metabolism, Inborn Errors↗
PubMed1995

Neutrophil-derived long-lived oxidants in cystic fibrosis sputum.

We evaluated long-lived oxidant potential in the sputum of patients with cystic fibrosis (CF) by quantitating the methionine-inhibitable, long-lived oxidant fraction of sputum, referred to as the chloramines. Taurine, the preferred amino acid substrate for chloramine formation, and myeloperoxidase (MPO), the chlorinated oxidant-generating enzyme, were also quantitated. As compared with the sputum of asthmatic subjects, the sputum of CF patients contained high concentrations of chloramines along with high levels of taurine and active MPO. A negative correlation between chloramine and taurine was found in the sputum of CF patients. No correlation was found between the density of Pseudomonas aeruginosa and the level of chloramines, taurine, or MPO. In contrast, respiratory parameters (%FEV or %FVC) and a nutritional index correlated positively with chloramine levels, whereas negative correlations were observed with taurine and MPO. In addition, the effect of antibiotic therapy, which significantly increased chloramine and decreased taurine levels, supported a beneficial effect of chloramines on overall clinical status. Our findings support a dual role of long-lived oxidants at the site of airway inflammation in CF, one component of which is their ability to mediate oxidative stress and the other a beneficial effect that may be partly explained by their inhibitory effect on antiprotease defense systems.

Adolescent↗