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Biomedical subjects

J B Thambo

Publications and source records attributed to J B Thambo.

5 recordsLinked to original sources
PubMed2003

[Ectopic junctional tachycardia of the neonate].

Congenital ectopic junctional tachycardia (EJT) is a rare arrhythmia presenting in the first 6 months of life. It is often resistant to antiarrhythmic drugs and its poor prognosis (35% mortality) explains its often complex management. The authors report two cases which illustrate its unpredictability with a potential to degenerate to serious ventricular arrhythmias. The possibility of progression to atrioventricular block, increased by antiarrhythmic therapy, may lead to implantation of a cardiac pacemaker. The poor outcome of the two babies underlines the severity of these arrhythmias.

Adrenergic beta-Antagonists↗
PubMed2002

[Ebstein's anomaly].

Since Ebstein's first description in 1866 and the first surgical attempts at treatment in the 1950's, the natural history of this condition remains obscure. The anatomical description contrasts with the clinical and prognostic variability of this malformation. The form observed in the foetal or prenatal periods has a very different prognosis to that observed in adults. The risk factors are not the same even though the anatomical entity is comparable. The difficulty in managing these patients is due to the problems of diagnosis and determination of these prognostic factors. Advances in echocardiography, the key investigation which facilitates diagnosis, and in surgical and ablation techniques, have improved our understanding of this condition and its prognosis.

Adult↗
PubMed2002

[Outcome of operated Fallot's tetralogy].

Fifty years after the beginning of cardiac surgery, a large percentage of operated congenital heart disease patients attain adulthood. The tetralogy of Fallot is one of the malformations in which the natural outcome was unfortunately nearly fatal in the long-term. Open heart surgery has radically transformed the prognosis of this, the most common of all cyanotic congenital cardiac malformations. Nowadays, most operated patients lead normal professional and family lives. Lonf-term survival after correction is between 90-95% after 30-35 years. Although surgical repair is satisfactory, the operated heart is not anatomically normal. The patients have a variable degree of devalvulation of the pulmonary outflow tract, a scar on the right ventricle, a patch repairing the ventricular septal defect and scars on the atrium (cannulation for cardiopulmonary bypass). These sequellae expose the patients to a number of complications, notably arrhythmic and sometimes haemodynamic, affecting the right ventricle. The late mortality rate varies from 5 to 13% in the literature. The main causes of death are sudden death and reoperation. Sudden death is the most severe long-term complication but it is uncommon, affecting less than 5% of the population. It is mainly due to ventricular arrhythmias. Certain predisposing factors should be identified during long-term follow-up, among them the presence of haemodynamic abnormalities: systolic overload (residual pulmonary stenosis) or diastolic overload of the right ventricle (pulmonary regurgitation), infundibular aneurysm, right ventricular dysfunction. It would appear to be important to prevent pulmonary regurgitation by preserving the pulmonary valve even if it means persistence of a mild transvalvular pressure gradient. When pulmonary regurgitation is inevitable, follow-up is essential to evaluate the timing of valvulation of the pulmonary orifice. Despite these different complications which must be understood for proper follow-up of these patients, the long-term outcome of operated tetralogy of Fallot remains very good.

Adult↗
PubMed2001

Cardioprotection by ischemic preconditioning preserves mitochondrial function and functional coupling between adenine nucleotide translocase and creatine kinase.

M. N. Laclau, S. Boudina, J. B. Thambo, L. Tariosse, G. Gouverneur, S. Bonoron-Adèle, V. A. Saks, K. D. Garlid and P. Dos Santos. Cardioprotection by Ischemic Preconditioning Preserves Mitochondrial Function and Functional Coupling Between Adenine Nucleotide Translocase and Creatine Kinase. Journal of Molecular and Cellular Cardiology (2001) 33, 947-956. This study investigates the effect of ischemic preconditioning on mitochondrial function, including functional coupling between the adenine nucleotide translocase and mitochondrial creatine kinase, which is among the first reactions to be altered in ischemia. Three groups of Langendorff-perfused rat hearts were studied: a control group, a group subjected to 30 min ischemia followed by 15 min reperfusion, and a group subjected to ischemic preconditioning prior to 30 min ischemia and 15 min reperfusion. Ischemic preconditioning significantly delayed the onset and amplitude of contracture during ischemia, decreased enzymatic release, and improved the recovery of heart contractile function after reperfusion. Mitochondrial function was assessed in permeabilized skinned fibers. The protective effect of preconditioning was associated with preservation of mitochondrial function, as evidenced by maintenance of the high K(1/2)for ADP in regulation of mitochondrial respiration and V(max)of respiration, the near absence of respiratory stimulation by exogenous cytochrome c, and preservation of functional coupling between mitochondrial creatine kinase and adenine nucleotide translocase. These data suggest that ischemic preconditioning preserves the structure-function of the intermembrane space, perhaps by opening the mitochondrial ATP-sensitive K(+)channel. The consequence is preservation of energy transfer processes from mitochondria to ATP-utilizing sites in the cytosol. Both of these factors may contribute to cardioprotection and better functional recovery of preconditioned hearts.

Adenosine Diphosphate↗