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A 77-year-old female was admitted in our hospital for uterine prolapse surgery. She developed ventricular tachycardia during induction of general anaesthesia and after initial symptomatic measures, she was transferred to the coronary care unit. Heart failure persisted and electrocardiographic changes mimicking acute myocardial infarction appeared. Coronary angiography was normal and left ventriculography revealed akinesis of the apical region of the left ventricle and apical ballooning during systole, with relative sparing of the base of the heart. Complete recovery of left ventricular function occurred 8 days after the initial onset of symptoms. A diagnosis of Takotsubo syndrome was made on the basis of consistent clinical and laboratory findings, typical echocardiography and angiography findings, and reversible course. This case emphasises the importance of being aware of uncommon causes of cardiac dysfunction in stressful situations, especially during induction of general anaesthesia.

Rapid advancement in telecommunication technology has made possible automatic periodic transmission of pacemaker and implantable defibrillator data to the attending physician (home monitoring). Furthermore, technology using remote control software allows, through device programmers, interrogation of the device memory, permitting remote monitoring by physicians or technical support of the manufacturer. Potential applications of these two capabilities include a close watch over the functioning of the devices, ability to obtain an earlier diagnosis (and management) of arrhythmic events, and assistance at the time of implant procedure and routine follow up. Finally these new tools raise several questions concerning safety aspects (including reliability of transmission, encrypted transfer, restricted access of the central database), economic aspects, and physician and manufacturer's liability.

Introduction et but de l’etude L’insuffisance cardiaque evolue dans 16% des cas vers un etat de denutrition caracterise par une perte importante du muscle squelettique, appelee cachexie cardiaque. La cachexie cardiaque pourrait faire intervenir de profondes modifications du metabolisme proteique, ainsi que des perturbations des fonctions mitochondriales au sein du muscle. Notre but etait donc d’etudier la proteosynthese et les fonctions mitochondriales de differents types musculaires (squelettiques types 1 et 2, cardiaque) durant la cachexie cardiaque chez le rat. Materiel et methodes Un infarctus du myocarde (IDM) a ete realise chez 7 rats LEWIS de 3 mois par ligature chirurgicale de l’IVA. La dysfonction ventriculaire gauche etait confirmee par echocardiographie. Un animal ayant maigri de plus de 7,5% etait considere comme cachectique cardiaque (CC) et etait alors sacrifie simultanement a un rat temoin sain (TS). Apres l’injection d’un traceur isotopique ([13C]valine), le sang, les muscles (soleus, gastrocnemius, tibialis anterior), le coeur, le foie et le tissu adipeux intra-abdominal etaient preleves. Le taux de synthese (FSR) des proteines mitochondriales etait calcule a partir de l’enrichissement en [13C]valine des proteines mesure par spectrometrie de masse. Les activites enzymatiques mitochondriales de la citrate synthase (CS) et de la cytochrome c oxydase (COX) etaient mesurees par spectrophotometrie. L’analyse statistique utilisait un test non parametrique de Mann-Withney. Resultats 6 rats sur les 7 ayant subi l’IDM sont devenus cachectiques, en moyenne en 85 jours. Le poids du foie etait statistiquement superieur dans le groupe CC par rapport aux TS (11,4±2,4 g vs 8,6±1,3 g, P Conclusions Cette etude confirme que la CC est associee a de profondes alterations de la fonction mitochondriale musculaire dans les muscles squelettiques de type oxydatif (soleus), associees a une augmentation de la vitesse de synthese des proteines de cet organite. Ce dernier phenomene pourrait etre lie a des mecanismes de compensation tentant de limiter les perturbations fonctionnelles.