[Rhythmic pitfalls in cardiac pacing]. / Pièges rythmologiques en stimulation cardiaque.

Some electrocardiographic appearances in cardiac pacing may suggest pacemaker dysfunction but in fact the unit may be functioning normally or have a minor fault which is easy to correct by reprogramming. A pacing rate different to that programmed may be due to the rate-response hysteresis or rate smoothing functions. Irregular pacing is often due to phenomena of inappropriate sensing. A pacemaker in the bipolar AAI mode may seem to have no output if the spike is not visible: function in AAI mode should not be interpreted as pacing catheter displacement. The practician may wrongly interpret faulty ventricular sensing in patients with AAI pacemakers and atrial fibrillation when irregular pacing is observed or when ventricular extrasystoles do not inhibit the pacemaker. In dual chamber pacing, the blanking period may result in inadequate ventricular stimulation. The phenomenon of crossed detection or cross-talk is a cause of inappropriate inhibition. Applications of the magnet blocks the sensing function: the magnet pacemaker rate is an indicator of pacemaker end of life. In fact, the magnet induces different behaviours depending on the model of pacemaker which makes it essential to know the special characteristics of each pacemaker. The application of the magnet may trigger arrhythmias or no output of pacemakers at the end of life. The A-V interval may vary with respect to its response to the heart rate, when there is a hysteresis function of the A-V interval, sensing in the "safety" gap or when anti-atrial trachycardia algorithms are activated. The acceleration of a dual-chamber pacemaker may be related to electronic reentrant tachycardia or to an atrial tachycardia: a fault or delayed activation of various anti-arrhythmic algorithms may also cause difficulties in the interpretation of the electrocardiogram.

[Intrinsic sinus node dysfunction in adolescence during anorexia nervosa]. / Dysfonction sinusale intrinsèque de l'adolescence au cours d'une anorexie mentale.

A seventeen year old girl with anorexia nervosa (32 kg; 165 cm) was admitted as an emergency after syncope with severe bradycardia resistant to atropine monitored over a one week period. Autonomic blockade confirmed the intrinsic character of the sinus node dysfunction with chronotropic incompetence on exercise. Secondarily, a Mobitz I second degree AVB was observed. A DDDR pacemaker was implanted with an excellent functional result. With a one year follow-up, the bradycardia persists but body weight has increased. The authors discuss the physiopathology of this case: in the literature, the classical bradycardia of anorexia nervosa is sensitive to vagolytic drugs and only exceptionally as intense as in this patient. Sinus node dysfunction is very rare in the young in the absence of congenital heart disease. It is possible that the bradycardia had become chronic in this case.