Inappropriate shocks delivered by implantable cardiac defibrillators during oversensing of activity of diaphagmatic muscle

Two cases are reported (both men, one 72 and one 54 years old) of inappropriate shocks delivered by an implantable cardiac defibrillator (ICD) device, which oversensed the myopotentials induced by deep breathing and Valsalva manoeuvre. No damage to leads was associated with the oversensing of myopotentials. The mechanism of the inappropriate shocks was determined using real time electrograms. Modification of the duration of ventricular detection and decrease in sensitivity made it possible to avoid the oversensing of myopotentials and to deliver ICD treatment.

 Keywords: implantable cardiac defibrillator;  inappropriate shocks;  myopotential

Inappropriate shocks delivered by implantable cardiac defibrillators during oversensing of activity of diaphagmatic muscle

International audienceTwo cases are reported (both men, one 72 and one 54 years old) of inappropriate shocks delivered by an implantable cardiac defibrillator (ICD) device, which oversensed the myopotentials induced by deep breathing and Valsalva manoeuvre. No damage to leads was associated with the oversensing of myopotentials. The mechanism of the inappropriate shocks was determined using real time electrograms. Modification of the duration of ventricular detection and decrease in sensitivity made it possible to avoid the oversensing of myopotentials and to deliver ICD treatment

Antagonist-like activity of antibodies against the cardiac h5-HT4 receptor

International audienc

Catecholaminergic automatic activity in the rat pulmonary vein: electrophysiological differences between cardiac muscle in the left atrium and pulmonary vein.

International audienc

[Non-invasive exploration methods of supraventricular arrhythmia in current practice].

International audienceIn patients with supraventricular rhythm disorders ambulatory electro-cardiographic recording (Holter system) is an indispensable examination as it detects attacks that pass unrecorded by conventional ECG, being asymptomatic, too brief or too rare. It confirms the diagnosis, defines the factors triggering the attacks, detects the association of rhythm and conduction disorders, guides the treatment and monitors its effectiveness. Sequential ambulatory recording lends itself particularly well to this last objective. Biochemical examinations explain the cause of certain relapses (potassium depletion, high alcohol blood level) or detect the origin, clinically more or less obvious, of these disorders of rhythm (essays of thyroid hormones). Measuring blood levels of therapeutic drugs makes the handling of these various drugs safer. Finally, echocardiography detects an underlying heart disease, evaluates the size of the left atrium (a factor of relapse when it is dilated and of embolism when it harbours thrombi) and assesses the left ventricular function before administration of antiarrhythmics which, to varying extents, are all negative inotropic drugs

[Anti-arrhythmic therapy and cardiac failure].

International audienceIn cardiac failure, continuous ambulatory electrocardiographic recording for 24 hours (Holter system) enables detection of 60 to 80% of complex ventricular arrhythmias, 15 to 40% of atrial arrhythmias and sudden death accounts for about 40% of fatalities but its causes are multiple and sometimes unrelated to arrhythmias. Abnormalities of cardiac structure, metabolic and neuro-hormonal changes and some drug therapies are implicated in the genesis of these arrhythmias, the management of which is discussed in two different situations with respect to the functional incapacity: in paucisymptomatic ventricular arrhythmias in patients with cardiac failure, class I antiarrhythmics and d-sotalol should be avoided and betablockers prescribed with caution; the indications of amiodarone have not yet been determined. When the arrhythmia is symptomatic (sustained ventricular tachycardia or ventricular fibrillation), class I antiarrhythmics are not effective enough in the prevention of sudden death; betablockers and amiodarone may give good results but should be compared with implantable defibrillators in the future. The multiplicity and complexity of the mechanisms of arrhythmias in cardiac failure, and the inadequate results obtained with classical antiarrhythmics necessitate the development of new antiarrhythmics based on blockade of non-selective channels probably activated in cardiac failure by the stretching of myocardial fibres