Arythmie ventriculaire

Extrasystoles ventriculaires isolées, répétitives ou organisées en tachycardie ventriculaire. La classification repose sur :

Des critères ECG

·      Extrasystoles ventriculaires : isolées ou répétitives, monomorphe ou polymorphe, à couplage long ou couplage court (cf. cf. Extrasystoles ventriculaires bénignes, Extrasystoles ventriculaires malignes)

·      Tachycardie ventriculaire : salve de > 3 ESV, non soutenue ou soutenue (> 30 sec) « commune » ou « spécifique » (TV fasciculaire, TV infundibulaire, TV catécholergique, TV bidirectionnelle, torsades de pointes, flutter ventriculaire ou fibrillation ventriculaire)

Des critères cliniques

·      mode déclenchement : au repos, à l’effort, après l’effort

·      symptômes : asymptomatique, symptômes minimes, pré-syncope, syncope, arrêt cardiaque (récupéré) ou mort subite

Le terrain cardiologique 

·      cœur structurellement normal

·      cardiopathie ischémique, cardiomyopathie, cardiopathie congénitale…

·      canalopathie (syndrome de Brugada, syndrome du QT long…)

·      existence d’un trouble métabolique ou toxique

Le mécanisme

·      Voir arythmie [2]

Traitement (2014) [3]


Vidéo (P.T.) sur la reconnaissance ECG des arythmies/cardiopathie du sujet jeune: Arythmie ventriculaire, Brugada, QT long



[1] Zipes DP et al. ACC/AHA/ESC guidelines for management of patients with ventricular arrhythmias and the prevention of sudden cardiac death—executive summary. Circulation 2006; 114;1088-1132. (téléchargeable)

[2] Binah O, Rosen MR. Mechanisms of ventricular arrhythmias. Circulation 1992; 85(1 Suppl):I25-31. Review. (pas d’accès on line) Ventricular arrhythmias may result from abnormalities of impulse initiation and/or impulse propagation. The former include automatic arrhythmias, which may occur at high (normal) levels of membrane potential or at low (abnormal) levels of membrane potential. They also include triggered activity, which may result from early (occurring before complete repolarization) or delayed (occurring after complete repolarization) afterdepolarizations. Arrhythmias resulting from abnormal impulse propagation may be reentrant, determined in part by anatomic or functional conduction block, or the result of reflection. The factors determining various arrhythmogenic mechanisms are discussed.

[3] Pedersen CT, et al; EP-Europace,UK. EHRA/HRS/APHRS expert consensus on ventricular arrhythmias. Heart Rhythm. 2014;11(10):e166-96

—> For treatment of patients with non-sustained VAs, we propose the following consensus recommendations. Expert consensus recommendations on non-sustained Vas

  • (1) Infrequent ventricular ectopic beats, couplets, and triplets without other signs of an underlying SHD or an inherited arrhythmia syndrome should be considered as a normal variant in asymptomatic patients. IIa LOE C
  • (2) An invasive electrophysiological study (EPS) should be considered in patients with significant SHD and non-sustained VAs especially if accompanied by unexplained symptoms such as syncope, near-syncope, or sustained palpitations IIa LOE C
  • (3) No treatment other than reassurance is needed for patients with neither SHD nor an inherited arrhythmogenic disorder who have asymptomatic or mildly symptomatic PVCs. I LOE C
  • (4) It is recommended to treat survivors of a myocardial infarction (MI) and other patient with reduced left ventricular (LV) function and non-sustained VAs with a betablocker unless these agents are contraindicated. I LOE A
  • (5) A therapeutic trial of beta-blockers may be considered in symptomatic patients with non-sustained VAs. IIb LOE C
  • (6) In suitable patients without SHD, a non-dihydropyridine calcium channel antagonist may be considered as an alternative to beta-blocker treatment. IIb C
  • (7) In patients who suffer from symptomatic non-sustained VAs on an adequately dosed beta-blocker or a nondihydropyridine calcium channel antagonist, treatment with an antiarrhythmic drug (AAD; amiodarone, flecainide, mexiletine, propafenone, sotalol) may be considered to improve symptoms associated with arrhythmia episodes. IIb LOE C (a) Flecainide and propafenone are not recommended to suppress PVCs in patients with reduced LV function (unless caused by ventricular ectopy itself), myocardial ischaemia, or myocardial scar. III LOE A (b) Sotalol should be used with caution in patients with chronic kidney disease and should be avoided in patients with a prolonged QT interval at baseline or with excessive prolongation of QT interval (40.50 s) upon therapy initiation. I LOE B (c) Amiodarone appears to have less overall proarrhythmic risk than other AADs in patients with heart failure and may be preferred to other membrane-active AADs unless a functioning defibrillator has been implanted. IIb LOE C
  • (8) Catheter ablation may be beneficial by improving symptoms or LV dysfunction in patients suffering from frequent nonsustained VAs (e.g. 4PVC 10 000 per 24 h) in patients with significant symptoms or LV dysfunction without another detectable cause. IIa LOE B
  • (9) Amiodarone, sotalol, and/or other beta-blockers are useful pharmacological adjuncts to implantation of a defibrillator (e. g. to reduce shocks) and to suppress symptomatic NSVT in patients who are unsuitable for ICD therapy, in addition to optimal medical therapy for patients with heart failure. IIb LOE B