[Ventricular tachycardia--etiology, mechanisms and therapy]

Prevention and therapy of cardiovascular diseases have undergone enormous changes over the last decades. However, ventricular tachycardias (VT) still pose a major problem in a number of cardiac patients. Analysis of the etiology and mechanism of the tachycardia is of paramount importance for initiation of specific therapies. The morphology of VTs on the surface ECG can be either polymorphic or monomorphic. Polymorphic VTs have a constantly changing QRS-morphology due to the variable ventricular activation, without specific origin. This kind of VT is mainly caused by an acute, often reversible condition, such as ischemia or QT-prolongation. These VTs are potentially malignant, they cannot be treated by catheter ablation. In contrast, monomorphic VTs have a constant QRS-morphology, indicative of repetitive ventricular depolarisation in the same activation sequence. This kind of VT is either caused by focal abnormal activity (triggered activity, automaticity, micro-reentry) or by an arrhythmogenic substrate (macro-reentry). Focal idiopathic VTs usually have a benign prognosis and catheter ablation is potentially curative. The majority of ventricular arrhythmias, however, are substrate-related reentry tachycardias, most commonly based on an infarct scar Therapy of first choice for these patients is the treatment with an implantable Cardioverter/Defibrillator (ICD). Catheter ablation is indicated in case of drug refractory recurrent VTs triggering repeated ICD therapies. The different therapeutic strategies are not alternative but complementary options in many patients.