Catheter Ablation of Ventricular Arrhythmias: Clinical Vignettes
نویسندگان
چکیده
Ventricular arrhythmias (VA) can develop in patients with structural heart disease (SHD) including prior myocardial infarction and nonischemic cardiomyopathy. When VAs manifest in structurally normal hearts, they are usually a result of intra-cellular calcium overload (triggered activity) or an abnormal response to adrenergic stimulation (automaticity).1 Reentry within the Purkinje fibers and specialized conduction system causes ~ 5% of all VAs in patients undergoing catheter ablation.2 This may occur in patients with severe dilated cardiomyopathy due to idiopathic or valvular heart disease etiologies, or in ischemic heart disease in which damaged His-Purkinje fibers can facilitate macro-reentrant bundle-branch reentry VT. In patients without structural heart disease, intra-fascicular reentry involving a portion of the LV Purkinje fibers can lead to VT. This most commonly is associated with the left posterior fascicle giving rise to a characteristic narrow complex right bundle branch block (RBBB) superior axis QRS configuration (Belhassen’s VT).
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