Left ventricular idiopathic ventricular tachycardia can be terminated by intravenous verapamil infusion, hence the term verapamil-sensitive ventricular tachycardia. Left ventricular idiopathic ventricular tachycardia is caused by the formation of a folding loop in the distal segment of the posterior branch of the left bundle branch (left posterior branch) or the anterior branch (left anterior branch), the former being more common. Echocardiography reveals the presence of left ventricular pseudotendinous cords (a striated inotropic structure across the ventricular cavity that is not usually considered physiologically significant) in most patients and therefore suggests that pseudotendinous cords may be involved in the development of left ventricular idiopathic ventricular tachycardia, but not all patients with pseudotendinous cords develop left ventricular idiopathic ventricular tachycardia, so there is no more definitive evidence of a relationship between the two. Similar to right ventricular outflow tract ventricular tachycardia, left ventricular idiopathic ventricular tachycardia has a good prognosis and rarely (but may) cause serious complications such as sudden death. Long-term pharmacological treatment includes beta-blockers, verapamil, and thiazepam. Ablation may be considered for patients who fail to respond to medications or who do not want to take them. The location of ablation therapy is also determined by both pacing and agonist labeling. The ideal ablation target is located at the earliest point where the Purkinje potential (a specific electrical impulse signal) can be measured on the left ventricular septal surface or anterior wall during an episode of ventricular tachycardia. The success rate of ablation of left ventricular idiopathic ventricular tachycardia is over 90%.