Ventricular False Tendons and Ventricular Arrhythmias: Distinguishing Incidental Findings From Culprit Substrates

Ventricular false tendons are fibrous or fibromuscular cords that cross the ventricular cavity. Some contain Purkinje tissue and have been implicated in premature ventricular complexes, left posterior fascicular ventricular tachycardia, and, rarely, ventricular fibrillation. However, false tendons are also common in healthy hearts, so their visibility does not establish causality. This narrative review critically appraises the evidence and addresses three unresolved mechanistic questions. First, it is unclear whether a posteroseptal tendon forms the circuit of fascicular tachycardia or carries part of the adjacent Purkinje network. Control data are lacking, and ablation lesions involve both structures. Second, the slow, decremental, and verapamil-sensitive conduction of the P1 pathway may reflect abnormal Purkinje tissue, reduced electrical coupling, or mixed tissue composition. Third, successful ablation sites cluster at tendon insertions. We propose a junctional hypothesis in which the insertion, where a thin Purkinje-containing cord must depolarize a large myocardial mass, may form an arrhythmogenic interface. This model is untested but may account for insertion-based targets, verapamil sensitivity, and exit shifts. We also propose a graded framework that classifies a tendon as an unlikely, possible, probable, or definite culprit. A definite grade requires concordant anatomical, electrical, imaging, and procedural evidence plus at least one observation that separates the tendon from adjacent tissue. By these criteria, most reported culprit tendons are probable rather than definite. A false tendon is best regarded as a visible segment of the Purkinje network whose arrhythmogenic potential may depend on how and where it couples to the myocardium.