Idiopathic ventricular arrhythmias (VAs) with diverse mechanisms have been described in the left ventricle (LV).The predilection sites for these VAs are LV outflow tract, aortic cusps, mitral annulus, or epicardium (LV summit) and epicardial venous tissue (LV crux).Recently, idiopathic ventricular tachycardias (VT) or premature ventricular contractions (PVC) originating from the papillary muscles (PM) in the LV have been reported as a distinct clinical syndrome.[1][2][3][4][5][6][7] The elegant studies by Rawling et al. 8) showed that the PM has a rich network of Purkinje fibers, that the distribution of subendocardial Purkinje to ventricular muscle electrical coupling is spatially inhomogeneous, and that the junctional regions themselves have variable degrees of electrical coupling.They indicated that ventricular muscle activation by the Purkinje network occurs only at discrete, localized regions near the PM base.8)The PM has been known to be implicated in arrhythmogenesis of both idiopathic left VAs and VAs due to structural heart diseases.[1][2][3][4][5][6][7] Experimental studies showed that the PM is important in the generation and the maintenance of reentry during VT and VF as a spiral wave anchoring site that stabilizes wave conduction.9) These findings were confirmed again by Pak et al. 10) Idiopathic VAs from the PM are uncommon and rare in a sustained form.4) They are not reproducibly induced by programmed stimulation and sensitive to