Ventricular tachycardia (VT) in structurally normal hearts or nonischemic cardiomyopathy can originate from the aortic sinuses of Valsalva (SoV). It is unknown whether VT can originate from the SoVs in patients with prior myocardial infarction (MI). To evaluate the prevalence, arrhythmogenic substrate, and ablation outcomes of postinfarction VT originating from the SoVs. Among 217 consecutive patients with postinfarction VT undergoing ablation, we identified 13 (6%) patients who had ≥1 VT mapped in a SoV. Control groups of 13 patients with idiopathic SoV VT and 13 postinfarction patients without SoV VT were included. In the study group, 17 VTs were mapped in a SoV (right n = 5, left-right commissure n = 6, left n = 6). SoV VT target sites had low bipolar voltage during sinus rhythm [median 0.42 (IQR: 0.16-0.53) mV] which was significantly lower than target sites in patients with idiopathic SoV VTs [median 1.02 (IQR: 0.89-1.52) mV; p < .001]. An area of endocardial low voltage was found below the aortic valve in all patients with postinfarction SoV VTs compared to 9 (69%) of the patients in the postinfarction control group without SoV VT (p = .02). Morphology characteristics of postinfarction SoV VTs differed from idiopathic SoV VTs. None of the postinfarction SoV VTs were inducible after ablation and none recurred after a median follow-up of 14 months. In patients with prior MI, VT can be targeted in an aortic SoV. The SoVs should be routinely investigated in postinfarction patients with inferior axis VT and an area of low voltage below the aortic valve.