With an increased risk of sudden death in ischemic and non-ischemic heart disease and the risk of arrhythmic events in patients with HCM. In addition, the occurrence of NSVT is a risk factor for sudden cardiac death. However, conventional ambulatory ECG recordings, which last up to 24 h, may underestimate the arrhythmic risk of HCM patients or miss NSVT events due to their relatively short duration. Conversely, HyT2 may be detected.1 month after the acute event, and this timing provides a clinical advantage because HyT2 detection may permit the identification of patients with electrical instability, who have a higher arrhythmic risk and require strict clinical surveillance and enhanced therapeutic effort, even when NSVT is absent on ECG recordings. Although HyT2 is a sign of myocardial edema on CMR, this relationship remains incompletely understood. In ischemic heart disease, myocardial edema occurs secondary to prolonged acute ischemic events. In the setting of acute myocardial infarction, edema highlights the presence of ischemic but viable myocardium surrounding necrotic areas, and the ratio between edema and the extent of necrosis is used to assess the myocardial salvage index. In myocarditis, HyT2 is considered a sign of active inflammation and is usually located in the subepicardial layer or in the midwall. HyT2 usually lasts one month after a myocardial infarction, whereas it may be detected 6 months after myocarditis. In our HCM patients, HyT2 was located in the midwall of hypertrophic myocardial segments and was localized with or without LGE. Previously, Melacini et al. hypothesized that these T2 abnormalities in HCM could be attributed to ischemia caused by microvascular dysfunction, impaired diastolic relaxation, mismatch between capillary density, myocardial tissue interstitial fibrosis and/or myocardial bridging. In this setting, prolonged ischemia involving the hypertrophic myocardial segments may cause small intramural, rather than subendocardial, myocardial Torin 1 1222998-36-8 damage, which presents on CMR as both HyT2 and LGE. HyT2 may be detectable in the acute/subacute phase but may subsequently disappear, while LGE may persist as a chronic scar. However, Frustaci and colleagues found histopathological evidence of acute myocarditis in biopsies in a significant fraction of their HCM cohort, which was related to the patient’s clinical status ; therefore, HyT2 may indicate the presence of inflammatory myocardial damage. The hypothesis that microvascular disease and ischemia result in HyT2 is strongly supported by the observation that the area of HyT2 closely matched the region of hypoperfusion based on the first-pass gadolinium CMR technique. Moreover, a global decrease in myocardial blood flow was previously demonstrated in patients with HCM in CMR and positron emission tomography studies. Specifically, the extent of LGE was inversely related to the global myocardial blood flow, suggesting a close relationship between ischemic events and chronic myocardial damage. Furthermore, repetitive episodes of ischemia could explain the rapid progression of myocardial fibrosis in HCM, as recently demonstrated. In the current study, we detected HyT2 in 42% of patients with HCM. In particular, patients with HyT2 demonstrated higher LV mass indexes, lower ejection fractions and a greater extent of LGE than those without HyT2. Moreover, patients with HyT2 had more arrhythmic risk factors than those without. Together, these findings suggest the presence of more advanced disease in patients with HyT2. A higher LV mass index has also been associated with microvascular disease, a lower blood supply/demand ratio and increased interstitial fibrosis.