“…2) In general, it is accepted that PM-LE indicates that replacement fibrosis seen after PM infarction results from occlusion of one or more feeder arteries. Given that PM-LE has been reported in patients with hypertrophic cardiomyopathy [7], cardiac sarcoidosis [11], and post cardiopulmonary resuscitation [9], PM-LE is not solely related to MI. Development of PM-LE probably results not only from coronary artery occlusion, but also from microcirculation impairment [21] and increased interstitial fibrosis associated with mechanical stress [22] within PMs due to severe LV remodeling.…”