BackgroundThe pathophysiology and behavior of acute type B intramural hematoma (TBIMH) is poorly understood. The purpose of this study is to characterize the pathophysiology, fate and outcomes of TBIMH in the endovascular era. MethodsA retrospective analysis of a U.S. Aortic Database identified 70 patients with TBIMH from 2008-2022. Patients were divided into groups and analyzed based upon subsequent management: early thoracic endovascular aortic repair(TEVAR; Group 1) or hospital discharge on OMT(Group 2). ResultsOf 70 total patients, 43%(30/70) underwent TEVAR(Group 1) and 57%(40/70) were discharged on OMT(Group 2). There were no significant differences in age, demographics, or comorbidities between groups. Indications for TEVAR in Group 1:1)Penetrating aortic ulcer(PAU) or ulcer-like projection(ULP)(n=26); 2)Descending thoracic aortic aneurysm(n=3); or 3)Progression to TBAD(n=2). Operative mortality was zero. No patient suffered a stroke or spinal cord ischemia. During the follow-up period, 50%(20/40) of Group 2 patients required delayed surgical intervention, including TEVAR in 14 patients and open repair in 6 patients. Indications for surgical intervention were:1)Development of a PAU/ULP(n=13); 2)Progression to TBAD(n=3), 3)Concomitant aneurysmal disease(n=4). 20 patients did not require surgical intervention. Of the initial cohort, 71% of patients required surgery, 9% progressed to TBAD, and 19% had regression or stability of TBIMH with OMT alone. ConclusionsThe most common etiology of TBIMH is an intimal defect. Progression to TBAD and IMH regression without an intimal defect occurs in a small percentage of patients. An aggressive strategy with endovascular therapy and close surveillance for TBIMH results in excellent short and long-term outcomes.