Acute Type B Intramural Hematoma: Novel Insights in the Endovascular Era

Background: The 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. Methods: A retrospective analysis of a US Aortic Database identified 70 patients with TBIMH from 2008 to 2022. Patients were divided into groups and analyzed based upon subsequent management: early thoracic endovascular aortic repair (TEVAR; Group 1) or hospital discharge on optimal medical therapy (OMT) (Group 2). Results: Of 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 were as follows: 1) Penetrating atheroscletoic ulcer (PAU) or ulcer-like projection (n = 26); 2) Descending thoracic aortic aneurysm (n = 3); or 3) Progression to type B aortic dissection (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 as follows: 1) Development of a PAU / ulcer-like projection (n = 13); 2) Progression to TBAD (n = 3), or 3) Concomitant aneurysmal disease (n = 4). Twenty 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. Conclusions: The most common etiology of TBIMH is an intimal defect. Progression to TBAD and intramural hematoma 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-term and long-term outcomes.