Thoracic endovascular aortic repair for symptomatic penetrating aortic ulcers and intramural hematomas is associated with poor outcomes

• Published in: Journal of vascular surgery Vol. 74; no. 1; pp. 63 - 70.e1
• Main Authors: Rokosh, Rae S., Rockman, Caron B., Patel, Virendra I., Milner, Ross, Osborne, Nicholas H., Cayne, Neal S., Jacobowitz, Glenn R., Garg, Karan
• Format: Journal Article
• Language: English
• Published: United States Elsevier Inc 01.07.2021
• Subjects: Intramural hematoma; Penetrating aortic ulcer; Thoracic endovascular aortic repair; Intramural hematoma; Thoracic endovascular aortic repair; Penetrating aortic ulcer
• ISSN: 0741-5214; 1097-6809
• DOI: 10.1016/j.jvs.2020.11.045

The natural history of penetrating aortic ulcers (PAUs) and intramural hematomas (IMHs) of the aorta has not been well described. Although repair is warranted for rupture, unremitting chest pain, or growth, no threshold has been established for treating those found incidentally. Thoracic endovascular aortic repair (TEVAR) offers an attractive approach for treating these pathologic entities. However, the periprocedural and postoperative outcomes have not been well defined. Patients aged ≥18 years identified in the Vascular Quality Initiative database who had undergone TEVAR for PAUs and/or IMHs from January 2011 to February 2020 were included. We identified 1042 patients, of whom 809 had follow-up data available. The patient demographics and comorbidities were analyzed to identify the risk factors for major adverse events (MAEs) and postoperative and late mortality. The cohort was 54.8% female, and 69.9% were former smokers, with a mean age of 71.1 years. Comorbidities were prevalent, with 57.8% classified as having American Society of Anesthesiologists class 4. Of the 1042 patients, 89.8% had hypertension, 28.3% chronic obstructive pulmonary disease, 17.9% coronary artery disease, and 12.2% congestive heart failure. Patients were predominately symptomatic (74%), and 44.5% had undergone nonelective repair. The MAE incidence was 17%. The independent predictors of MAEs were a history of coronary artery disease, nonwhite race, emergent procedural indication, ruptured presentation, and deployment of two or more endografts. In-hospital mortality was 4.3%. Of the index hospitalization mortalities, 73% were treatment related. For the 809 patients with follow-up (mean, 25.1 ± 19 months), the all-cause mortality was 10.6%. The predictors of late mortality during follow-up included age >70 years, ruptured presentation, and a history of chronic obstructive pulmonary disease and end-stage renal disease. A subset analysis comparing symptomatic (74%) vs asymptomatic (26%) patients demonstrated that the former were frequently women (58.2% vs 45.3%; P < .001), with a greater incidence of MAEs (20.6% vs 6.9%; P < .001), including higher in-hospital reintervention rates (5.9% vs 1.5%; P = .002) and mortality (5.6% vs 0.7%; log-rank P = .015), and a prolonged length of stay (6.9 vs 3.7 days; P < .0001), despite similar procedural risks. During follow-up, late mortality was greater in the symptomatic cohort (12.2% vs 6.5%; log-rank P = .025), with all treatment-related mortalities limited to the symptomatic group. We found significantly greater morbidity and mortality in symptomatic patients undergoing repair compared with asymptomatic patients, despite similar baseline characteristics. Asymptomatic patients treated with TEVAR had no treatment-related mortality during follow-up, with the overall prognosis largely dependent on preexisting comorbidities. These findings, in conjunction with increasing evidence highlighting the risk of disease progression and attendant morbidity associated with these aortic entities, suggest a need for natural history studies and definitive guidelines on the elective repair of IMHs and PAUs.