Anatomy determines etiology in thoracic aortic aneurysm

Abstract

BACKGROUND: It is well established that thoracic aortic aneurysms (TAA) and abdominal aortic aneurysms (AAA) have different risk factors, clinical features, and genetic influences. Differences between and amongst subtypes of TAAs have received less attention. Despite observations of divergent clinical outcomes between ascending thoracic aortic aneurysms (ATAAs) and descending thoracic aortic aneurysms (DTAAs), etiologic factors determining the anatomic distribution of these aneurysms are not well understood.

METHODS: From 3,247 patients registered in an institutional Thoracic Aortic Center Database from July 1992 through August 2013, we identified 921 patients with full aortic dimensional imaging by CT or MRI scan with TAA > 3.5 cm and without evidence of aortic dissection (AoD). Patients were analyzed in three groups: isolated ATAA (n=677), isolated DTAA (n=97), and combined ATAA and DTAA (n=146).

RESULTS: Patients with a DTAA, alone or with coexistent ATAA, had significantly more hypertension (80.6% vs. 61.8%, p<.001) and a higher burden of atherosclerotic disease ( 86.7% vs. 7.5%, p<.001) ) and were more likely to be female (59.3% vs. 29.5%, P<.001). Conversely, patients with isolated ATAA were significantly younger (average age 59.5 vs. 71, p<.001), and contained almost every case of overt genetically-triggered TAA. Patients with isolated DTAA were demographically indistinguishable from patients with combined ATAA and DTAA. In follow up, patients with isolated DTAA, or with ATAA and DTAA, experienced significantly more aortic events (aortic dissection/rupture) and had higher mortality than patients with isolated ATAA.

CONCLUSIONS: Based on patient characteristics and outcomes, subtypes of TAA emerge. DTAA with or without associated ATAA or AAA appears to be a disease more highly associated with atherosclerosis, hypertension, and advanced age. In contrast, isolated ATAA appears to be a clinically distinct entity with a higher burden of genetically triggered disease. These data have important implications for familial screening recommendations for TAA.