Aortic Dissection Rethought: A New Classification System Adding Clarity and Allowing Prediction of In-Hospital Mortality

Objectives: The Stanford aortic dissection classification is helpful for an initial triage but does not take the location of the primary entry tear or the presence or absence of malperfusion into account.

Methods: We extended the Stanford aortic dissection classification (A and B) by the entity of Non-A-Non-B aortic dissection and defined subgroups including the location of the primary entry tear (E) and the presence or absence of malperfusion (M) adding 0 if a primary entry tear was not visible, adding 1 if the primary entry tear was located in the ascending aorta, adding 2 if in the arch and 3 if located in the descending aorta (E0, E1, E2, E3). Regarding malperfusion we added 0 if absent, 1 if malperfusion affected the coronary arteries, 2 if the supraaortic vessels were affected and 3 if visceral/ renal and/or extremity organ malperfusion was present (M0, M1, M2, M3). This new classification system was validated in 357 patients having had aortic dissection.

Results: The distribution was 59% for Type A, 31% for Type B, and 10% for Non-A-Non-B aortic dissection. The majority of Type A patients (80%) had primary entry tear in ascending aorta (E1). Nine per cent Type A patients had primary entry tear in the aortic arch (E2). Four percent had primary entry tear in the descending aorta (E3). In Non-A-Non-B patients, 44 and 53% had primary entry in the aortic arch (E2) and in the descending aorta (E3), respectively. In 17% Type B patients the location of primary entry tear could not be determined (E0) whereas 83% had their primary entry tear in the descending aorta (E3). Coronary malperfusion (M1) was observed only in patients with Type A dissection. Supraaortic malperfusion (M2) was most frequently (26%) seen in Type A E1 patients. In-hospital mortality was 16, 5, and 8% in A, B, and non-A non-B, respectively (p = 0.01). In-hospital mortality was 14, 21, and 0% in Type A E1, E2, and E3, respectively (p = 0.018). In-hospital mortality was 10 and 23% in Type A M0 and M3, respectively (p = 0.13). Postoperative stroke was 14, 1, and 3% in A, B, and non-A non-B, respectively (p < 0.001). Two years after dissection onset, the worst survival was observed in A, followed by non-A non-B and B patients (83 ± 3 vs. 88 ± 6 vs. 93 ± 3%, p = 0.042).

Conclusion: This extension and modification of the Stanford aortic dissection classification system adds clarity with regard to the extent of the disease process and allows an initial prediction of outcome regarding in-hospital mortality.

No conflict of interest has been declared by the author(s).