Three-Channeled Aortic Dissection in a Patient without Marfan Syndrome.

A 64-year-old man was admitted for evaluation of back pain. He did not have a Marfan syndrome (MFS)-like appearance, and had a history of a type B aortic dissection and total arch replacement. A connective tissue disorder had been suspected because of the histologic findings of the resected aortic wall. On admission, a computed tomography (CT) scan demonstrated a three-channeled aortic dissection (3ch-AD) measuring 63 mm in diameter. We planned to perform elective surgery during his hospitalization. On the fourth hospital day, he complained of severe back pain, and enhanced CT scan revealed an aortic rupture. The patients with 3ch-AD often have MFS. However, even if they do not have an MFS-like appearance, clinicians should consider fragility of the aortic wall in patients with 3ch-AD. If the aortic diameter is enlarged, early surgery is recommended. In particular, if a connective tissue disorder is obvious or suspected, emergent surgery is warranted.

A Fever in Acute Aortic Dissection is Caused by Endogenous Mediators that Influence the Extrinsic Coagulation Pathway and Do Not Elevate Procalcitonin.

Objective A fever is observed in approximately one-third of cases of acute aortic dissection (AAD); however, the causes remain unclear. We investigated the mechanism of a fever in AAD by measuring the serum concentrations of inflammatory markers, mediators of coagulation and fibrinolysis, and procalcitonin, a marker of bacterial infection. Methods We retrospectively studied 43 patients with medically treated AAD without apparent infection. Patients were divided into those with (Group A; n=19) and without (Group B; n=24) a maximum body temperature >38°C. We established which patients fulfilled the criteria for systemic inflammatory response syndrome (SIRS), and its relationship with a fever was examined. Mediators of inflammation, coagulation and fibrinolysis were compared by a univariate analysis. Factors independently associated with a fever were established by a multivariate analysis. Results The criteria for SIRS were fulfilled in a greater proportion of patients in Group A (79%) than in Group B (42%, p=0.001). There was no difference in the procalcitonin concentration between Groups A and B (0.15±0.17 ng/mL vs. 0.11±0.12 ng/mL, respectively; p=0.572). Serum procalcitonin concentrations lay within the normal range in all patients in whom it was measured, which showed that the fever was caused by endogenous mediators. On the multivariate analysis, there was a borderline significant relationship between a fever and the prothrombin time-International Normalized Ratio (p=0.065), likely reflecting the extrinsic pathway activity initiated by tissue factor. Conclusion Our findings suggest that a fever in AAD could be caused by SIRS, provoked by endogenous mediators that influence the extrinsic coagulation pathway without elevating the serum procalcitonin concentration.