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Objectives It is difficult to predict the evolution of uncomplicated type B intramural hematoma (IMHB) with a focal intimal disruption (FID) in the acute phase. The aims of this study were to investigate the predictors of FIDs and summarize the risk factors for the evolution of uncomplicated IMHB in the acute phase. Methods Eighty‐six patients with uncomplicated IMHB were included and were divided according to the development of an FID during the acute phase: the FID group (n = 32) and the no‐FID group (n = 54). Geometric measurements and computed fluid dynamic calculations were based on a computed tomography scan performed on admission. Multivariate logistic regression analysis was used to estimate the predictors of FID development. Results Thirty‐two (37%) patients developed an FID. Patients with an FID had higher C‐reactive protein levels (18.6 ± 2.3 vs 8.1 ± 0.2 mg/dL, P < 0.001) and white blood cell counts (10.3 ± 2.1 vs 7.5 ± 1.7 109/L, P < 0.001). The no‐FID group had lower occurrences of disease progression (15% vs 64%, P < 0.001) and aorta‐related mortality (6% vs 25%, P = 0.016). Multivariate logistic regression analysis indicated a significant risk for the occurrence of an FID with a larger maximum aortic diameter (OR, 1.35; 95% CI, 1.05‐1.73, P = 0.020), thicker hematoma (OR, 2.20; 95% CI, 1.40‐3.48, P = 0.001), and higher oscillatory shear index (per 0.01 unit, OR, 1.74; 95% CI, 1.21‐2.49, P = 0.003). The aorta‐related mortality during the acute phase was 25% (n = 8). Conclusions Certain aortic conditions, including ta larger aortic diameter, thicker hematoma and higher oscillatory shear stress, are associated with the FID development and result in worse clinical outcomes.

BackgroundSTAT1/4 has been suggested to be involved in cardiac allograft rejection. However, no direct evidence regarding STAT3 has been established in cardiac allograft rejection. Here, we hypothesized that inhibition of STAT3 attenuates cardiac allograft rejection.Material/MethodsTo test our hypothesis, homotopic mouse heart transplantation was carried out in syngeneic C57BL/6 to C57BL/6 strain mice with or without oral gavage with NSC 74859, an inhibitor of STAT3. The immune response was investigated using real-time PCR for CD4 and CD8 surface makers of T cells and CD14 of monocytes and cytokines, including IL-2, IL-15, and IL-6 of allografts at 3, 6, and 9 days after transplantation. Prognosis was also evaluated.ResultsWe found that allografts with oral gavage of NSC 74859 whose CD4, CD8 T, and CD14 monocytes were significantly lower than that of allograft without oral gavage of NSC 74859, and the same was true for the expression of IL-2, IL-15, and IL-6. Immunohistochemical analysis of grafts showed reduced infiltration of monocytes/macrophages into the graft myocardium. Survival was also markedly extended in the NSC 74859 group.ConclusionsInhibition of IL-6/STAT3 using NSC 74859 was shown to remarkably alleviate cardiac allograft rejection in mice, indicating that the target against IL-6/STAT3 pathway might be clinically used as an alternative therapy for cardiac allograft rejection.