Morphologic prognostic factor for thoracoabdominal aortic dilation after acute type A dissection repair.

OBJECTIVES: Risk factors for late-term aortic dilation after acute type A aortic dissection repair have not been well examined. The goal of this study was to determine the relationship between the abdominal aortic true lumen location and thoraco-abdominal aortic dilation after surgical repair for acute type A aortic dissection. METHODS: Patients who were preoperatively diagnosed with acute type A aortic dissection between April 2014 and July 2022 were included in this study. We evaluated the renal artery-level dissected aortic morphology and classified the study population into 2 groups: the ventral (those with the true lumen located on the ventral side) and the dorsal (other patients not assigned to the ventral group) groups, based on the location of the true lumen. Aortic dilation was defined as thoraco-abdominal aortic expansion ≥5 mm on 1-year postoperative computed tomography images. RESULTS: We examined 49 surgical patients who were assigned to the ventral (n = 22) and dorsal (n = 27) groups. The number of patients with ≥5 mm thoraco-abdominal aortic dilation after the operation was significantly higher in the ventral group than in the dorsal group (90.9% vs 51.9%, P = 0.009). The multivariable logistic regression analysis showed that the ventral type was an independent prognostic factor for thoraco-abdominal aortic dilation after the operation (odds ratio, 6.01; 95% confidence interval, 1.56-23.77; P = 0.009). CONCLUSIONS: The location of the true lumen of the abdominal aorta in acute type A aortic dissection may be a prognostic factor for thoraco-abdominal aortic dilation after surgical repair.

Recurrent and Multiple Intracerebral Hemorrhages in Polycythemia Vera Secondary to Myelofibrosis: A Case Report and Literature Review.

Polycythemia vera (PV) is one of the myeloproliferative neoplasms and has higher frequency of the JAK2 V617F mutation. Hemorrhagic stroke is rare in PV, and myelofibrosis is secondary to PV. A 76-year-old Japanese man was diagnosed as PV with the JAK2 V617F mutation at the age of 63 years. He developed anemia together with secondary myelofibrosis, and then 40 mg ruxolitinib was started at 70 years. At 76 years, he presented with apathy and was diagnosed with intracerebral hemorrhage (ICH) in the right thalamus. Six months later, he developed multiple ICHs in bilateral cerebellar hemispheres. Leukocyte count was 57,600/µL, platelet count was 66,000/µL, and the level of hemoglobin was 8.7 g/dL. Bleeding time was 6 min. The agglutination ability when adding collagen was 41%. A patient with the JAK2 V617F mutation developing hemorrhagic stroke due to late-stage PV and secondary myelofibrosis was reported, implying various mechanisms for recurrent and multiple ICH.