Acute aortic dissection is a cardiovascular emergency that requires prompt diagnosis and treatment. Helical computed tomography (CT) allows diagnosis of acute aortic dissection with a sensitivity and specificity of nearly 100%. With helical CT, a dissection involving the ascending aorta (type A in the Stanford classification) can be differentiated from one distal to the left subclavian artery (type B). Helical CT can also be used to identify atypical forms of aortic dissection such as intramural hematoma, penetrating atherosclerotic ulcer, ruptured type B dissection, and atypical configurations of the intimal flap. Helical CT is useful in follow-up of aortic dissection by allowing assessment of early and late changes after surgery or medical treatment. Such changes include postoperative complications of type A dissection, healing of intramural hematoma, progression of intramural hematoma, and aneurysms of the true or false lumen. Helical CT can also be used to monitor potentially life-threatening ischemic complications of abdominal branch vessels.

Intramural haematoma mortality in the first 3 months of evolution is high (19%). Maximum aortic diameter >50 mm and ascending aorta involvement are predictive of early mortality.

BACKGROUND Undifferentiated pleomorphic sarcoma (UPS) constitutes the most common subtype of soft tissue sarcoma. However, UPS is clinically and molecularly poorly understood, in great extent due to its intrinsic phenotypic and cytogenetic complexity, which in turn results in the absence of specific prognostic or predictive biomarkers. The RAS/mitogen‐activated protein kinases (MAPK) and phosphoinositide 3‐kinase inhibitor (PI3K)/mammalian target of rapamycin (mTOR) pathways are considered to be 2 major mechanisms for sarcoma proliferation and survival and to the authors' knowledge their role in UPS remains unclear. The objective of the current study was to investigate whether the RAS/MAPK and PI3K/mTOR pathways are activated in UPS, and whether pathway activation is associated with outcome. METHODS Records for patients diagnosed and treated for UPS in the study institution between 2000 and 2009 were reviewed. Phosphorylation status of 4E‐binding protein (4E‐BP1), eukaryotic translation initiation factor 4E (eIF‐4E), S6‐RP, and ERK 1/2, together with total forms of 4E‐BP1 and eIF‐4E, were assessed using immunohistochemistry in paraffin‐embedded tumor tissue. Mutational analysis for KRAS; NRAS; BRAF; and phosphatidylinositol‐4,5‐bisphosphate 3‐kinase, catalytic subunit alpha (PIK3CA) oncogenic mutations was performed as well. RESULTS Critical lymph nodes within the RAS/MAPK and PI3K/mTOR pathways were found to be activated in >80% of UPS cases. Hyperactivation of the RAS/MAPK pathway, as assessed by expression of phosphorylated ERK 1/2, was found to independently predict a higher risk of disease recurrence and impaired overall survival. Only a KRAS A146V mutation was detected in 1 tumor. CONCLUSIONS The RAS/MAPK and PI3K/mTOR pathways are activated in the majority of cases of UPS. The RAS/MAPK pathway distinguishes a subgroup of patients with localized UPS with a worse outcome. Cancer 2016;122:99–107. © 2015 American Cancer Society.

This pilot trial has not found differences between triflusal and aspirin in the prevention of vascular complications after TIA or ischemic stroke, although given the wide CI, potentially important group differences could not be ruled out. Triflusal may be associated with a lower risk of hemorrhagic complications. A larger, prospective clinical trial is necessary to verify these results.

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