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Surgical aortic specimens are usually examined in Pathology Departments as a result of treatment of aneurysms or dissections. A number of diseases, genetic syndromes (Marfan syndrome, Loeys–Dietz syndrome, etc.), and vasculopathic aging processes involved in vascular injury can cause both distinct and nonspecific histopathologic changes with degeneration of the media as a common denominator. Terminology for these changes has varied over time leading to confusion and inconsistencies. This consensus document has established a revised, unified nomenclature for the variety of noninflammatory degenerative aortic histopathologies seen in such specimens. Older terms such as cystic medial necrosis and medionecrosis are replaced by more technically accurate terms such as mucoid extracellular matrix accumulation (MEMA), elastic fiber fragmentation and/or loss, and smooth muscle cell nuclei loss. A straightforward system of grading is presented to gauge the extent of medial degeneration and synoptic reporting tables are provided. Herein we present a standardized nomenclature that is accessible to general pathologists and useful for future publications describing these entities.

Inflammatory diseases of the aorta include routine atherosclerosis, aortitis, periaortitis, and atherosclerosis with excessive inflammatory responses, such as inflammatory atherosclerotic aneurysms. The nomenclature and histologic features of these disorders are reviewed and discussed. In addition, diagnostic criteria are provided to distinguish between these disorders in surgical pathology specimens. An initial classification scheme is provided for aortitis and periaortitis based on the pattern of the inflammatory infiltrate: granulomatous/giant cell pattern, lymphoplasmacytic pattern, mixed inflammatory pattern, and the suppurative pattern. These inflammatory patterns are discussed in relation to specific systemic diseases including giant cell arteritis, Takayasu arteritis, granulomatosis with polyangiitis (Wegener's), rheumatoid arthritis, sarcoidosis, ankylosing spondylitis, Cogan syndrome, Behcet's disease, relapsing polychondritis, syphilitic aortitis, and bacterial and fungal infections. (C) 2015 Elsevier Inc. All rights reserved

s S315 Methods: Q-PCR analysis of CAV intima samples showed 5 miRs to have a significant up(miR-21, -223, and -146b-5p) or down-regulation (miR886-5p and -214) compared to control intima. The four main cell types within the intima (mononuclear cells, endothelial cells, vascular smooth muscle cells, and fibroblasts) were analyzed in vitro for their miR expression by Q-PCR. Using LNA-probes for In Situ Hybridization of these specific miRs the localization within each cell and between different cells types was determined in CAV tissue sections. Eight HTx-patients, with or without CAV, were included in this analysis. Results: Literature and in vitro experiments suggested two main cell categories that could express these miRs: miR-146b and -223 are mainly detected in immune cells and miR-21, -214, and -886-5p mainly in fibroblasts, smooth muscle, and/or endothelial cells. Most miRs show no or little expression in healthy coronary arteries. In CAV arteries miR-214 and -886-5p are highly expressed in macrophages. In more fibrotic CAV lesions less mR-214 and -886-5p was observed and the expression of miR-223 is highly increased in the extra cellular matrix. MiR-21 and -223 remain low, but when present located in elongated, probably fibroblast like, cells and lymphocytes, respectively. Conclusion: The type of cells positive for one miR did not change as CAV progresses, but because the cellular profile changes in the arterial wall, miR expression patterns change. This study confirms that these miRs play a role in the immunological or fibrotic process of CAV. Interfering with this miR expression could be an interesting new therapeutic approach. is too recent to document visitation. Altogether, the tutorial is available to over 1.2 billion people in their native language. The utility of the tutorial is being assessed through an on-line evaluation. Conclusion: The AECVP and SCVP have together generated the first complete web-tutorial for the interpretation of ACR on EMB available at www. scvp.net. With its translation into multiple languages, the tutorial has become the most universal treatise on acute cellular rejection. This should improve inter-institution agreement on cellular rejection.