The medial layer of the aorta confers elasticity and strength to the aortic wall and is composed of alternating layers of smooth muscle cells (SMCs) and elastic fibers. The SMC elastin-contractile unit is a structural unit that links the elastin fibers to the SMCs and is characterized by the following: 1. Layers of elastin fibers that are surrounded by microfibrils. 2. Microfibrils that bind to the integrin receptors in focal adhesions on the cell surface of the SMCs. 3. SMC contractile filaments that are linked to the focal adhesions on the inner side of the membrane. The genes that are altered to cause thoracic aortic aneurysms and aortic dissections encode proteins involved in the structure or function of the SMC elastin – contractile unit. Included in this gene list are the genes encoding protein that are structural components of elastin fibers and microfibrils, FBN1, MFAP5, ELN, and FBLN4. Also included are genes that are structural proteins in the SMC contractile unit, including ACTA2, which encodes SMC-specific α-actin and MYH11, which encodes SMC-specific myosin heavy chain, along with MYLK and PRKG1, which encode kinases that control SMC contraction. Finally, mutations in the gene encoding the protein linking integrin receptors to the contractile filaments, FLNA, also cause thoracic aortic disease. Thus, these data suggest that functional SMC elastin-contractile units are important for maintaining the structural integrity of the aorta.

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AKI after TAVR is associated with worse outcomes. Blood transfusion should be administered restrictively in TAVR. Patients with CKD, PAD, prior CABG, and TA approach require close surveillance as they are at risk for AKI through seven days after TAVR. doi: 10.1111/jocs.12768 (J Card Surg 2016;31:416-422).