Endovascular Vertebral Artery Transposition Using Flow Reversal Technique for Left Subclavian Artery Stump Syndrome.

BACKGROUND: Cerebellar strokes are a rare complication related to thoracic endovascular aortic repair (TEVAR). This can manifest in an indolent manner or as a neurological catastrophe. Often it is unclear when a surgical intervention would be needed. Patients at risk for this relatively rare complication are not easily identified. CASE: We describe an endovascular option with flow reversal for left vertebral artery transposition using stent grafts for relocating arterial inflow and excluding a floating thrombus at the proximal subclavian artery (SCA) related to a previous TEVAR. CONCLUSIONS: Ligation of the subclavian artery proximal to the vertebral artery should be considered when performing a carotid subclavian bypass for elective TEVAR. This case details a unique, less invasive approach for vertebral artery transposition and thrombus exclusion in a high-risk patient with previous neck dissection.

Hybrid approach to deep vein arterialization as an adjunct for patients with severe medial calcinosis.

Patients with no-option chronic limb-threatening ischemia are not candidates for conventional revascularization options and will inevitably require major amputation. Deep venous arterialization (DVA) is a potential option for these patients. A complete endovascular system to perform DVA has recently received great acclaim and US Foor and Drug Administration approval. However, patients with severe tibial medial calcinosis such as those with diabetes or renal failure may not be candidates for this because most endovascular needles cannot penetrate severe calcium. Here we describe a novel hybrid approach to DVA that provided technical success in three patients with end-stage renal disease and severe medial calcinosis.

LRP1 protects against excessive superior mesenteric artery remodeling by modulating angiotensin II-mediated signaling.

Vascular smooth muscle cells (vSMCs) exert a critical role in sensing and maintaining vascular integrity. These cells abundantly express the low-density lipoprotein receptor-related protein 1 (LRP1), a large endocytic signaling receptor that recognizes numerous ligands, including apolipoprotein E-rich lipoproteins, proteases, and protease-inhibitor complexes. We observed the spontaneous formation of aneurysms in the superior mesenteric artery (SMA) of both male and female mice in which LRP1 was genetically deleted in vSMCs (smLRP1-/- mice). Quantitative proteomics revealed elevated abundance of several proteins in smLRP1-/- mice that are known to be induced by angiotensin II-mediated (AngII-mediated) signaling, suggesting that this pathway was dysregulated. Administration of losartan, an AngII type I receptor antagonist, or an angiotensinogen antisense oligonucleotide to reduce plasma angiotensinogen concentrations restored the normal SMA phenotype in smLRP1-/- mice and prevented aneurysm formation. Additionally, using a vascular injury model, we noted excessive vascular remodeling and neointima formation in smLRP1-/- mice that was restored by losartan administration. Together, these findings reveal that LRP1 regulates vascular integrity and remodeling of the SMA by attenuating excessive AngII-mediated signaling.