Alternative Techniques for Treatment of Thoracic Aneurysms without Ideal Anatomy

The combination of open surgery and thoracic endovascular repair [TEVAR] are considered hybrid procedures, they are used today to solve the different pathologies of the thoracic aorta, these procedures are presented as a therapeutic alternative for those patients who are not candidates for a procedure conventional surgical procedure, either because they are considered “high risk” patients, due to their pathological history, or in those patients who present a complex anatomy that makes it difficult to complete the repair with endovascular therapies in its entirety. To familiarize ourselves with these therapies, we consider it important to classify them by anatomical segments according to the Ishimaru classification to facilitate their understanding.

Ascending Aortic Length and Its Association With Type A Aortic Dissection

Background The aim of this study was to determine the role of ascending aortic length and diameter in type A aortic dissection. Methods and Results Computed tomography scans from patients with acute type A dissections (n=51), patients with proximal thoracic aortic aneurysms (n=121), and controls with normal aortas (n=200) were analyzed from aortic annulus to the innominate artery using multiplanar reconstruction. In the control group, ascending aortic length correlated with diameter ( r 2 =0.35, P <0.001), age ( r 2 =0.17, P <0.001), and sex ( P <0.001). As a result of immediate changes in aortic morphology at the time of acute dissection, predissection lengths and diameters were estimated based on models from published literature. Ascending aortic length was longer in patients immediately following acute dissection (median, 109.7 mm; interquartile range [IQR], 101.0–115.1 mm), patients in the estimated predissection group (median, 104.2 mm; IQR, 96.0–109.3 mm), and patients in the aneurysm group (median, 107.0 mm; IQR, 99.6–118.7 mm) in comparison to controls (median, 83.2 mm; IQR, 74.5–90.7 mm) ( P <0.001 all comparisons). The diameter of the ascending aorta was largest in the aneurysm group (median, 52.0 mm; IQR, 45.9–58.0 mm), followed by the dissection group (median, 50.3 mm; IQR, 46.6–57.5 mm), and not significantly different between controls and the estimated predissection group (median, 33.4 mm [IQR, 30.7–36.7 mm] versus 35.2 mm [IQR, 32.6–40.3 mm], P =0.09). After adjustment for diameter, age, and sex, the estimated predissection aortic lengths were 16 mm longer than those in the controls and 12 mm longer than in patients with nondissected thoracic aneurysms. Conclusions The length of the ascending aorta, after adjustment for age, sex, and aortic diameter, may be useful in discriminating patients with type A dissection from normal controls and patients with nondissected thoracic aneurysms.

Regulation of SMC traction forces in human aortic thoracic aneurysms

Smooth muscle cells (SMCs) usually express a contractile phenotype in the healthy aorta. However, aortic SMCs have the ability to undergo profound changes in phenotype in response to changes in their extracellular environment, as occurs in ascending thoracic aortic aneurysms (ATAA). Accordingly, there is a pressing need to quantify the mechanobiological effects of these changes at single cell level. To address this need, we applied Traction Force Microscopy (TFM) on 759 cells coming from three primary healthy (AoPrim) human SMC lineages and three primary aneurysmal (AnevPrim) human SMC lineages, from age and gender matched donors. We measured the basal traction forces applied by each of these cells onto compliant hydrogels of different stiffness (4, 8, 12, 25 kPa). Although the range of force generation by SMCs suggested some heterogeneity, we observed that: 1. the traction forces were significantly larger on substrates of larger stiffness; 2. traction forces in AnevPrim were significantly higher than in AoPrim cells. We modelled computationally the dynamic force generation process in SMCs using the motor-clutch model and found that it accounts well for the stiffness-dependent traction forces. The existence of larger traction forces in the AnevPrim SMCs were related to the larger size of cells in these lineages. We conclude that phenotype changes occurring in ATAA, which were previously known to reduce the expression of elongated and contractile SMCs (rendering SMCs less responsive to vasoactive agents), tend also to induce stronger SMCs. Future work aims at understanding the causes of this alteration process in aortic aneurysms.

Bioinformatics analysis of common key genes and pathways of intracranial, abdominal, and thoracic aneurysms

Background Aneurysm is a severe and fatal disease. This study aims to comprehensively identify the highly conservative co-expression modules and hub genes in the abdominal aortic aneurysm (AAA), thoracic aortic aneurysm (TAA) and intracranial aneurysm (ICA) and facilitate the discovery of pathogenesis for aneurysm. Methods GSE57691, GSE122897, and GSE5180 microarray datasets were downloaded from the Gene Expression Omnibus database. We selected highly conservative modules using weighted gene co‑expression network analysis before performing the Gene Ontology, Kyoto Encyclopedia of Genes and Genomes pathway and Reactome enrichment analysis. The protein–protein interaction (PPI) network and the miRNA-hub genes network were constructed. Furtherly, we validated the preservation of hub genes in three other datasets. Results Two modules with 193 genes and 159 genes were identified as well preserved in AAA, TAA, and ICA. The enrichment analysis identified that these genes were involved in several biological processes such as positive regulation of cytosolic calcium ion concentration, hemostasis, and regulation of secretion by cells. Ten highly connected PPI networks were constructed, and 55 hub genes were identified. In the miRNA-hub genes network, CCR7 was the most connected gene, followed by TNF and CXCR4. The most connected miRNAs were hsa-mir-26b-5p and hsa-mir-335-5p. The hub gene module was proved to be preserved in all three datasets. Conclusions Our study highlighted and validated two highly conservative co-expression modules and miRNA-hub genes network in three kinds of aneurysms, which may promote understanding of the aneurysm and provide potential therapeutic targets and biomarkers of aneurysm.

Anatomic Suitability for Branched Thoracic Endovascular Repair in Patients with Aortic Arch Pathological Features

Background Endovascular repair has become a viable alternative for aortic pathological features, including those located within the aortic arch. We investigated the anatomic suitability for branched thoracic endovascular repair in patients previously treated with conventional open surgery for aortic arch pathological features. Methods and Results Patients who underwent open surgery for aortic arch pathological features at our institution between 2000 and 2018 were included. Anatomic suitability was determined by strict compliance with the anatomic criteria within manufacturers’ instructions for use for each of the following branched thoracic stent grafts: Relay Plus Double‐Branched (Terumo‐Aortic), TAG Thoracic Branch Endoprosthesis (W.L. Gore & Associates), Zenith Arch Branched Device (Cook‐Medical), and Nexus Stent Graft System (Endospan Ltd/Jotec GmbH). Computed tomography angiography images were analyzed with outer luminal line measurements. A total of 377 patients (mean age, 64±14 years; 64% men) were identified, 153 of whom had suitable computed tomography angiography images for measurements. In total, 59 patients (15.6% of the total cohort and 38.6% of the measured cohort) were eligible for endovascular repair using at least one of the devices. Device suitability was 30.9% for thoracic aneurysms, 4.6% for type A dissections, 62.5% for type B dissections, and 28.6% for other pathological features. Conclusions The anatomic suitability for endovascular repair of all aortic arch pathological features was modest. The highest suitability rates were observed for thoracic aneurysms and for type B dissections, of which repair included part of the aortic arch. We suggest endovascular repair of arch pathological features should be reserved for high‐volume centers with experience in endovascular arch repair.