Staging Endovascular Thoracic and Thoracoabdominal Aortic Aneurysm Repairs and the Risk of Post-operative Spinal Cord Ischemia.

OBJECTIVE: Staged aortic aneurysm repair is one method used to decrease the risk of spinal cord ischemia (SCI) following endovascular aortic intervention. Sequential sacrifice of arteries perfusing the spine may allow for improved spinal perfusion through the development of collateral networks over time. To evaluate the impact of staging endovascular aortic aneurysm repairs on SCI, we conducted a conservative analysis of Vascular Quality Initiative (VQI) data. METHODS: De-identified VQI data were queried for cases of endovascular thoracic and thoracoabdominal aneurysm repairs from year 2014 to 2019. Cases were selected based on inclusion criteria: aneurysmal disease, no ruptures, no prior aortic surgeries, no retreatments, and only cases with complete data on aortic zones and SCI. Chi-square, Student's t-tests, and Mann-Whitney U tests were used for univariable analyses, as appropriate. Logistic regression analyses were used to identify independent predictors of outcome. RESULTS: There were 116 staged aortic repairs (SARs) (8.2%) performed out of a total of 1421 endovascular aortic repairs that fit study criteria. The overall rate of SCI within the study cohort was 3.4% (n = 48). The distribution of SARs and SCI events according to aortic zone coverage are displayed in Table 1. Patients who underwent staged endovascular aortic repairs had higher rates of SCI, pre-op spinal drain placement, non-African-American race, COPD, smoking history, positive stress tests, aspirin and statin use, increased estimated blood loss, physician-modified endografts, number of aortic zones covered, lower pre-op hemoglobin levels, larger aneurysm sac size, fusiform aneurysms, and longer total procedure times, Table 2. After adjusting for factors associated with SCI, a priori, and factors with a P < 0.1 univariable analysis, SAR was not associated with SCI (odds ratio [OR] = 1.86, 95% confidence interval [CI] = 0.77-4.50, P = 0.17). Of the six factors associated with SCI on univariable analysis, only procedure time ≥6 hours (OR = 2.49, 95% CI = 1.09-5.70, P = 0.031) and the number of aortic zones covered (OR = 1.15, 95% CI = 1.00-1.32, P = 0.047) were predictive of SCI. Staged repairs had a lower proportion of permanent SCI (38%, 3 of 8 cases) compared with repairs that were not staged (68%, 27 of 40 cases), with a relative risk reduction of 44% for those who developed SCI, P = 0.21. CONCLUSIONS: In a large national data set, SARs were performed for patients with more extensive aortic disease. SARs were only performed in about 8% of cases and the rate of SCI remained low. After adjusting for baseline comorbidities, extent of aortic disease, and other factors that may potentiate SCI, staged aortic aneurysm repair had a similar risk of SCI compared with non-staged repairs. However, there was a trend toward decreased permanent SCI risk in the SAR group.

Alk3 mediated Bmp signaling controls the contribution of epicardially derived cells to the tissues of the atrioventricular junction.

Recent studies using mouse models for cell fate tracing of epicardial derived cells (EPDCs) have demonstrated that at the atrioventricular (AV) junction EPDCs contribute to the mesenchyme of the AV sulcus, the annulus fibrosus, and the parietal leaflets of the AV valves. There is little insight, however, into the mechanisms that govern the contribution of EPDCs to these tissues. While it has been demonstrated that bone morphogenetic protein (Bmp) signaling is required for AV cushion formation, its role in regulating EPDC contribution to the AV junction remains unexplored. To determine the role of Bmp signaling in the contribution of EPDCs to the AV junction, the Bmp receptor activin-like kinase 3 (Alk3; or Bmpr1a) was conditionally deleted in the epicardium and EPDCs using the mWt1/IRES/GFP-Cre (Wt1(Cre)) mouse. Embryonic Wt1(Cre);Alk3(fl/fl) specimens showed a significantly smaller AV sulcus and a severely underdeveloped annulus fibrosus. Electrophysiological analysis of adult Wt1(Cre);Alk3(fl/fl) mice showed, unexpectedly, no ventricular pre-excitation. Cell fate tracing revealed a significant decrease in the number of EPDCs within the parietal leaflets of the AV valves. Postnatal Wt1(Cre);Alk3(fl/fl) specimens showed myxomatous changes in the leaflets of the mitral valve. Together these observations indicate that Alk3 mediated Bmp signaling is important in the cascade of events that regulate the contribution of EPDCs to the AV sulcus, annulus fibrosus, and the parietal leaflets of the AV valves. Furthermore, this study shows that EPDCs do not only play a critical role in early developmental events at the AV junction, but that they also are important in the normal maturation of the AV valves.