Aichi Medical University

Spinal cord ischemia (SCI) is a serious complication after thoracic endovascular aortic repair (TEVAR). However, the pathophysiology of SCI after TEVAR is not fully understood. The aim of this study was to evaluate the association between the density of mural thrombi in the descending thoracic aorta (DTA) and SCI.

Clinical data from all patients who underwent TEVAR at 9 institutions between October 2008 and December 2022 were retrospectively reviewed. At each institution, all patients who developed SCI were included, and an equal number of patients without SCI were included in the control group. This approach aimed to minimize the influence of treatment length, which is widely recognized as one of the most significant risk factors for SCI. We analyzed preoperative computed tomography angiography (CTA) images. We used the plaque analysis module of the workstation to distinguish the sites of mural thrombi distributed throughout the DTA. The volume of each defined tissue category was automatically calculated. A low-density thrombus (LDT) was < 30 Hounsfield unit (HU), an intermediate-density thrombus was ≥ 30 but < 150 HU, and a high-density thrombus was > 150 HU.

Thirty-two patients with SCI and 32 patients without SCI were included in the study. Univariate analysis revealed that total thrombus volume (P = 0.032) and LDT volume (P = 0.006) were significantly higher in SCI group. Multivariate analysis revealed that the LDT volume was the only predicter of SCI.

We observed that LDT in the DTA is associated with SCI after TEVAR. This data indicated that the mechanism of SCI after TEVAR may be related to embolism of vulnerable thrombi in the DTA.

To evaluate the dose-dependent renoprotective effects of sacubitril/valsartan in heart failure patients. This retrospective observational study included patients with heart failure (Stage B or higher, B-type natriuretic peptide (BNP) >100 pg/mL or N-terminal proBNP >300 pg/mL) who initiated sacubitril/valsartan (SV) treatment. Patients were classified by final SV daily dose (50, 100, 200, or 400 mg) at 18 months. Factors associated with eGFR changes were identified using multiple regression analysis. A total of 157 patients (mean age 74.8-77.9 years, 64.3% male) were stratified by daily SV dosage groups (50 mg, n = 20; 100 mg, n = 46; 200 mg, n = 62; 400 mg, n = 29). Baseline characteristics were similar across groups for eGFR, heart failure stage, diabetes history, myocardial infarction, atrial fibrillation, proteinuria, and use of most heart failure medications. However, hypertension prevalence and systolic blood pressure differed significantly between groups (p < 0.05). One-way ANOVA revealed significant dose-dependent differences in eGFR changes among SV dosage groups (p < 0.05). In the final multiple linear regression model, SV dosage (p < 0.05) was a significant factor associated with eGFR changes, with proteinuria showing a trend toward significance. Sex and BNP levels ≥400 pg/dL were not significant. Sensitivity analysis converting SV dosage to a categorical variable confirmed these findings. Stratification by proteinuria status demonstrated dose-dependent relationships in both proteinuria-positive and proteinuria-negative subgroups, with more pronounced dose dependency in the proteinuria-positive group (p < 0.001). SV exhibits dose-dependent renoprotective effects in heart failure patients. Optimizing SV dosage may be beneficial for heart failure patients with concurrent kidney dysfunction, especially those with proteinuria.