Risk factors for target vessel endoleaks after physician-modified fenestrated or branched endovascular aortic repair for postdissection thoracoabdominal aortic aneurysms.

OBJECTIVE: Patients with postdissection thoracoabdominal aortic aneurysms (TAAAs) have been more likely to develop endoleaks than those with degenerative TAAAs after fenestrated or branched endovascular aortic repair (F/BEVAR). In the present study, we aimed to determine the risk factors for target vessel (TV)-related endoleaks after visceral segment F/BEVAR for postdissection TAAAs. METHODS: We performed a retrospective analysis of all patients with degenerative and postdissection TAAAs treated with F/BEVAR between 2017 and 2021. All the patients had undergone computed tomography angiography before and 3 months, 6 months, and annually after discharge. Two experienced vascular surgeons had used data from computed tomography angiography and vascular angiography to judge the presence of endoleaks. The study end points were mortality, aneurysm rupture, and the emergence of and reintervention for TV-related endoleaks. RESULTS: A total of 195 patients (mean age, 66 ± 10 years; 69% men) had undergone F/BEVAR for 99 postdissection TAAAs and 96 degenerative TAAAs. During a mean follow-up of 16 ± 12 months, we found that the patients with postdissection TAAAs were younger (age, 64 ± 10 years vs 69 ± 9 years; P = .001), had required more prior aortic repairs (58% vs 40%; P = .012), and had had a higher body mass index (26.1 ± 3.4 kg/m2 vs 24.8 ± 3 kg/m2; P = .008), a larger visceral segment aortic diameter (47.1 ± 7.5 mm vs 44.5 ± 7.5 mm; P = .016), and more TV-related endoleaks (18% vs 7%; P = .023) compared with those with degenerative TAAAs. Of the 99 patients with postdissection TAAAs, 327 renal-mesenteric arteries were revascularized using 12 scallops, 141 fenestrations, and 174 inner or outer branch stents. A total of 25 TV-related endoleaks were identified among 18 patients during follow-up, including 6 type Ic (retrograde from the distal end of the branch), 3 type IIIb (bridging stent fabric tear), and 16 type IIIc endoleaks (detachment or loose connection of the bridging stent). The patients with an endoleak had had a larger visceral aortic diameter (52.7 ± 6.4 mm vs 45.8 ± 7.2 mm; P < .001) and had undergone revascularization of more TVs (3.7 ± 0.7 vs 3.2 ± 0.9; P = .032). In contrast, true lumen compression did not seem to affect the occurrence of TV endoleaks (39% vs 27%; P = .323). The use of presewn branch stents in the fenestration position was associated with a lower risk of TV-related endoleaks (5% vs 11%; P = .025). In addition, TVs derived entirely or partially from the false lumen were more prone to the development of endoleaks after reconstruction (19% vs 4% [P < .001]; and 15% vs 4% [P = .047], respectively). CONCLUSIONS: We found that patients with postdissection TAAAs were more likely to have TV-related endoleaks after F/BEVAR in the visceral region than those with degenerative TAAAs. Additionally, patients with a larger aortic diameter and a greater number of fenestrations in the visceral region were more likely to have experienced TV-related endoleaks. Branch vessels deriving from the false lumen were also more likely to develop endoleaks after reconstruction, and prefabricated branch stents were related to a lower possibility of TV-related endoleaks.

[Effect of low density carotid plaque on the development of cerebral small vessel disease in patients with carotid stenosis].

Objective: To investigate the correlation between cerebral small vessel disease (CSVD) and carotid low-density plaque on multi-slice spiral CT angiography (MSCTA) in patient with carotid stenosis. Methods: The clinical data of 221 patients with carotid stenosis who admitted to Nanjing Drum Tower Hospital, the Affiliated Hospital of Nanjing University Medical School, from January 2016 to January 2021 were retrospectively analyzed. There were 195 males and 26 females, with the age of (70.0±8.4) years (range: 48 to 88 years). According to MRI, the patients were divided into carotid stenosis combined with CSVD group (the CSVD group) and carotid stenosis without CSVD group (the non-CSVD group). Lowest density in the carotid atherosclerotic plaque area (CAPALD) was analyzed by MSCTA. The t-test, Mann-Whitney U test and Chi-square test were used for comparison between the two groups. Univariate and multivariate Logistic regression analysis were performed on CAPALD and other clinical indicators with CSVD. Receiver operating characteristic (ROC) curves of CAPALD and CAPALD combined with the demographics (sex, age and body mass index) were plotted for predicting CSVD, and the area under the curve (AUC), sensitivity and specificity were calculated. Results: There were 169 patients in the CSVD group and 52 patients in the non-CSVD group. In the CSVD group, 88.8% (150/169) were males and 11.2% (19/169) were females, with the age of (70.5±8.2) years (range: 48 to 88 years). In the non-CSVD group, 86.5% (45/52) were males and 13.5% (7/52) were females, with the age of (68.4±9.1) years (range: 51 to 85 years). CAPALD and the score of Montreal cognitive assessment were lower in the CSVD group than those in the non-CSVD group (21.0 HU vs. 35.0 HU, Z=-3.760, P<0.01; 22.6±3.9 vs. 24.8±3.3, t=-2.064, P<0.05). Multivariate Logistic regression analysis showed that CAPALD was an independent factor for CSVD (OR=1.044, 95%CI:1.020 to 1.070, P<0.01). The AUC of the ROC curve for CAPALD predicting carotid stenosis with CSVD was 0.672 (P<0.01), with cut-off value of 34.5 HU, sensitivity of 82.8%, and specificity of 50.0%. The AUC of ROC curve for CAPALD combined with the demographics predicting CSVD was 0.733 (P<0.01), with sensitivity of 82.9% and specificity of 64.0%. Conclusions: The decreased CAPALD is a risk factor for CSVD in patients with carotid stenosis. The analysis of carotid plaque density by MSCTA may help to identify the patients at high risk of CSVD.

Risk factors for target vessel endoleaks after physician-modified fenestrated or branched endovascular aortic arch repair: A retrospective study.

Objective: Fenestrated or branched endovascular aortic arch repair (fb-arch repair) is an effective option for treating complex aortic arch lesions, including thoracic aortic aneurysms and aortic dissections. However, the relatively high rate of re-intervention due to target vessel (TV)-related endoleaks have raised concerns. This study aimed to determine risk factors for TV-related endoleaks after fb-arch repair. Methods: This was a retrospective analysis of all patients undergoing fb-arch repair between 2017 and 2021in nanjing drum tower hospital of China. All the patients underwent computed tomography angiography (CTA) before surgery; at discharge; and at 3 months, 6 months, and yearly post-discharge. All procedures are performed with physician modified grafts. Two experienced vascular surgeons used CTA and vascular angiography data to assess endoleaks. The study endpoints were mortality, aneurysm rupture, and emergence of and re-intervention for TV-related endoleaks. Results: During the follow-up period, 218 patients underwent fb-arch repair. There were seven perioperative deaths and four deaths during follow-up (two myocardial infarctions and two malignancies). There were nine additional patients who were excluded from the study (two strokes, three with abnormal aortic arch anatomy, and four with insufficient clinical data). Among the 198 patients considered (mean age, 59 ± 13.3 years; 85% male), 309 branch arteries were revascularized. A total of 35 TV-related endoleaks were identified in 28 patients during a mean follow-up of 23 ± 14 months (median 23, IQR 26.3): six type Ic, 4 type IIIb, and 20 type IIIc endoleaks. Patients in the endoleak group had greater aortic arch segment diameters (43.1 ± 5.1 vs. 40.3 ± 4.7; P = 0.004) and a greater number of TVs revascularized (2.0 ± 0.8 vs. 1.5 ± 0.8; P = 0.004) than those in the non-endoleak group. However, the morphological classification of the aortic arch did not seem to affect the occurrence of TV endoleaks (13%, 14%, and 15% for type І, II, and III aortic arches, respectively; P = 0.957). Pre-sewing branch stents in the fenestration position reduced the risk of TV endoleaks (5% vs. 14%; P = 0.037). Additionally, in TVs affected by aortic aneurysm or dissection, the risk of endoleaks increased after reconstruction (17% vs. 8%; P = 0.018). The incidence of secondary TV-related endoleaks after fb-arch repair was 14.1%. Conclusion: The data from this study showed that the incidence of secondary target vessel related endoleaks after fb-arch repair is approximately 14.1%. Additionally, patients with a larger aortic arch diameter or more revascularized arteries during surgery were at increased risk TV-related endoleaks. The target vessels originating from the false lumen or aneurysm sac are more prone to endoleaks after reconstruction. Finally, prefabricated branch stents reduced risk of TV-related endoleaks.

Oridonin attenuates low shear stress-induced endothelial cell dysfunction and oxidative stress by activating the nuclear factor erythroid 2-related factor 2 pathway.

BACKGROUND: Atherosclerosis (AS) is the primary cause of cardiovascular disease and the incidence is extremely common; however, there are currently few drugs that can effectively treat AS. Although oridonin has been widely used to treat inflammation and cancer for numerous years, to the best of our knowledge, its protective effect against AS has not been reported. Therefore, the present study aimed to investigate whether oridonin attenuated AS. METHODS: By using text mining, chemometric and chemogenomic methods, oridonin was predicted to be a beneficial agent for the treatment of AS. A parallel flow chamber was used to establish a low shear stress (LSS)-induced endothelial cell (EC) dysfunction model. Briefly, ECs were exposed to 3 dyn/cm2 LSS for 30 min and subsequently treated with oridonin or transfected with a small interfering RNA (siRNA) targeting nuclear factor erythroid 2-related factor 2 (NRF2). Reactive oxygen species (ROS), superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH) and glutathione disulfide (GSSG) in EA.hy926 cells were analyzed to determine the level of oxidative stress. The nitric oxide (NO) levels and mRNA expression levels of endothelial NO synthase (eNOS), endothelin-1 (ET-1) and prostaglandin synthase (PGIS) in EA.hy926 cells were analyzed to determine EC dysfunction. Furthermore, the mRNA and protein expression levels of NRF2 were analyzed using reverse transcription-quantitative PCR and western blot. In addition, zebrafish were fed with a high-cholesterol diet to establish a zebrafish AS model, which was used to observe lipid accumulation and inflammation under a fluorescence microscope. RESULTS: We found LSS led to oxidative stress and EC dysfunction; this was primarily indicated through the significantly decreased SOD and GSH content, the significantly increased MDA, GSSG and ROS content, the upregulated mRNA expression levels of ET-1, and the downregulated NO levels and mRNA expression levels of eNOS and PGIS in ECs. Notably, oridonin could improve LSS-induced oxidative stress and EC dysfunction, and the effects of oridonin were reversed by the transfection with NRF2 siRNA. Oridonin also attenuated lipid accumulation and neutrophil recruitment at the LSS regions in the zebrafish AS model. CONCLUSIONS: In conclusion, the results of the present study suggested that oridonin may ameliorate LSS-induced EC dysfunction and oxidative stress by activating NRF2, thereby attenuating AS.