The impact of endovascular treatment on clinical outcomes of stable symptomatic patients with spontaneous superior mesenteric artery dissection.

OBJECTIVE: To evaluate the efficacy and clinical outcomes of endovascular treatment for superior mesenteric artery dissection (SMAD) and its effect on superior mesenteric artery (SMA) remodeling compared with medical management alone after successful initial medical management. METHODS: In this retrospective analysis, all patients with spontaneous SMAD at a single institution were identified from March 2007 to August 2019. The primary outcomes were freedom from major adverse events (MAEs, a composite of dissection-related death, the recurrence of mesenteric ischemia symptoms, and a requirement for intervention). The secondary outcomes were morphologic remodeling of the dissections and stenosis or occlusion of the SMA. RESULTS: A total of 94 patients with SMAD who underwent successful initial medical management (91 males; mean age, 50.4 ± 6.3 years) were enrolled in the study. Fifty-seven (60.6%) received medical management alone, and 37 (39.4%) underwent endovascular repair after initial medical management. In the endovascular group, the technical success rate was 86.5% (32 of 37). During a mean follow-up period of 33.6 ± 26.2 months (range, 1-120 months), nine (9.6%) patients experienced a recurrence of abdominal pain, and six had additional interventions for SMAD. The patients in the endovascular group showed more complete or partial remodeling (22 [81.1%] vs 24 [44.4%]; P < .0001) or unchanged dissections (5 [13.5%] vs 23 [42.6%]; P = .0001) than those in the conservative group. Survival analysis showed that the estimated MAE-free survival rates were 95.6%, 88.9%, and 85.4% at 1, 3, and 5 years, respectively. There was a higher freedom from SMA stenosis or occlusion in the endovascular group (log rank P = .046). CONCLUSIONS: Endovascular treatment and medical management alone result in similar MAE-free survival for patients with SMAD after successful initial medical management. Moreover, endovascular therapy is associated with a higher complete remodeling rate and greater freedom from SMA stenosis or occlusion.

Betanin Prevents Experimental Abdominal Aortic Aneurysm Progression by Modulating the TLR4/NF-κB and Nrf2/HO-1 Pathways.

Betanin, a bioactive ingredient mostly isolated from beetroots, exhibits a protective effect against cardiovascular diseases. However, its effects on abdominal aortic aneurysm (AAA) have not been elucidated. In this study, an AAA model was constructed by infusion of porcine pancreatic elastase in C57BL/6 mice. Mice were then administered with betanin or saline intragastrically once daily for 14 d. Our results showed that treatment with betanin remarkably limited AAA enlargement and mitigated the infiltration of inflammatory cells in the adventitia. The increased expression of proinflammatory cytokines and matrix metalloproteinases (MMPs) was also significantly alleviated following betanin treatment. Furthermore, betanin suppressed the activation of toll-like receptor 4 (TLR4)/nuclear factor-kappaB (NF-κB) signaling in the aortic wall, and downregulated the levels of tissue-reactive oxygen species as well as circulating 8-isoprostane by stimulating the nuclear factor-E2-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway. Taken together, these data suggest that betanin may attenuate AAA progression and may be used as a therapeutic drug against AAA.

Paeonol Ameliorates Abdominal Aortic Aneurysm Progression by the NF-κB Pathway.

OBJECTIVE: Abdominal aortic aneurysm (AAA) is a chronic inflammatory disease characterized by localized progressive dilatation. Currently, paeonol has been shown to possess anti-inflammatory and protective cardiovascular properties. Our study aimed to investigate the potential influences of paeonol on AAA progression. METHODS: Experimental AAAs were created in C57BL/6J mice by intra-aortic infusion of porcine pancreatic elastase, and then intragastrically administered paeonol (20 mg/kg/day) for 14 days. The effects of paeonol on experimental AAA were measured by ultrasound imaging, histopathology, and western blot analyses. RESULTS: Paeonol treatment limited the enlargement of the aneurysmal diameter and alleviated the depletion of elastic fibers and vascular smooth muscle cells (VSMCs). Furthermore, the infiltration of CD68+ macrophages and CD8+ lymphocytes was obviously attenuated after paeonol administration, along with mural neoangiogenesis. Western blot results showed that paeonol inhibited the expression of matrix metalloproteinase (MMP) and the NF-κB pathway activation. CONCLUSIONS: Paeonol might prevent experimental AAA progression by inhibiting the NF-κB pathway, which suggests that it is a potential drug for AAA.

Effect of isoflavone on balloon catheter-induced neointimal hyperplasia in ovariectomised rabbit carotid artery.

BACKGROUND: This study was designed to investigate the effects of phytoestrogen isoflavone on balloon catheter-induced hyperplasia of carotid artery. METHODS: Forty-eight female New Zealand rabbits were randomly divided into four groups: control (balloon-induced carotid artery injury only); ovariectomy control (ovariectomy and carotid artery injury), oestrogen (ovariectomy, carotid artery injury and nilestriol, 5mg/kg daily for 28 days), and isoflavone (ovariectomy, carotid artery injury and isoflavone 120 mg/kg daily for 28 days). The arterial wall thickness was assessed by coloured ultrasonography, and the oestrogen-α and oestrogen-ß receptors in the abdominal aorta were measured by Western blotting. RESULTS: The medial layer thickness in the isoflavone group was less than in the ovariectomy control group (0.28±0.03 vs. 0.35±0.04 mm, p<0.01), and the intimal/medial layer (I/M) ratio is the isoflavone group was also less than in the ovariectomy control group (16.85±3.79 vs. 48.94±8.92, p<0.01). There was no statistically significant difference in the medial layer thickness or I/M ratio between the isoflavone and the oestrogen groups. The optical density of the oestrogen-α receptors in the isoflavone group (0.317±0.002) was less than in the oestrogen (0.633±0.002) or ovariectomy control group (0.590±0.001, p<0.01). The optical density of the oestrogen-ß receptors in the isoflavone group (1.350±0.002) and the ovariectomy control group (1.2033±0.002) was less than in the oestrogen group (1.7699±0.003, p<0.01). CONCLUSIONS: Isoflavone therapy in the ovariectomised rabbit model attenuated balloon catheter-induced intimal and medial layer hyperplasia in the carotid arteries. Down-regulation of the oestrogen-α receptors may be involved in the hyperplasia-preventative effect.