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Objective:To summarize the safety and efficacy of aortic banding in the treatment of refractory endoleaks after endovascular abdominal aortic aneurysm repair (EVAR).Methods:The clinical and follow-up data of 10 patients with refractory endoleaks EVAR undergoing aortic banding at Peking University People's Hospital from Jun 2019 to Aprl 2022 were retrospectively analyzed.Results:The aortic banding was indicated for type Ⅰ endoleak in 6 patients, type Ⅱ endoleak in 3 patients and internal tension in 1 patient with persistent aneurysm enlargement or rupture. The surgical procedure was based on laparotomy. The proximal aortic neck was exposed and re-fixation with artificial strip to prevent bleeding. The surgical procedures was successful in all the 10 cases without residual endoleak or re-bleeding. The post-operative contrast-enhanced ultrasonography revealed neither new-onset endoleak nor occlusion of stent-grafts. Perioperative complications included one case of delayed wound healing and one case of incomplete ileus. No perioperative deaths occurred. Midterm follow-up was achieved in 10 patients with a mean follow-up time of 13 months. No recurrence of endoleak was found. One patient underwent endovascular repair for independent thoracic aortic aneurysm 6 months after surgery. There were no other aorta-related secondary surgeries or aortic-related deaths.Conclusion:Aortic banding for refractory endoleaks after EVAR is minimally invasive and reliable. It can effectively eliminate the refractory endoleaks, and reduce the risks of aortic-related secondary surgery or death.
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Objective To investigate the expression of PLP2 protein in the process of cardiac remodeling.Methods Mice were subjected to left anterior descending coronary artery ligation to induce cardiac remodeling model.Mice were subjected to isoproterenol (ISO) subcutaneous injection for 2 weeks to establish acute cardiac injury model.Mice were subjected to aortic banding (AB) surgery to establish a myocardial hypertrophy model.Cardiac myocytes hypertrophy model was induced by phenylephrine (PE) stimulation.Transforming growth factor (TGF) beta was used to stimulate cardiac fibroblasts.The PLP2 transcription level was detected by RT-PCR.Results PLP2 expression was significantly increased in 2 weeks after myocardial infarction (P ＜ 0.05),as well as in acute cardiac injury induced by ISO injection (P ＜ 0.05).After 1 week of AB surgery,the PLP2 expression began to increase (P ＜ 0.05),peaked at 2 weeks post AB (P ＜ 0.05),preserved to 8 weeks after AB (P ＜ 0.05).The expression of PLP2 in PE stimulated cardiomyocytes was increased as well as TGFβ stimulated fibroblast.Conclusion The expression of PLP2 were dynamically changed significantly in different cardiac remodeling model,suggesting that it may be involved in the occurrence and development of cardiac remodeling.
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Objective To investigate the expression changes of SSR in the process of cardiac remodeling.Methods Myocardial infarction (MI) was induced by left anterior descending coronary artery ligation in mice to establish cardiac remodeling model.Mice subjected to isoproterenol (ISO) subcutaneous injection for 2 weeks to establish acute cardiac injury model.Mice subjected to aortic banding (AB) to establish a mouse model of cardiac hypertrophy.RT-PCR was used to detect the expression change of SSR in various cardiac remodeling models.Results The expression levels of SSR subunit 1 (SSR1) and 3 (SSR3) were significantly decreased in mice after 2 weeks of MI (P ＜ 0.05),and were also decreased in acute cardiac injury induced by 2 weeks of ISO injection (P ＜ 0.05),and reduced afterl week of AB operation (P ＜ 0.05).However,the expression of SSR1 and SSR3 increased at 2 weeks after AB (P ＜ 0.05),and sustained to 8 wccks after AB (P ＜ 0.05).Conclusion The expression of SSR3 and SSR1 in different models of cardiac remodeling were significantly changed,and showed dynamic changes,suggesting that it may participate in the occurrence and development of cardiac remodeling.
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Objective To investigate the role of RhoA /Rho-kinase pathway in rat models of left heart disease-as-sociated pulmonary hypertension ( PH-LHD) .Methods Twenty male SD rats (3-4 week-old, 90-100 g) were randomly divided into two groups (10 rats in each group):the group C ( control group) with sham operation, and group H ( pulmo-nary arterial hypertension) .The rat model of left heart disease-associated pulmonary hypertension was established by supra-coronary aortic banding in the group H, and the sham surgery was applied for the rats in the group C ( The titanium clip was fixed at the mediastinal tissue adjacent to the artery rather than the ascending aorta).On day 60 after the operation, the cardiac functions, including right ventricular systolic pressure and pulmonary artery pressure were evaluated.After that, all rats were sacrificed and treated with cardiopulmonary lavage in vivo until the lung became white.Then the left lung tissues were fixed in 4%paraformaldehyde for pathological observation while the right lung tissues were frozen for mRNA detec-tion.Results Compared with the group C, both ventricular systolic pressure and pulmonary artery pressure in the group H were increased significantly (P<0.01).Pathological data demonstrated that the pulmonary artery walls in H group were much thicker than that in the group C.Moreover, vascular wall hypertrophy index in the group H was increased greatly compared with that in the group C (P<0.01).QPCR data showed that mRNA levels of Rho kinase, RhoA and ET-A R in the group H were up-regulated compared with the group C ( P<0.01) .Conclusions Rat model of left heart disease-asso-ciated pulmonary arterial hypertension can be successfully established by supracoronary aortic banding.Rho-kinase-media-ted pathway may contribute to the pathogenesis and progress of left heart disease-associated pulmonary arterial hypertension.
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BACKGROUND: Aortic banding and debanding models have provided useful information on the development and regression of left ventricular hypertrophy (LVH). In this animal study, we aimed to evaluate left ventricular (LV) deformation related to the development and regression of LVH. METHODS: Minimally invasive ascending aorta banding was performed in rats (10 Sprague Dawley rats, 7 weeks). Ten rats underwent a sham operation. Thirty-five days later, the band was removed. Echocardiographic and histopathologic analysis was assessed at pre-banding, 35 days of banding and 14 days of debanding. RESULTS: Banding of the ascending aorta created an expected increase in the aortic velocity and gradient, which normalized with the debanding procedure. Pressure overload resulted in a robust hypertrophic response as assessed by gross and microscopic histology, transthoracic echocardiography [heart weight/tibia length (g/m); 21.0 +/- 0.8 vs. 33.2 +/- 2.0 vs. 26.6 +/- 2.8, p < 0.001]. The circumferential (CS) and radial strains were not different between the groups. However, there were significant differences in the degree of fibrosis according to the banding status (fibrosis; 0.10 +/- 0.20% vs. 5.26 +/- 3.12% vs. 4.03 +/- 3.93%, p = 0.003), and global CS showed a significant correlation with the degree of myocardial fibrosis in this animal model (r = 0.688, p = 0.028). CONCLUSION: In this animal study, simulating a severe LV pressure overload state, a significant increase in the LV mass index did not result in a significant reduction in the LV mechanical parameters. The degree of LV fibrosis, which developed with pressure overload, was significantly related to the magnitude of left ventricular mechanics.