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BACKGROUND: Aortic dissection (AD) is a fatal cardiovascular disorder without effective medications due to unclear pathogenic mechanisms. Bestrophin3 (Best3), the predominant isoform of bestrophin family in vessels, has emerged as critical for vascular pathological processes. However, the contribution of Best3 to vascular diseases remains elusive. METHODS: Smooth muscle cell–specific and endothelial cell–specific Best3 knockout mice (Best3 SMKO and Best3 ECKO , respectively) were engineered to investigate the role of Best3 in vascular pathophysiology. Functional studies, single-cell RNA sequencing, proteomics analysis, and coimmunoprecipitation coupled with mass spectrometry were performed to evaluate the function of Best3 in vessels. RESULTS: Best3 expression in aortas of human AD samples and mouse AD models was decreased. Best3 SMKO but not Best3 ECKO mice spontaneously developed AD with age, and the incidence reached 48% at 72 weeks of age. Reanalysis of single-cell transcriptome data revealed that reduction of fibromyocytes, a fibroblast-like smooth muscle cell cluster, was a typical feature of human ascending AD and aneurysm. Consistently, Best3 deficiency in smooth muscle cells decreased the number of fibromyocytes. Mechanistically, Best3 interacted with both MEKK2 and MEKK3, and this interaction inhibited phosphorylation of MEKK2 at serine153 and MEKK3 at serine61. Best3 deficiency induced phosphorylation-dependent inhibition of ubiquitination and protein turnover of MEKK2/3, thereby activating the downstream mitogen-activated protein kinase signaling cascade. Furthermore, restoration of Best3 or inhibition of MEKK2/3 prevented AD progression in angiotensin II–infused Best3 SMKO and ApoE −/− mice. CONCLUSIONS: These findings unveil a critical role of Best3 in regulating smooth muscle cell phenotypic switch and aortic structural integrity through controlling MEKK2/3 degradation. Best3–MEKK2/3 signaling represents a novel therapeutic target for AD.

In this study, we compared the early results between the extensive arch repair with a novel two-branched stent graft (TSG) and the traditional technique.Between 2013 July and 2015 March, 63 acute type A aortic dissection (ATAAD) patients from four cardiac centers with indications for extensive arch repair were included in this study. Finally, 28 patients were involved in the traditional procedure (TP) group (23 males with the age of 49.75 ± 9.26 years) and 35 patients were involved in the TSG group (29 males with the age of 53.82 ± 8.17 years).The operation was successful in all patients. The selective cerebral perfusion time, total operation time, and chest drainage within 24 hours after the operation in the TSG group were significantly less than those in the TP group (P ≤0.05). The mean follow-up time was 11.17 ± 1.74 months in the TP group and 11.94 ± 4.29 months in the TSG group. No statistical differences were found in aortic diameter, false lumen diameter, and true lumen diameter at the diaphragmatic level during the follow-up.Our technique with a novel TSG simplified the extensive arch repair procedure and was an effective way for the treatment of ATAAD.

OBJECTIVE: To explore the diagnosis and treatment of pregnancy-associated acute Stanford type A aortic dissection to improve the maternal and fetal outcomes. METHODS: We analyzed the perioperative data of 5 pregnant women with acute Stanford type A aortic dissection treated between June, 2009 and February, 2017. RESULTS: The median age of the women was 30 years (range, 22-34 years) with gestational weeks of 23-38 weeks upon diagnosis. All the 5 patients received surgical interventions. Three patients underwent caesarean delivery and hysterectomy, and the fetuses survived after the surgery; 2 patients chose to continue pregnancy following the surgery, among whom one died due to postoperative complications and the other underwent termination of pregnancy. During follow-up, the surviving patients showed no endoleak in the descending aorta stent and the distal dissection remained stable. CONCLUSION: The maternal and fetal outcomes of pregnancyassociated acute Stanford type A aortic dissection can be improved by multidisciplinary cooperation and optimization of the surgical approaches according to the time of pregnancy, fetal development and conditions of the aortic lesions.

To study the benefit of prophylactic antibiotics (PA) in totally percutaneous aortic endovascular repair (PEVAR) in the catheterization laboratory for reducing stent-graft infection and postimplantation syndrome (PIS).The clinical data were analyzed of patients undergoing thoracic endovascular aortic repairs. The patients were divided into non-PA group and PA group according to the use of prophylactic antibiotics before PEVAR. The diagnosis of infection was made by two senior physicians with reference to Hospital Acquired Infection Diagnostic Criteria Assessment released by the Ministry of Health of China.The 95 enrolled patients included 35 with PA and 60 without PA group, who were comparable for baseline characteristics. Infection-related deaths occurred in 1 case in non-PA group and retrograde Stanford type A dissection and death occurred in 1 case in PA group (1.67% vs 2.85%, P=1.00). The PA and non-PA groups showed no significant difference in the incidence of postoperative infection (5% vs 2.86%, P=1.000), hospital stay (9.30±7.21 vs 10.06±5.69, P=0.094), infection-related mortality (1.67% vs 0%, P=1.00), or postoperative fever (70.90% vs 91.43%, P=0.20). The body temperature showed significant variations at different time points after procedure (F=19.831, P0.001) irrelevant to the use of prophylactic antibiotics (F=0.978, P=0.326).The current data do not support the benefit of PA in reducing postoperative infection and PIS in patients undergoing PEVAR, but the patients without PA may have worse clinical outcomes in the event of postoperative infections.

Decreasing the intracranial pressure has been advocated as one of the major protective strategies to prevent spinal cord ischemia after endovascular aortic repair. However, the actual changes of cerebrospinal fluid (CSF) pressure and its relation with spinal cord ischemia have been poorly understood. We performed CSF pressure measurements and provisional CSF withdrawal after thoracic endovascular aortic repair, and compared the changes of CSF pressure in high risk patients and in patients with new onset paraplegia and paraparesis.Four hundred and nineteen patients were evaluated for the risk of spinal cord ischemia after thoracic endovascular aortic repair. Patients with identified risk factors before the procedure constituted group H and received prophylactic sequential CSF pressure measurement and CSF withdrawal. Patients who actually developed spinal cord ischemia constituted group P and received rescue CSF pressure measurements and CSF withdrawal.Among the 419 patients evaluated, 17 were graded as high risk. Four patients actually developed spinal cord ischemia after endovascular repair. The incidence of spinal cord ischemia in this investigation was 0.9%. The patients who actually developed spinal cord ischemia had no identified risk factors and had elevated CSF pressure, ranging from 15.4 to 30.0 mmHg. Six of the 17 patients graded as high risk had elevated CSF pressure:20 mmHg in two patients and15 mmHg in four patients. Sequential CSF pressure measurements and provisional withdrawal successfully decrease CSF pressure and prevented symptomatic spinal cord ischemia in high-risk patients. However, these measurements could only successfully reverse the neurologic deficit in two of the patients who actually developed spinal cord ischemia.Cerebrospinal fluid pressure was elevated in patients with spinal cord ischemia after thoracic endovascular aortic repair. Sequential measurements of CSF pressure and provisional withdrawal of CSF decreased CSF pressure effectively in high risk patients and provided effective prevention of spinal cord ischemia. Risk factor identification and prophylactic measurements play the key role in prevention of spinal cord ischemia after thoracic endovascular aortic repair.

The perioperative aortic dissection (AD) rupture is a severe event after endovascular stent graft placement for treatment of type B AD. However, this life-threatening complication has not undergone systematic investigation. The aim of the study is to discuss the reasons of AD rupture after the procedure.The medical record data of 563 Stanford type B AD patients who received thoracic endovascular repair from 2004 to December 2011 at our institution were collected and analyzed. Double entry and consistency checking were performed with Epidata software.Twelve patients died during the perioperation after thoracic endovascular repair, with an incidence of 2.1%, 66.6% were caused by aortic rupture and half of the aortic rupture deaths were caused by retrograde type A AD. In our study, 74% of the non-rupture surviving patients had the free-flow bare spring proximal stent implanted, compared with 100% of the aortic rupture patients (74% vs. 100%, P = 0.213). The aortic rupture patients are more likely to have ascending aortic diameters = 4 cm (62.5% vs. 9.0%, P = 0.032), involvement the aortic arch concavity (62% vs. 27%, P = 0.041) and have had multiple stents placed (P = 0.039).Thoracic AD endovascular repair is a safe and effective treatment option for AD with relative low in-hospital mortality. AD rupture may be more common in arch stent-graft patients with an ascending aortic diameter = 4 cm and with severe dissection that needs multi-stent placement. Attention should be paid to a proximal bare spring stent that has a higher probability of inducing an AD rupture. Post balloon dilation should be performed with serious caution, particularly for the migration during dilation.

To summarize the experience with surgical treatment of constrictive pericarditis.A retrospective analysis of the post-operative clinical data was conducted in 128 surgical patients with chronic constrictive pericarditis.Two early postoperative death occurred in this group due to severe low cardiac output syndrome, with the mortality rate of 1.57%. The postoperative complications included low cardiac output syndrome (13.2%), arrhythmia (7.02%), acute renal insufficiency (3.9%), respiratory insufficiency (3.1%), wound infection (2.3%), postoperative chest bleeding (1.6%) and cerebral infarction (0.78%). Relapse occurred in one case because of incomplete pericardial resection.Constrictive pericarditis should be confirmed as soon as possible with actively surgery, and the extent of pericardial resection should be decided according to the individual conditions. Complete untethering of the diseased pericardium should be performed with active prevention of postoperative complications.