An Off-Pump Repair Technique for Postinfarction Apical Left Ventricular Aneurysm.

PURPOSE: The conventional surgical treatment for postinfarction left ventricular aneurysm (LVA) is open-heart repair with cardiopulmonary bypass. However, the risk of the open-heart surgery under cardiopulmonary bypass may result in an unacceptable risk for many patients with multiple comorbidities. Here, we reported a new off-pump repair technique for postinfarction apical LVA. METHODS: A new off-pump repair technique, circular banding and occlusion technique, was applied to repair the postinfarction apical LVA in 12 patients. Clinical data of all those 12 patients were retrospectively reviewed. Patients were followed up prospectively by direct interviews and echocardiographic examination. RESULTS: The new repair technique was successfully performed in all these 12 patients. Acute reduction of the LVA mouth diameter, the left ventricular (LV) end-diastolic volume and end-systolic volume, and an increase in the LV ejection fraction (EF) were immediately obtained after the repair. Patients had an uneventful postoperative course. They were in New York Heart Association class 1-2, and the LV volume and EF detected by echocardiography remained unchanged during an average 28.4 ± 9.9 months (range 13 to 45 months) follow-up. CONCLUSIONS: Circular banding and occlusion is a simple, safe, and effective off-pump repair technique for postinfarction apical LVA. It can allow effective LV remodeling and improve heart function.

Upregulation of miR-222-3p alleviates the symptom of aortic dissection through targeting STAT3.

OBJECTIVE: This study sought to investigate the differentially expressed miRNAs in Aortic dissection (AD) and explore the downstream mechanisms in regulating AD. METHODS: Exosomes of AD patients and healthy people were isolated by differential centrifugation, and the differentially expressed miRNAs were evaluated by RNA sequencing. The downstream target of miR-222-3p was predicted by bioinformatics method and validated by dual-luciferase assay. Angiotensin II and Promethazine were used to establish AD mouse model and platelet-derived growth factor BB (PDGF-BB) was used to induce human vascular smooth muscle cells (HVSMCs) to elucidate the effect of miR-222-3p upregulation on AD in vivo and in vitro. The relative level of miR-222-3p was evaluated by RT-qPCR. The level of several proteins was investigated by Western blot. Immunofluorescence staining was used to detect the stress fiber formation. Cell migration was evaluated by wound healing and Transwell assay. The proliferation, cell cycle and apoptosis of HVSMCs were assessed by CCK-8 and flow cytometry, respectively. RESULTS: MiR-222-3p was downregulated in AD and PDGF-BB induced HVSMCs. The upregulation of miR-222-3p alleviated the symptom of AD in vivo by targeting STAT3, and inhibited stress fiber formation, abnormal migration, proliferation and apoptosis of HVSMCs induced by PDGF-BB by regulating the expression of α-SMA, SM22α, MMP2, MMP9 and p-Smad2. CONCLUSION: The upregulation of miR-222-3p attenuates the progression of AD. Our study provides a theoretical basis for exploring new strategies against AD.

Changes in aortic collagen in ß-aminopropionitrile-induced acute aortic dissection.

BACKGROUND: The precise role collagen plays in acute aortic dissection (AAD) was investigated in an animal model of ß-aminopropinitrile (BAPN)-induced AAD. METHODS: The 30 3-week-old male specific-pathogen free (SPF)-grade Sprague-Dawley (SD) rats were randomly divided into two groups: 10 in the Control group and 20 in the Model group. The Model group was treated with 0.1% BAPN for 4 weeks, while the Control group received untreated water. Histopathological staining and western blot were used to detect changes of the extracellular matrix (ECM) and collagen content in the aorta. RESULTS: At the end of the experiment, the incidence of AAD was 25%, the aortic ECM of surviving rats was severely damaged, and the arrangement was disordered. Fibroblast cells are unevenly distributed, with wide gaps, collagen fibers were also distributed unevenly in a disordered arrangement and their thickness was uneven. The elastic membrane disappeared over a large area. Compare to Control group, the Collagen types I, III and their subunits were upregulated (P<0.05), while matrix metalloproteinase (MMP) 2 and MMP9 were downregulated in the aorta of Model group (P<0.05). CONCLUSIONS: In the animal model of BAPN-induced AAD, collagen types I, III and subunits were increased, while MMP2 and MMP9 were decreased in thoracic aorta, which may lead to stiffness of the aorta and be the cause of dissection.

Establishment and effect evaluation of an aortic dissection model induced by different doses of ß-aminopropionitrile in rats.

INTRODUCTION: Given the controversy regarding the appropriate dose of ß-aminopropionitrile for induction of aortic dissection models in rats, the purpose of this study was to explore the most suitable concentration of ß-aminopropionitrile to establish a high-incidence and low-mortality aortic dissection model. METHODS: Eighty three-week-old male Sprague-Dawley rats were equally divided into four groups: a control group, a 0.06% ß-aminopropionitrile group, a 0.08% ß-aminopropionitrile group and a 0.1% ß-aminopropionitrile group. Initial experiments were performed on the control group, which was not treated with ß-aminopropionitrile (and drank water freely), and the other three groups, which were given different concentrations of ß-aminopropionitrile solution daily (0.06%, 0.08% and 0.1%). Subsequently, on the 40th day, osmotic minipumps administering 1 µg/kg per min angiotensin II (Ang II) were implanted subcutaneously into the ß-aminopropionitrile groups, while the control group was continuously pumped with normal saline. The rats were euthanized 48 h after implantation. All rats that died before the expected end time of the experiment were autopsied immediately, and the aortas were dissected. The rats surviving at the end of the experiment were sacrificed by an overdose of sodium pentobarbital, and tissue samples were harvested for further analyses. RESULTS: The mean survival days were significantly different among the groups, with 39.1 ± 6.04 days in the 0.08% ß-aminopropionitrile group and 32.7 ± 9.85 days in the 0.1% ß-aminopropionitrile group (P = 0.0178) at the end of the experiment. Compared with those in the 0.06% ß-aminopropionitrile group, the rates of aortic dissection were significantly higher in the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (P = 0.0015 and P = 0.0005, respectively), while there was no significant difference between the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (P = 0.723) at 70% and 75%, respectively. However, the rupture rates were significantly different between the 0.08% ß-aminopropionitrile group and the 0.1% ß-aminopropionitrile group (55% versus 20%, P = 0.022). Hematoxylin-eosin staining of the aortic tissue sections of the ß-aminopropionitrile group showed that red blood cells entered the pseudocavity in the vascular wall, while the vascular wall structure of the control group was intact. Compared with control rats, which were intact and free from fracture, ß-aminopropionitrile-treated rats had fewer collagen fibers and exhibited fracture. Magnetic resonance imaging showed that the aortic intimae of the aortic dissection rats showed double lumens and intimal tears. CONCLUSIONS: An aortic dissection model with a high incidence and low mortality was successfully and stably developed with 0.08% ß-aminopropionitrile. This model will enable further studies investigating aortic dissection pathogenesis and drug therapy. Magnetic resonance imaging may be a reliable technique for imaging the aorta in rats.

Anti­inflammatory effect of salusin­ß knockdown on LPS­activated alveolar macrophages via NF­κB inhibition and HO­1 activation.

Inflammation of alveolar macrophages is the primary pathological factor leading to acute lung injury (ALI), and NF­κB activation and HO­1 inhibition are widely involved in inflammation. Salusin­ß has been reported to contribute to the progression of the inflammatory response, but whether salusin­ß could regulate inflammation in lipopolysaccharide (LPS)­induced ALI remains unknown. The present study aimed to investigate the role of salusin­ß in LPS­induced ALI and to uncover the potential underlying mechanisms. Sprague­Dawley rats were subjected to LPS administration, and then pathological manifestations of lung tissues, inflammatory cytokines levels in bronchoalveolar lavage fluid (BALF) and expression of salusin­ß in macrophages of lung tissues were assessed. NR8383 cells with or without salusin­ß knockdown were treated with LPS, and then the concentration of inflammatory cytokines, and the expression of high mobility group box­1 (HMGB1), NF­κB signaling molecules and heme oxygenase­1 (HO­1) levels were detected. The results showed that LPS caused injury of lung tissues, increased the levels of proinflammatory cytokines in BALF, and led to higher expression of salusin­ß or macrophages in lung tissues of rats. In vitro experiments, LPS also upregulated salusin­ß expression in NR8383 cells. Knockdown of salusin­ß using short hairpin (sh)RNA inhibited the LPS­induced generation of inflammatory cytokines. LPS also enhanced HMGB1, phosphorylated (p)­IκB and p­p65 expression, but reduced HO­1 expression in both lung tissues and NR8383 cells, which were instead inhibited by the transfection of sh­salusin­ß. In addition, knockdown of HO­1 using shRNA reversed the inhibitory effect of sh­salusin­ß on the LPS­induced generation of inflammatory cytokines, activation of NF­κB signaling and inactivation of HO­1. In conclusion, this study suggested that knockdown of salusin­ß may inhibit LPS­induced inflammation in alveolar macrophages by blocking NF­κB signaling and upregulating HO­1 expression.

Efficacy and safety of corticosteroids prophylaxis in cardiac surgery: A protocol for systematic review and meta-analysis.

BACKGROUND: Although corticosteroid prophylaxis in adult cardiac surgery has been studied extensively for 40 years, its role remains controversial, and the optimal dose remains uncertain. The objective of this meta-analysis was to estimate the clinical benefits and risks of corticosteroid use in cardiopulmonary bypass. METHODS: We will search Pubmed, Web of Science, Embase, Clinical Trials, and Cochrane Central Register of Controlled Trials for relevant clinical trials published in any language before August 1, 2020. Randomized controlled trials (RCTs) of interest which meet inclusion criteria published or unpublished will be included. We will divide the included studies into child and adult groups for analysis. If sufficient data are available, the included trials will be divided into 4 subgroups: ≤20 mg/kg (low dose), 20-40 mg/kg (slightly high dose), 40-100 mg/kg (high dose), and >100 mg/kg (ultra high dose) based on the equivalent hydrocortisone dose. INPLASY registration number: INPLASY2020100044. RESULTS: The results of this study will be published in a peer-reviewed journal. CONCLUSION: This study will compare the efficacy of tprophylactic corticosteroids for adults and children undergoing cardiac surgery with CPB. Due to the nature of the disease and intervention methods, randomized controlled trials may be inadequate, and we will carefully consider inclusion in high-quality, non-randomized controlled trials, but this may result in high heterogeneity and affect the reliability of the results.

Mechanical stretch aggravates aortic dissection by regulating MAPK pathway and the expression of MMP-9 and inflammation factors.

This study aimed to explore whether mechanical stretch aggravated aortic dissection through regulating MAPK pathway, MMP-9, and inflammation factors. We first established aortic dissection model rats. Mechanical stretch (3 g) was exerted on vascular ring of aortic dissection which was also treated by inhibitors of MAPK pathway (SB203580, SP600125, and U0126). HE and Masson staining showed that aortic dissection severity with 3 g tension was worse than that without tension (0 g); after the treatments of diverse inhibitors, the fracture and breakage of the elastic fibers decreased. The expression of MMP-9, TNF-α, IL-1ß) p38/p-p38, JNK1/p-JNK1, and ERK1/2/p-ERK1/2 were determined by immunohistochemical analysis, RT-PCR, and western blot. No matter whether tension was exerted or inhibitors were added, there was no change in the expression of p38, JNK1, and ERK1/2. However, compared to the 0 g group, the expression of MMP-9, TNF-α, IL-1ß, p-p38, p-JNK1, and p-ERK1/2 was significantly upregulated in the 3 g group (P < 0.05). In both 0 g and 3 g groups, the expression of MMP-9, TNF-α, IL-1ß, p-p38, p-JNK1, and p-ERK1/2 was remarkably downregulated after inhibitors treatment (P < 0.05). In conclusion, mechanical stretch aggravated aortic dissection by regulating the MAPK pathway and the consequent expression of MMP-9 and inflammation factors.

Ascending Aorta and Hemiarch Replacement Combined With Modified Triple-Branched Stent Graft Implantation for Repair of Acute DeBakey Type I Aortic Dissection.

BACKGROUND: To simplify extensive repair of acute DeBakey type I aortic dissection, ascending aorta and hemiarch replacement combined with modified triple-branched stent graft implantation was developed. The descriptions and early results of this technique are reported. METHODS: From August 2014 to September 2015, 116 patients with acute DeBakey type I aortic dissection underwent ascending aorta and hemiarch replacement combined with modified triple-branched stent graft implantation. Clinical data of all patients were retrospectively reviewed. Survivors were followed up prospectively by computed tomography angiography. RESULTS: The cardiopulmonary bypass time was 131.5 ± 10.7 minutes, the aortic cross-clamp time was 50.0 ± 9.9 minutes, and the selective cerebral perfusion and lower body arrest time was 17.2 ± 2.2 minutes. The in-hospital mortality rate was 3.4%. Two patients were lost during follow-up. One patient died of a cerebrovascular accident 2 months after discharge, and another died of chronic renal failure 5 months after discharge. At the 3-month postoperative scans, complete thrombus formation of the false lumen around the implanted modified triple-branched stent graft occurred in all survivors, at the diaphragmatic level in 69.7% patients, and at the superior mesenteric arterial level in 8.3% patients. CONCLUSIONS: Extensive thoracic aorta repair of acute type I aortic dissection can be performed simply by combining ascending aorta and hemiarch replacement with modified triple-branched stent graft implantation. This technique can reduce the risk and technical difficulty of extensive thoracic aorta repair to levels close to those seen with ascending aorta and hemiarch graft replacement with open distal anastomosis.

Repair of Acute Type A Aortic Dissection With Ascending Aorta Replacement Combined With Open Fenestrated Stent Graft Placement.

BACKGROUND: In the conventional ascending replacement for acute type A aortic dissection, the distal aortic anastomosis is frequently performed at the dissected site, and postoperative residual dissection in the arch and downstream aorta still occurs in most patients. We used open placement of a fenestrated stent graft during this operation. METHODS: During the conventional ascending replacement in 41 patients with acute type A aortic dissection, a fenestrated stent graft was inserted into the arch and the proximal descending aorta through the distal ascending transection. The distal ascending transection incorporating the proximal end of the fenestrated stent graft was directly anastomosed to the Dacron (DuPont, Wilmington, DE) tube graft. Survivors were examined by computed tomography angiography. RESULTS: The cardiopulmonary bypass time was 134.46 ± 19.03 minutes, aortic cross-clamp time was 46.38 ± 8.57 minutes, and selective cerebral perfusion and lower body arrest time was 12.50 ± 2.19 minutes. There was 1 in-hospital death but no difficult bleeding from the distal aortic anastomosis. On postoperative computed tomography, the false lumen closed, with complete thrombus formation around the inserted fenestrated stent graft found in all survivors (100%), at the diaphragmatic level in 28 patients (70%), and at the superior mesenteric arterial level in 3 (8%). CONCLUSIONS: An open fenestrated stent graft placement provided extensive primary repair of the thoracic aorta and a strong distal aortic stump during the conventional ascending aorta replacement for acute type A aortic dissection but did not increase the risk or technical difficulty of the operation.

Echocardiographic Evaluation of Changes in Cardiac Hemodynamics and Loading Conditions after Transthoracic Minimally Invasive Device Closure of Atrial Septal Defect.

PURPOSE: To evaluate transthoracic minimally invasive device closure of atrial septal defects by performing transthoracic echocardiography to measure changes in cardiac hemodynamics and loading conditions. METHODS: Between January 2012 and December 2012, we performed transthoracic minimally invasive device closure of atrial septal defects in 95 patients with secundum atrial septal defects (ASD), and performed transthoracic echocardiography to measure blood flow velocities at the tricuspid valve orifice and at the pulmonary valve orifice, sizes of the left and right atria and ventricles, right ventricular fractional area change, right ventricular Tei index, three-dimensional right ventricular ejection fraction, tricuspid annular plane systolic excursion and left ventricular ejection fractions before the procedure and 1 week, 3 months, and 1 year post-procedure. RESULTS: Varying degrees of improvement were observed post-procedure at later time points. The maximum blood flow velocity at the pulmonary valve orifice, mean flow velocity, velocity-time integral, and A peak and E peak blood flow velocity at the tricuspid valve orifice decreased significantly post-procedure (P<0.05). In 3 months and 1 year's follow-up, the inner diameter of the middle portion of the pulmonary artery, and diameters of the right atrium and right ventricle decreased significantly post-procedure (P<0.05). The diameters of the left atrium and left ventricle increased after the procedure (P<0.05). One week after the procedure, the right ventricular fractional area change, three-dimensional right ventricular ejection fraction, right ventricular Tei index and tricuspid annular plane systolic excursion had significantly reduced compared with the preoperative data (P<0.05). While these four parameters were still decreased at the 3 months and at 1 year's follow-up, but the differences were not statistically significant compared with the 1 week's postoperative data (P>0.05). One week post-procedure, left ventricular ejection fraction had not changed significantly, but at 3 months and at 1 year post-procedure, left ejection fraction had increased significantly compared with the preoperative data (P<0.05). CONCLUSION: Echocardiographic evaluation has demonstrated that cardiac hemodynamics and loading conditions improved significantly after transthoracic minimally invasive device closure of atrial septal defects.

A clinical study of thoracoscopy-assisted mitral valve replacement concomitant with tricuspid valvuloplasty, with domestically manufactured pipeline products for cardiopulmonary bypass.

OBJECTIVE: To discuss the feasibility and experience of treating valvular heart diseases with thoracoscopy-assisted mitral valve replacement concomitant with tricuspid valvuloplasty, with domestically manufactured pipeline products for cardiopulmonary bypass. METHODS: A total of 135 patients with valvular heart disease were admitted to our hospital between January 2011 and January 2013. They received thoracoscopy-assisted mitral valve replacement concomitant with tricuspid valvuloplasty, with domestically manufactured pipeline products. A cardiopulmonary bypass with domestically-manufactured pipeline products was established during the surgery. The procedure was accomplished with the assistance of thoracoscopy through a small incision in the right chest wall. RESULTS: All 135 patients underwent a successful surgery, and were followed up for the duration of half a year to two years. None of them displayed any evidence of complications. Our procedure had the advantage of fewer complications and a significantly shortened time period for the patient care and hospitalization. As opposed to imported pipeline products for cardiopulmonary bypass, our procedure had the advantage of similar clinical results at a lower cost. CONCLUSIONS: Thoracoscopy-assisted mitral valve replacement concomitant with tricuspid valvuloplasty was proved to be a safe and effective method for cardiopulmonary bypass, with the use of domestically manufactured pipeline products.

Use of a simply modified drainage catheter for peritoneal dialysis treatment of acute renal failure associated with cardiac surgery in infants.

Acute renal failure (ARF) is a common complication in infants who undergo cardiac surgery in the intensive care unit. We report on a modified drainage catheter used in peritoneal dialysis (PD) for the treatment of ARF associated with cardiac surgery in infants. Thirty-nine infants with congenital heart disease undergoing cardiac surgery who developed ARF at our center between January 2009 and January 2012 were assessed. A modified drainage catheter for PD was used in these infants. Their demographic, clinical, and surgical data were analyzed. Thirty infants with ARF were cured by PD, and the other 9 died in the first 48 hours because of the severity of the acute cardiac dysfunction. All these infants were dependent upon mechanical ventilation during the postoperative period and used vasoactive drugs. In the survival group, the interval between the procedure and initiation of PD was 13.6 ± 6.5 (range, 6-30) hours. PD duration was 3.9 ± 0.9 (3-6) days. Minor complications were encountered in some patients (asymptomatic hypokalemia, hyperglycemia, and thrombocytopenia). These complications were readily treated by drugs or resolved spontaneously. Hemodynamics, cardiac function, and renal function improved significantly during PD. These data suggest that PD using a modified drainage catheter for ARF after cardiac surgery in infants is safe, feasible, inexpensive, and yields good results.

Dexmedetomidine attenuates hypoxemia during palliative reconstruction of the right ventricular outflow tract in pediatric patients.

The objective of this study was to investigate whether the α agonist dexmedetomidine has the ability to attenuate hypoxemia in pediatric patients undergoing palliative pulmonary artery reconstruction.From January 2009 to January 2013, a total of 25 pediatric patients with Tetralogy of Fallot, pulmonary atresia (ventricular septal defect), or persistent truncus arteriosus (I) were enrolled in our study. Due to hypoplastic pulmonary arteries, all patients received palliative pulmonary artery reconstruction. During the perioperative period, they were allocated to receive either dexmedetomidine (bolus dose of 0.3 µg/kg followed by an infusion of 0.2-0.3 µg/kg/h, n = 15) or control drug (n = 10) intravenously. Any desaturation was recorded. Heart rate, mean arterial pressure, pulse oximetry, and arterial blood gas parameters were measured during the perioperative period.There were no significant differences between the groups in hemodynamic variables. The arterial oxygen saturation and arterial blood gas parameters increased in the dexmedetomidine groups (P < 0.05).These findings suggest that the injection of dexmedetomidine can attenuate hypoxemia during palliative pulmonary artery reconstruction in pediatric patients.