A New Aortic Arch Inclusion Technique With Frozen Elephant Trunk for Type A Aortic Dissection.

OBJECTIVE: Our aims were to describe a new surgical technique for the treatment of type A aortic dissection (TAAD) and to report the operative outcomes of 154 patients. SUMMARY BACKGROUND DATA: Surgical treatment of TAAD is complicated and carries a high mortality risk. To lower this risk, we developed a simplified procedure in which a stent graft was implanted as frozen elephant trunk (FET), and the proximally trimmed vascular graft was sutured from the inside of the aortic arch using the inclusion technique under moderate hypothermic circulatory arrest and antegrade selective cerebral perfusion. METHODS: We conducted a retrospective analysis of 154 cases of TAAD treated with our novel technique (93 men and 61 women, 52.5 ±â€Š11.4 years). Computed tomography angiography was performed before discharge and at 6 months postoperatively. RESULTS: In-hospital mortality rate was 5.19%, with paraplegia occurring in 2 patients (1.3%) and stroke in 6 (3.9%). The rate of closure of the aortic arch false lumen was 77.8%, with a 69.2% rate of descending thoracic aorta thrombosis at discharge. The survival rate was 91.1% at a mean follow-up of 21 ±â€Š10 months, with rates of aortic arch false lumen closure of 92.4% and descending thoracic aorta thrombosis of 74.3% at 6 months postoperatively. CONCLUSIONS: The aortic arch inclusion technique with FET provides a safe alternative for TAAD treatment, with satisfactory operative results. Short-term follow-up results are encouraging, and long-term outcomes need further evaluation.

A New Aortic Arch Inclusion Technique with Frozen Elephant Trunk for Aortic Arch Aneurysm Treatment.

Various surgical techniques have been proposed for treating aortic arch aneurysm (AAA); however, the optimal treatment has not been well defined. This study introduces a new aortic arch inclusion technique with frozen elephant trunk (FET) for AAA treatment.A retrospective analysis was performed among 22 patients for AAA surgical treatment between March 2010 and March 2019. Patients were classified into Z1, Z2, and Z3 groups based on the origins of aneurysms. A stent graft with a 10 cm stented graft and 5-9 cm proximal vascular prosthesis was released into the descending thoracic aorta as FET through an incision in the aortic arch. The proximal vascular prosthesis was retracted into the aortic arch, trimmed to expose the orifices of the brachiocephalic vessels, and sutured inside the aortic arch using the inclusion technique. The proximal sealing location of the vascular graft was tailored to cover the origins of aneurysms.There was no 30-day mortality. No patient had postoperative stroke or paraplegia. Complete aneurysm thrombosis was achieved in all patients. One patient died of severe respiratory tract stenosis 3 months postoperatively. All other 21 patients were alive during 53.3 ± 36.5-month follow-up. Computed tomography angiography was obtained in 15 patients during follow-up. Endoleak was observed in one patient, and the other 14 patients were free from aneurysm-related or graft-related complications during follow-up.The aortic arch inclusion technique with FET provides an alternative technique in treating AAA with satisfactory mid-term follow-up results. A larger patient population with long-term follow-up results is warranted.

Extracorporeal Membrane Oxygenation in Stanford Type A Aortic Dissection.

The aim of this study was to summarize the clinical experience of postoperative extracorporeal membrane oxygenation (ECMO) support in Stanford type A aortic dissection (STAAD) patients.We retrospectively reviewed 246 consecutive acute STAAD patients undergoing operations at our institution from January 2012 to December 2016. Postoperative ECMO was used in 7 patients. There were 5 males and 2 females with a mean age of 43.1 ± 9.3 years. All 7 patients with acute STAAD underwent ascending aorta replacement and total arch repair with a self-designed stent graft (Micropart Corp, Shanghai, China). Concomitant procedures were aortic root replacement in 1 patient and coronary artery bypass grafting (CABG) in 2 patients. All patients received veno-arterial ECMO through the femoral artery and vein. Five patients were extubated before being removed from ECMO. The mean ECMO supporting time was 244.5 ± 57.8 hours. All 7 patients were successfully weaned from ECMO support, and 6 (85.7%) patients survived to discharge. The average hospital time was 26.3 ± 8.8 days. One patient died of cardiac arrest after being weaned from ECMO. Two patients underwent reoperation for bleeding and 1 patient showed transient delirium. The remaining patients all survived during a median follow-up of 19 months.ECMO provides a good temporary cardiopulmonary support in STAAD patients with refractory cardiogenic shock after surgery for aortic dissection. The early use of ECMO and preventing its complications actively can improve the patient survival rate.

A New Aortic Root Reinforcement Technique for Acute Type A Aortic Dissection Surgery.

Reinforcing the dissected and fragile aortic root is critical in acute type A aortic dissection (ATAAD) surgery. This study introduces our new aortic root reinforcement technique and reports our early operative results and midterm follow-up results.A retrospective analysis study was performed on 235 patients (aged 53.2 ±15.5 years) who were admitted to our hospital for ATAAD surgery and underwent the procedure with our new technique between October 2011 and June 2016. Two vascular graft rings were placed inside and outside aortic root, followed by a running horizontal mattress suture, placed just above the coronary artery ostiums and aortic valve commissures, with another horizontal suture at distal end of the aortic root stump, to reinforce the inner vascular graft, aortic wall, and outside vascular graft. Then additional 3-5 vertical mattress sutures were placed for further reinforcement within the reconstructed aortic root. Computed tomography angiography was performed at discharge and annually during follow-up.The patients' 30-day mortality was 5.1% (12/235). There was no uncontrollable intraoperative bleeding from the aortic root, and re-exploration for bleeding occurred in 0.79% (2/235). The survival rate was 90.2% during follow-up of 4.2 ± 2.1 years. There were no requests for aortic root reoperations during follow-up. All patients were free from aortic root disruptions, proximal anastomosis complications, and re-dissections of the reconstructed aortic root.Our new aortic root reinforcement technique provides a safe and effective technique for aortic root in ATAAD surgery, by reinforcing friable aortic root tissues and minimizing aortic root complications.

A Vaginal Stillbirth after Aortic Surgery of Type B Aortic Dissection in a Pregnant Woman.

Acute aortic dissection occurring during pregnancy poses great danger to both the mother and fetus. Cesareans are usually performed before or after the aortic repair depending on the conditions of the mother and fetus. Here we report our experience in treating a 32-week pregnant woman with a type B aortic dissection, whose baby had died before admission. A cesarean section was initially arranged after emergency aortic repair. However, the patient started to deliver the fetus vaginally after the aortic surgery and the stillborn baby was delivered vaginally. This case report provides new insight into the method of delivery in a pregnant woman with an aortic dissection.

Pioglitazone Suppresses CXCR7 Expression To Inhibit Human Macrophage Chemotaxis through Peroxisome Proliferator-Activated Receptor γ.

Cardiovascular disease is the leading cause of morbidity and mortality in patients with type 2 diabetes mellitus (T2DM). Pioglitazone, the widely used thiazolidinedione, is shown to be efficient in the prevention of cardiovascular complications of T2DM. In this study, we report that pioglitazone inhibits CXCR7 expression and thus blocks chemotaxis in differentiated macrophage without perturbing cell viability or macrophage differentiation. In addition, pioglitazone-mediated CXCR7 suppression and chemotaxis inhibition occur via activating peroxisome proliferator-activated receptor γ (PPARγ) but not PPARα in differentiated macrophage. More importantly, pioglitazone therapy-induced PPARγ activation suppresses CXCR7 expression in human carotid atherosclerotic lesions. Collectively, our data demonstrate that pioglitazone suppresses CXCR7 expression to inhibit human macrophage chemotaxis through PPARγ.

Liquid chromatography-tandem mass spectrometric assay for the determination of vaccarin in rat plasma: application to a pharmacokinetic study.

Vaccarin, a flavonoid glycoside, is considered one of the major active constituents of Vaccaria segetalis. A simple and specific liquid chromatography-tandem mass spectrometric method was developed and validated for quantifying vaccarin in rat plasma following intravenous dosing. Plasma samples were precipitated with methanol and separated on a Venusil-C18 analytical column (2.1 × 50 mm, 5 µm particles) with gradient elution consisting of methanol and 0.1% (v/v) formic acid as the mobile phase. The detection was performed on an Agilent Triple Quad LC/MS with electrospray ionization inlet in the positive multiple reaction monitoring mode. Good linearity was achieved over the concentration range of 12.5-25,000 ng/mL (r(2) > 0.99). Intra- and inter-day precisions were <9.1%, and accuracy ranged from -2.8 to 8.7%. The lower limit of quantification for vaccarin was 12.5 ng/mL, and the analyte was stable under various storage conditions. This validated method was successfully applied to the preliminary pharmacokinetic studies of vaccarin following intravenous administrations of 1.21, 2.41, and 4.82 mg/kg vaccarin in rats.

Effects of percutaneous closure of atrial septal defects via the right internal jugular vein.

Background: Percutaneous atrial septal defect (ASD) closure is the preferred treatment for patients with suitable ASD anatomy. The safety and effectiveness of transcatheter closure have been established. However, reports on transesophageal echocardiography (TEE)-guided percutaneous closure of ASD via the right internal jugular vein (RIJV) are limited. The study aims to discuss the safety and effectiveness of percutaneous trans-jugular vein closure of ASD. Methods: We conducted a retrospective analysis of patients (n=103) with secondary ASD who underwent surgical treatment in the Department of Cardiovascular Surgery, the Second Hospital of Jilin University between July 2015 to July 2022. The article is a cross-sectional study. Clinical data, including age, gender, weight, defect diameter, tricuspid regurgitation, left atrial (LA) size, and the operation results, were collected and evaluated. Nonparametric rank sum tests were used to assess tricuspid regurgitation before and after surgery, while paired sample t-tests were used to compare LA size before and after surgery. Results: TEE-guided percutaneous closure of ASD via the RIJV was successfully performed in 97 out of 103 (94.2%) cases. The average procedure time was 34.48±13.06 min, and the mean age at the time of the procedure and ASD size were 36±18 years and 15.45±5.82 mm, respectively. On analyzing medical records and echocardiographic images, postoperative complications were found to occur in four (3.9%) patients. Among these, three patients had residual shunt as indicated by echocardiography during the operation, which subsequently disappeared at the three-month follow-up. One patient developed atrial fibrillation after surgery but returned to normal sinus rhythm with medication. Percutaneous closure of ASD via the RIJV was unsuccessful in 6 patients (5.8%), with 5 of them undergoing transthoracic ASD closure and achieving satisfactory results. One patient refused further surgical treatment. No pericardial effusion, thrombosis, atrioventricular block, or other complications were observed during the 3-month to 1-year follow-up period. Conclusions: ASD closure via the RIJV is a safe and effective therapeutic approach. The initial results are satisfactory, but further studies with large sample sizes and long-term follow-up are warranted to assess the long-term outcomes.

Manganese boosts natural killer cell function via cGAS-STING mediated UTX expression.

Natural killer (NK) cells play a crucial role in both innate immunity and the activation of adaptive immunity. The activating effect of Mn2+ on cyclic GMP-AMP(cGAS)-stimulator of interferon genes (STING signaling has been well known, but its effect on NK cells remains elusive. In this study, we identified the vital role of manganese (Mn2+) in NK cell activation. Mn2+ directly boosts cytotoxicity of NK cells and promotes the cytokine secretion by NK cells, thereby activating CD8+ T cells and enhancing their antitumor activity. Furthermore, Mn2+ can simultaneously activate NK-cell intrinsic cGAS and STING and consequently augment the expression of ubiquitously transcribed tetratricopeptide repeat on chromosome X (UTX to promote the responsiveness of NK cells. Our results contribute to a broader comprehension of how cGAS-STING regulates NK cells. As a potent agonist of cGAS-STING, Mn2+ provides a promising option for NK cell-based immunotherapy of cancers.

Circ_0022920 Maintains the Contractile Phenotype of Human Aortic Vascular Smooth Muscle Cells Via Sponging microRNA-650 and Promoting Transforming Growth Factor Beta Receptor 1 Expression in Angiotensin II-Induced Models for Aortic Dissection.

Background Abnormal regulation of vascular smooth muscle cells is regarded as the iconic pathological change of aortic dissection (AD). Herein, we aim to identify circ_0022920 as a crucial regulator in AD. Methods and Results Microarray analysis of circular RNAs, messenger RNAs, and micro RNAs in patients with AD was performed, and we identified that circ_0022920 was significantly downregulated in these patients. The Pearson correlation analysis uncovered the negative correlation between miR-650 and circ_0022920 or TGFßR1 (transforming growth factor beta receptor 1). Angiotensin II was used to treat human aortic vascular smooth muscle cells (HASMCs) and mice as models for AD. Hematoxylin and eosin and Masson's trichrome staining were used to analyze AD histopathology. Cell proliferation was analyzed with Cell Counting Kit-8 assay and EdU incorporation. Cell migration was assessed with transwell and wound healing assays. Enhanced circ_0022920 expression dramatically inhibited HASMC proliferation and migration and maintained contractile marker expression induced by angiotensin II, whereas miR-650 exerted opposite effects. MiR-650 was a target of circ_0022920. MiR-650 targeted IRF1 (interferon regulatory factor 1) and thus negatively regulated TGFßR1 expression to promote HASMC proliferation and migration and inhibit contractile marker expression. Circ_0022920 suppressed the progression of AD in vivo. Conclusions Circ_0022920 modulates the contractile phenotype of HASMCs via regulating the miR-650-IRF1-TGFßR1 axis in angiotensin II-induced models for AD, which provides potential therapeutic targets for AD.

Preventing intimal thickening of vein grafts in vein artery bypass using STAT-3 siRNA.

BACKGROUND: Proliferation and migration of vascular smooth muscle cells (VSMCs) play a key role in neointimal formation which leads to restenosis of vein graft in venous bypass. STAT-3 is a transcription factor associated with cell proliferation. We hypothesized that silencing of STAT-3 by siRNA will inhibit proliferation of VSMCs and attenuate intimal thickening. METHODS: Rat VSMCs were isolated and cultured in vitro by applying tissue piece inoculation methods. VSMCs were transfected with STAT 3 siRNA using lipofectamine 2000. In vitro proliferation of VSMC was quantified by the MTT assay, while in vivo assessment was performed in a venous transplantation model. In vivo delivery of STAT-3 siRNA plasmid or scramble plasmid was performed by admixing with liposomes 2000 and transfected into the vein graft by bioprotein gel applied onto the adventitia. Rat jugular vein-carotid artery bypass was performed. On day 3 and7 after grafting, the vein grafts were extracted, and analyzed morphologically by haematoxylin eosin (H&E), and assessed by immunohistochemistry for expression of Ki-67 and proliferating cell nuclear antigen (PCNA). Western-blot and reverse transcriptase polymerase chain reaction (RT-PCR) were used to detect the protein and mRNA expression in vivo and in vitro. Cell apoptosis in vein grafts was detected by TUNEL assay. RESULTS: MTT assay shows that the proliferation of VSMCs in the STAT-3 siRNA treated group was inhibited. On day 7 after operation, a reduced number of Ki-67 and PCNA positive cells were observed in the neointima of the vein graft in the STAT-3 siRNA treated group as compared to the scramble control. The PCNA index in the control group (31.3 ± 4.7) was higher than that in the STAT-3 siRNA treated group (23.3 ± 2.8) (P < 0.05) on 7d. The neointima in the experimental group(0.45 ± 0.04 µm) was thinner than that in the control group(0.86 ± 0.05 µm) (P < 0.05).Compared with the control group, the protein and mRNA levels in the experimental group in vivo and in vitro decreased significantly. Down regulation of STAT-3 with siRNA resulted in a reduced expression of Bcl-2 and cyclin D1. However, apoptotic cells were not obviously found in all grafts on day 3 and 7 post surgery. CONCLUSIONS: The STAT-3 siRNA can inhibit the proliferation of VSMCs in vivo and in vitro and attenuate neointimal formation.

Early outcomes with a hybrid technique for repair of a non-A non-B aortic dissection.

OBJECTIVE: This study reports the early outcomes of patients with acute non-A non-B aortic dissection that involved the aortic arch but not the ascending aorta. METHODS: From January 2013 to December 2018, 825 patients presented with aortic dissection. Of these, 28 patients with non-A non-B dissection (classified as dissection extending into the aortic arch with entry between the left common carotid artery and the left subclavian arteries) underwent a novel hybrid surgery. Self modified stent-grafts (Micropart Corp, Shanghai, China) were implanted via median sternotomy. Clinical presentation, postoperative data, and early outcomes were recorded. RESULTS: All patients underwent an emergency operation. There were no in-hospital mortalities, reexplorations for hemorrhage, reports of paraplegia, cerebral infarctions, endoleaks, or left subclavian artery occlusions. No blood products were required during or after the operations. During the early follow-up at 39.12 ± 15.04 months (6.0-74.0 months), 1 patient was lost to follow-up, and 1 patient died suddenly. Computed tomography angiography showed false lumen patency persisted in the aortic arch and descending aorta without any symptoms. The 6-month computed tomography angiography showed significantly smaller distal aortic arch diameters (31.94 ± 6.95 mm) and descending aorta diameters (34.84 ± 4.15 mm) than measured preoperatively (36.76 ± 4.15 mm and 37.31 ± 4.7 mm, respectively). No paraplegia, cerebral infarction, upper limb ischemia, or left subclavian artery ischemia events were reported. CONCLUSIONS: Our inclusion aortic arch technique is a safe, effective, and simple treatment for non-A non-B aortic dissections that can avoid endoleaks, requires no blood products, and has satisfactory early outcomes.

Ministernotomy approach to aortic arch inclusion and frozen elephant trunk in the treatment of acute Stanford A aortic dissection.

This study aimed to report our results of ministernotomy approach to Liu's aortic root repair technique, Liu's aortic arch inclusion technique with frozen elephant trunk (FET) in the treatment in type A aortic dissection (TAAD). We retrospectively analyzed data on 68 Stanford A aortic dissection patients from October 2017 to March 2020. All patients underwent Liu's aortic root repair technique, Liu's aortic arch inclusion technique with FET and mild-moderate hypothermic circulatory arrest combined with ministernotomy approach. 154 TAAD patients between January 2014 and December 2016 underwent complete sternotomy were selected as control group. Clinical characteristics, data during operation, in-hospital and postoperative outcomes of these patients were observed. The mean hypothermic circulatory arrest time in ministernotomy Patients was 39.3 ± 7.9 min, aortic cross-clamp time was 105.9 ± 12.8 min, cardiopulmonary bypass time was 152.8 ± 24.3 min. Three patients died of multiple organ dysfunction syndrome in ministernotomy Patients. Perioperative temporary neurological dysfunction occurred in three (4.41%) patients, and 53 (77.9%) patients did not require any blood product transfusion during and after operation in ministernotomy Patients. Postoperative CT angiography (CTA) examination at 6-32 months showed excellent outcomes except in three (4.41%) cases where arch false lumen patency persisted. The Liu's aortic root repair technique, Liu's aortic arch inclusion technique with FET and mild-moderate hypothermia circulatory arrest simplify the surgical procedure and reduce bleeding, which can be accomplished through minimally invasive approach.

Progress in research on the role of exosomal miRNAs in the diagnosis and treatment of cardiovascular diseases.

Cardiovascular diseases are the most common diseases threatening the health of the elderly, and the incidence and mortality rates associated with cardiovascular diseases remain high and are increasing gradually. Studies on the treatment and prevention of cardiovascular diseases are underway. Currently, several research groups are studying the role of exosomes and biomolecules incorporated by exosomes in the prevention, diagnosis, and treatment of clinical diseases, including cardiovascular diseases. Now, based on the results of published studies, this review discusses the characteristics, separation, extraction, and identification of exosomes, specifically the role of exosomal miRNAs in atherosclerosis, myocardial injury and infarction, heart failure, aortic dissection, myocardial fibrosis, ischemic reperfusion, atrial fibrillation, and other diseases. We believe that the observations noted in this article will aid in the prevention, diagnosis, and treatment of cardiovascular diseases.

LINC01278 Sponges miR-500b-5p to Regulate the Expression of ACTG2 to Control Phenotypic Switching in Human Vascular Smooth Muscle Cells During Aortic Dissection.

Background Phenotypic switching in vascular smooth muscle cells (VSMCs) is involved in the pathogenesis of aortic dissection (AD). This study aims to explore the potential mechanisms of linc01278 during VSMC phenotypic switching. Methods and Results Twelve samples (6 AD and 6 control) were used for lncRNA, microRNA, and mRNA microarray analysis. We integrated the mRNA microarray data set with GSE52093 to determine the differentially expressed genes. Bioinformatic analysis, including Gene Expression Omnibus 2R, Venn diagram analysis, gene ontology, pathway enrichment, and protein-protein interaction networks were used to identify the target lncRNA, microRNA, and mRNA involved in AD. Subsequently, we validated the bioinformatics data using techniques in molecular biology in human tissues and VSMCs. Linc01278, microRNA-500b-5p, and ACTG2 played an important role in the vascular smooth muscle contraction pathway. Linc01278 and ACTG2 were downregulated and miR-500b-5p was upregulated in AD tissues. Molecular markers of VSMC phenotypic switching, including SM22α, SMA, calponin, and MYH11, were downregulated in AD tissues. Plasmid-based overexpression and RNA interference-mediated downregulation of linc01278 weakened and enhanced VSMC proliferation and phenotypic switching, respectively. Dual-luciferase reporter assays confirmed that linc01278 regulated miR-500b-5p that directly targeted ACTG2 in HEK293T cells. Conclusions These data demonstrate that linc01278 regulates ACTG2 to control the phenotypic switch in VSMCs by sponging miR-500b-5p. This linc01278-miR-500b-5p-ACTG2 axis has a potential role in developing diagnostic markers and therapeutic targets for AD.

Outcomes of Liu's aortic root repair and valve preservation in patients with type A dissection and aortic regurgitation.

OBJECTIVES: To evaluate short- and medium-term outcomes following Liu's aortic root repair and valve preservation in patients with acute type A aortic dissection complicated by moderate-to-severe aortic regurgitation (AR). METHODS: From October 2011 to July 2018, a total of 324 consecutive patients underwent emergency surgery for acute type A aortic dissection. There were 122 patients (38%) with moderate-to-severe AR, of whom 82 (67%) underwent Liu's aortic root repair and valve preservation. Aortic computed tomography angiography and echocardiography were performed at discharge, 6 and 12 months postoperatively, and annually thereafter. We focused on assessing the survival and aortic root and valve durability in the 82 patients. RESULTS: The 30-day, 1-year, 3-year and 6-year survival estimates were 94%, 90%, 85% and 81%, respectively. At a median follow-up of 36.5 (interquartile range 24.9-50.9) months, all patients were free from reoperation. No residual false lumens in the aortic root, recurrent aortic root dissections or aortic root pseudoaneurysms were observed during the follow-up period. Only 1 patient (1%) presented with moderate AR at 6 months, which remained asymptomatic with no significant changes over a 3-year period. The remaining patients showed satisfactory valve function with an AR grade of mild (27%) or trace or none (72%). In the competing risk analysis, the incidence of recurrence of AR was 2% at 8 years. CONCLUSIONS: Liu's aortic root repair and valve preservation is a safe and effective operative strategy that achieves favourable short- and medium-term outcomes for acute type A aortic dissection with moderate-to-severe AR.

Bioinformatics Analysis Reveals MicroRNA-193a-3p Regulates ACTG2 to Control Phenotype Switch in Human Vascular Smooth Muscle Cells.

Aortic dissection (AD) is among the most fatal cardiovascular diseases. However, the pathogenesis of AD remains poorly understood. This study aims to integrate the microRNAs (miRNA) and mRNA profiles and use bioinformatics analyses with techniques in molecular biology to delineate the potential mechanisms involved in the development of AD. We used the human miRNA and mRNA microarray datasets GSE98770, GSE52093, and GEO2R, Venn diagram analysis, gene ontology, and protein-protein interaction networks to identify target miRNAs and mRNAs involved in AD. RNA interference, western blotting, and luciferase reporter assays were performed to validate the candidate miRNAs and mRNAs in AD tissues and human vascular smooth muscle cells (VSMCs). Furthermore, we studied vascular smooth muscle contraction in AD. In silico analyses revealed that miR-193a-3p and ACTG2 were key players in the pathogenesis of AD. miR-193a-3p was upregulated in the AD tissues. We also found that biomarkers for the contractile phenotype in VSMCs were downregulated in AD tissues. Overexpression and depletion of miR-193a-3p enhanced and suppressed VSMC proliferation and migration, respectively. Dual luciferase reporter assays confirmed that ACTG2 was a target of miR-193a-3p. ACTG2 was also downregulated in human AD tissues and VMSCs overexpressing miR-193a-3p. Taken together, miR-193a-3p may be a novel regulator of phenotypic switching in VSMCs and the miR-193a-3p/ACTG2 axis may serve as a promising diagnostic biomarker and therapeutic candidate for AD.

The Role of Exosomes and Exosomal MicroRNA in Cardiovascular Disease.

Exosomes are small vesicles (30-150 nm in diameter) enclosed by a lipid membrane bilayer, secreted by most cells in the body. They carry various molecules, including proteins, lipids, mRNA, and other RNA species, such as long non-coding RNA, circular RNA, and microRNA (miRNA). miRNAs are the most numerous cargo molecules in the exosome. They are endogenous non-coding RNA molecules, approximately 19-22-nt-long, and important regulators of protein biosynthesis. Exosomes can be taken up by neighboring or distant cells, where they play a role in post-transcriptional regulation of gene expression by targeting mRNA. Exosomal miRNAs have diverse functions, such as participation in inflammatory reactions, cell migration, proliferation, apoptosis, autophagy, and epithelial-mesenchymal transition. There is increasing evidence that exosomal miRNAs play an important role in cardiovascular health. Exosomal miRNAs are widely involved in the occurrence and development of cardiovascular diseases, such as atherosclerosis, acute coronary syndrome, heart failure (HF), myocardial ischemia reperfusion injury, and pulmonary hypertension. In this review, we present a systematic overview of the research progress into the role of exosomal miRNAs in cardiovascular diseases, and present new ideas for the diagnosis and treatment of cardiovascular diseases.

A Complete Occlusion of Right Coronary Artery Due to Stanford Type A Aortic Dissection - Successful Treatment with Extracorporeal Membrane Oxygenation (ECMO).

We present a patient diagnosed Stanford Type A aortic dissection, who was misdiagnosed as acute myocardial infarction for 5 days. In the surgery, the right coronary ostium was totally occluded, and the right coronary artery (RCA) was bluish from the trunk to branches. The true lumen couldn't be found when we opened the RCA. We had to give up coronary artery bypass grafting (CABG). After a regular surgery of type A aortic dissection, the patient was failed to wean from cardiopulmonary bypass due to the right heart dysfunction. The Extracorporeal membrane oxygenation (ECMO) was instituted. The right ventricular wall motion was gradually improved during the post-operation period. This is the first report of using ECMO to successfully treat a complete occlusion of the right coronary artery due to a Type A aortic dissection. This case demonstrates the value of ECMO in assisting right heart function to ensure stable hemodynamics and myocardial recovery in the type A aortic dissection with coronary involvement.

Circular RNAs as potential biomarkers and therapeutics for cardiovascular disease.

Circular RNAs (circRNAs) are genetic regulators that were earlier considered as "junk". In contrast to linear RNAs, they have covalently linked ends with no polyadenylated tails. CircRNAs can act as RNA-binding proteins, sequestering agents, transcriptional regulators, as well as microRNA sponges. In addition, it is reported that some selected circRNAs are transformed into functional proteins. These RNA molecules always circularize through covalent bonds, and their presence has been demonstrated across species. They are usually abundant and stable as well as evolutionarily conserved in tissues (liver, lung, stomach), saliva, exosomes, and blood. Therefore, they have been proposed as the "next big thing" in molecular biomarkers for several diseases, particularly in cancer. Recently, circRNAs have been investigated in cardiovascular diseases (CVD) and reported to play important roles in heart failure, coronary artery disease, and myocardial infarction. Here, we review the recent literature and discuss the impact and the diagnostic and prognostic values of circRNAs in CVD.