Although extracorporeal membrane oxygenation (ECMO) has been in existence since the 1970s as a means of supporting respiratory or cardiac function, early application of this technology was plagued by high complication rates. Peripheral veno-arterial extracorporeal membrane oxygenation (V-A ECMO) causes higher left ventricular end-diastolic pressure, pulmonary edema, left ventricular distention, ventricular arrhythmia, low coronary perfusion, myocardial ischemia, substantial thrombus formation within left ventricule cavity and even multiple organ dysfunction. Mechanical left ventricular decompression is required to treat these related complications. In this article, we reviewed the problems associated with left ventricular decompression supported by peripheral V-A ECMO in patients with cardiogenic shock.
The cardiac conduction system (CCS) is a set of specialized myocardial pathways that spontaneously generate and conduct impulses transmitting throughout the heart, and causing the coordinated contractions of all parts of the heart. A comprehensive understanding of the anatomical characteristics of the CCS in the heart is the basis of studying cardiac electrophysiology and treating conduction-related diseases. It is also the key of avoiding damage to the CCS during open heart surgery. How to identify and locate the CCS has always been a hot topic in researches. Here, we review the histological imaging methods of the CCS and the specific molecular markers, as well as the exploration for localization and visualization of the CCS. We especially put emphasis on the clinical application prospects and the future development directions of non-destructive imaging technology and real-time localization methods of the CCS that have emerged in recent years.
ObjectiveBased on the rat in situ perfusion system, to explore the effect of up-regulating Chemokine (C-X-C motif) receptor 4 (CXCR4) expression on bone marrow neutrophils in modulating its ECC-related rapid release. MethodsTwelve SD rats were randomly divided into fucoidan perfusion group (F, n=6) and control group (C, n=6) after in situ perfusion system establishment. Rats in F group received perfusion of fucoidan solution (total volume 6 ml, 1 h) and C group received buffer only. Femurs from two groups were dissected after one-hour perfusion and bone marrow tissues were collected. The neutrophil CXCR4 expression in two groups were compared using flowcytometry. Eighteen SD rats were randomly divided into fucoidan perfusion group (F', n=6), fucoidan and AMD-3100 perfusion group (F+AMD3100, n=6) and control group (C', n=6) after in situ perfusion system establishment. Rats received desired interventions before stimulation from ECC plasma. After that, 40-min perfusions of buffer were added and total counts of neutrophil in perfusates were compared. ResultsThe percentages of CXCR4 (+) cell and CXCR4 expression fluorescence in F group were 4.71%±0.21% and 161.3±7.8 respectively while the values were 1.11%±0.11% and 58.4±6.5 respectively in C group. Values in F group were both significantly higher than those in C group (P<0.05). The total counts of neutrophil in perfusates from F' group, F+AMD3100 and C' group were 261 393.7±12 470.6, 872 635.2±10 430.6 and 818 675.2±10 708.8, respectively. Statistically differences were observed between each other (P<0.05). ConclusionBone marrow neutrophil CXCR4 expression of SD rat could be effectively up-regulated by perfusion of fucoidan within the in situ perfusion system. ECC-plasma-stimulated bone marrow neutrophil release in rat could be inhibited by fucoidan induced up-regulation of neutrophil CXCR4 expression, and this inhibition effect could be canceled by AMD-3100 intervention.
ObjectiveTo investigate the reliability and safety of the technique of percutaneous left ventricular transapical access guided by cardiac three dimensional CT angiography (3D-CTA) combined with echocardiography applied in structural heart defects.MethodsThe clinical data of 9 patients (7 males and 2 females with a median age of 50 years ranging from 43 to 64 years) with paravalvular leaks closed by percutaneous left ventricular transapical access in West China Hospital, from April 2015 to August 2018, were retrospectively analyzed. We applied preoperative cardiac 3D-CTA to define the puncture site and trace, which was established by combining with real-time guidance of transesophageal echocardiography (TEE/3D-TEE), and an occluder was deployed at the apical access point for hemostasis with real-time guidance of transthoracic echocardiography (TTE).ResultsThe puncture needles were successfully introduced into the left ventricular cavity at one time in all patients without injury of lung tissue, coronary artery or papillary muscle. There was no occluder displacement or apex bleeding. One patient developed pleural effusion caused by intercostal artery injury.ConclusionThat cardiac 3D-CTA is used to define puncture sites and trace with advantages of simplicity and repeatability. A safe access and secure exit of left ventricle can be achieved by combining with real-time guidance of echocardiography. There are acceptable technology-related complications.
Objective To analyze the metabolic characteristics of myocardial infarction (MI) using metabolomics to better understand its pathogenesis and to explore new therapeutic directions for MI. Methods Serum metabolites in ten acute MI mice and five sham-control mice were analyzed by UHPLC-QqQ/MS, and SPSS was used for statistical analysis. MetaboAnalyst 5.0 was used to analyze the metabolic pathways of the differential metabolites and build a metabolic network. Results One hundred and twenty-nine metabolites were detected by UHPLC-QqQ/MS. Significant serum metabolite differences were found between MI mice and normal controls. Fifty out of 129 metabolites in serum were associated with MI. In addition, the most important metabolic pathways were D-glutamate metabolism, alanine, aspartate and glutamate metabolism, glycine, serine and threonine metabolism, glyoxylate and dicarboxylate acid metabolism. ConclusionMetabolites in serine-related metabolic pathways reduce in serum in MI. We propose a new therapeutic direction for myocardial protection in MI.
Objective To study feasibility of retrograde infusion of hyperpolarization-activated cyclic nucleotide-gated channel protein 4 (HCN4) and connexin fluorescent dye (Alexa Fluor 633)-labeled antibodies through the aorta to image the cardiac conduction system (CCS) in rat hearts. The optimal dosage, infusion time and photochemical stability of fluorescent dyes were also studied. Methods Ex vivo rat heart anterograde perfusion models were established in 33 male SPFSD rats, and the primary and secondary antibody solutions were injected sequentially. The atrioventricular junction was observed and the fluorescence intensity of the area was recorded when the perfusion reaches the scheduled time. We set five dose gradients (3 rats per gradient), 5 perfusion time gradients (three rats per gradient) and 10 LED continuous illumination time gradients in 3 rats under specific dose and perfusion time, the fluorescence intensities of the region were observed and recorded. Standard immunofluorescence stained paraffin sections and frozen sections were prepared for histological comparison. Results A HCN4 red fluorescence signal aggregation region was observed in the atrioventricular junction, which was identified as the AVN structure based on HCN4/Cx43 semi-quantitative fluorescence intensity analysis and histological comparison. With increasing antibody perfusion time, both AVN and background fluorescence intensity showed no statistically significant difference. The ratio of AVN to background fluorescence intensity also increased with the increasing antibody perfusion time. When the illumination time of AVN was prolonged, the fluorescence intensity of both AVN and background showed a downward trend but no statistically significant difference. Conclusion The anterograde perfusion with fluorescent dye (Alexa Fluor 633)-labeled antibody can successfully image the AVN of the CCS in ex vivo rat hearts under stereoscopic fluorescence microscopy. Increasing the antibody dose results in different AVN imaging effects. The imaging effect of AVN improves with an increase antibody perfusion time. Even after long-term (8 h) exposure to light, Alexa Fluor 633 can still maintain a certain level of AVN image.
目的 观察和评价采用偏心型封堵器导管介入治疗干下型室间隔缺损的近期疗效和安全性。 方法 2011年8月－12月，6例经无主动脉瓣脱垂的干下型室间隔缺损（直径≤7 mm）患者（年龄＞3岁）在杂交手术室接受介入治疗。造影评估后，建立动静脉轨道，在保留导丝的情况下置入合适型号的国产偏心型室间隔缺损封堵器，并于术后定期随访复查。 结果 6例患者缺损直径4～7 mm（平均5.3 mm），其中5例成功地接受了导管介入封堵治疗，置入封堵器直径5～9 mm（平均6.4 mm）。仅1例因封堵器置入后出现主动脉瓣受压影响关闭，即改由外科微创经胸封堵成功。所有患者在随访期内，无栓塞、残余分流、瓣膜功能障碍、房室传导阻滞、死亡等并发症。 结论 无主动脉瓣脱垂的干下型室间隔缺损患者接受导管介入封堵治疗是安全、可行的，且短期随访结果良好。
ObjectiveTo evaluate the efficacy and reversible effect of anti-VCAM-1 ultrasound-targeted microbubbles on extracorporeal circulation (ECC) related bone marrow neutrophil releasing. MethodsThirty-six male SD rats were randomly divided into 6 groups with 6 rats in each group, including an antibody group (group A), antibody with ultrasound group (group AU), targeted microbubble group (group T), targeted microbubble rupture group (group TU), post-ECC plasma simulation group (group MC) and control group (group C) after in situ perfusion model establishment. Rats in group C received buffer perfusion for 4 cycles, and rats in other groups received perfusion for 5 cycles. After buffer perfusion for the first cycle, post-ECC plasma was infused to each group from the second cycle to the fifth cycle in group MC, A, AU, T and TU. Rats in group A and AU received injection with anti-VCAM-1 antibodies, while rats in group T and TU were given anti-VCAM-1 targeted microbubbles after the second perfusion cycle. Same ultrasound radiation was given to group AU and TU in the third perfusion cycle. Neutrophil counts from perfusate were compared among the 6 groups. ResultsUnder simulated inflammatory condition after ECC, compared with group MC, significant reduction of neutrophil count released from bone marrow was found in group A and T, especially in group T (P < 0.05). After ultrasonic radiation, neutrophil mobilization recovered in group TU and its neutrophil count was significantly higher than that of group T (P < 0.05). There was no significant difference in neutrophil count between group A and AU in each perfusion cycle (P > 0.05). ConclusionsAnti-VCAM-1 targeted microbubbles can block the binding of VCAM-1 and its ligand, and form a barrier on the surface of bone marrow sinusoids endothelium to inhibit neutrophils migrating and releasing. The binding of VCAM-1 and its ligand on microbubbles is separated by cavitation of disrupting microbubbles with ultrasound, and neutrophils recover the ability to cross the sinusoidal endothelium of bone marrow in inflammatory conditions to achieve the controllability of neutrophil releasing.