Combined cesarean delivery and repair of acute aortic dissection at 34 weeks of pregnancy during COVID-19 outbreak:A case report

BACKGROUND Since the outbreak of the coronavirus disease 2019(COVID-19)pandemic,the exclusion of a patient from COVID-19 should be performed before surgery.However,patients with type A acute aortic dissection(AAD)during pregnancy can seriously endanger the health of either the mother or fetus that requires emergency surgical treatment without the test for COVID-19.CASE SUMMARY A 38-year-old woman without Marfan syndrome was admitted to the hospital because of chest pain in the 34th week of gestation.She has diagnosed as having a Stanford type-A AAD involving an aortic arch and descending aorta via aortic computed tomographic angiography.The patient was transferred to the isolated negative pressure operating room in one hour and underwent cesarean delivery and ascending aorta replacement.All medical staff adopted third-level medical protection measures throughout the patient transfer and surgical procedure.After surgery,the patient was transferred to the isolated negative pressure intensive care unit ward.The nucleic acid test and anti-COVID-19 immunoglobulin(Ig)G and IgM were performed and were negative.The patient and infant were discharged without complication nine days later and recovered uneventfully.CONCLUSION The results indicated that the procedure that we used is feasible in patients with a combined cesarean delivery and surgery for Stanford type-A AAD during the COVID-19 outbreak,which was mainly attributed to rapid multidisciplinary consultation,collaboration,and quick decision-making.

Delayed xenon post-conditioning mitigates spinal cord ischemia/reperfusion injury in rabbits by regulating microglial activation and inflammatory factors

The neuroprotective effect against spinal cord ischemia/reperfusion injury in rats exerted by delayed xenon post-conditioning is stronger than that produced by immediate xenon post-conditioning. However, the mechanisms underlying this process remain unclear. Activated microglia are the main inflammatory cell type in the nervous system. The release of pro-inflammatory factors following microglial activation can lead to spinal cord damage, and inhibition of microglial activation can relieve spinal cord ischemia/reperfusion injury. To investigate how xenon regulates microglial activation and the release of inflammatory factors, a rabbit model of spinal cord ischemia/reperfusion injury was induced by balloon occlusion of the infrarenal aorta. After establishment of the model, two interventions were given： （1） immediate xenon post-conditioning—after reperfusion, inhalation of 50% xenon for 1 hour, 50% N2/50%O2 for 2 hours; （2） delayed xenon post-conditioning—after reperfusion, inhalation of 50% N2/50%O2 for 2 hours, 50% xenon for 1 hour. At 4, 8, 24, 48 and 72 hours after reperfusion, hindlimb locomotor function was scored using the Jacobs locomotor scale. At 72 hours after reperfusion, interleukin 6 and interleukin 10 levels in the spinal cord of each group were measured using western blot assays. Iba1 levels were determined using immunohistochemistry and a western blot assay. The number of normal neurons at the injury site was quantified using hematoxylin-eosin staining. At 72 hours after reperfusion, delayed xenon post-conditioning remarkably enhanced hindlimb motor function, increased the number of normal neurons at the injury site, decreased Iba1 levels, and inhibited interleukin-6 and interleukin-10 levels in the spinal cord.Immediate xenon post-conditioning did not noticeably affect the above-mentioned indexes. These findings indicate that delayed xenon post-conditioning after spinal cord injury improves the recovery of neurological function by reducing microglial activation and the release of interleukin-6 and interleukin-10.

Serine-threonine protein kinase activation may be an effective target for reducing neuronal apoptosis after spinal cord injury

The signaling mechanisms underlying ischemia-induced nerve cell apoptosis are poorly understood. We investigated the effects of apoptosis-related signal transduction pathways following ischemic spinal cord injury, including extracellular signal-regulated kinase（ERK）, serine-threonine protein kinase（Akt） and c-Jun N-terminal kinase（JNK） signaling pathways. We established a rat model of acute spinal cord injury by inserting a catheter balloon in the left subclavian artery for 25 minutes. Rat models exhibited notable hindlimb dysfunction. Apoptotic cells were abundant in the anterior horn and central canal of the spinal cord. The number of apoptotic neurons was highest 48 hours post injury. The expression of phosphorylated Akt（pAkt） and phosphorylated ERK（p-ERK） increased immediately after reperfusion, peaked at 4 hours（p-Akt） or 2 hours（p-ERK）, decreased at 12 hours, and then increased at 24 hours. Phosphorylated JNK expression reduced after reperfusion, increased at 12 hours to near normal levels, and then showed a downward trend at 24 hours. Pearson linear correlation analysis also demonstrated that the number of apoptotic cells negatively correlated with p-Akt expression. These findings suggest that activation of Akt may be a key contributing factor in the delay of neuronal apoptosis after spinal cord ischemia, particularly at the stage of reperfusion, and thus may be a target for neuronal protection and reduction of neuronal apoptosis after spinal cord injury.

Investigation on the mechanisms of Wuling Powder in treating myocardial ischemia-reperfusion injury based on network pharmacology and molecular docking with experiment verification

Background Myocardial ischemia-reperfusion injury is characterized by the inability of tissue and organ function to recover after the perfusion blood flow is restored followed by myocardial ischemia.Previous studies have shown that many Chinese herbal compounds can reduce myocardial ischemia-reperfusion injury,but the efficacy of Wuling Powder in treating myocardial ischemia-reperfusion injury has not been reported.The present study aimed to investigate the mechanism of Wuling Powder in treating myocardial ischemia-reperfusion injury by network pharmacology and molecular docking.Methods The active constituents of Wuling Powder were obtained by the Traditional Chinese Medicine Systems Pharmacology Database and Analysis Platform(TCMSP),and the related targets of active constituents of Wuling Powder were screened by the Swiss Target Prediction database.Disease targets of myocardial ischemia-reperfusion injury were obtained by Gene Cards,Dis Ge NET and OMIM gene databases.The active compound-target network of Wuling Powder was constructed using Cytoscape software.The drug prediction targets were mapped to the disease target set,and the intersection targets were obtained.The Gene Ontology(GO)function and Kyoto Encyclopedia of Genes anf Genomes(KEGG)pathway enrichment analysis were performed on the intersection targets obtained by using String database.Auto Dock Vina was used for molecular docking of core targets and the top 3 key active ingredients with degree values.Results Through screening,56 active ingredients and 116 targets of Wuling Powder were obtained.There were 27 common targets of Wuling Powder and myocardial ischemia-reperfusion injury in Myocardial ischemia-reperfusion injury(MIRI).Protein-Protein Interaction(PPI)network analysis in this study showed that CASP3,PTGS2,CAT,JUN,ESR1,CASP8,CASP9 and RELA may be the key targets of Wuling Powder to exert the protective effect of MIRI.GO functional analysis and KEGG pathway enrichment analysis showed that biological processes such as apoptosis,lipopolysaccharide response,steroid hormone response and signal transduction pathways such as PTGS2,TNF-α,nuclear transcription factor-κB(NF-κB),MAPK,PI3K/AKT,NLRP3,and autophagy play an important role in the occurrence and development of MIRI.Molecular docking results showed thatβ-sitosterol and hederagenin had good binding activities with key targets such as PTGS2,CASP3,and CAT.Conclusions Wuling Powder may act on CASP3,PTGS,CAT,JUN,ESR1,CASP8,CASP9 and other targets throughβ-sitosterol,hederagenin,3β-acetoxyatractylone,taxifolin and other active ingredients.[S Chin J Cardiol 2024;25(3):179-192]

Myocardial autophagy variation during acute myocardial infarction in rats： the effects of carvedilol

Background The loss of cardiac myocytes is one of the mechanisms involved in acute myocardial infarction （AMI）-related heart failure. Autophagy is a common biological process in eukaryote cells. The relationship between cardiac myocyte loss and autophagy after AMI is still unclear. Carvedilol, a non-selective α1-and β-receptor blocker, also suppresses cardiac myocyte necrosis and apoptosis induced by ischemia. However, the association between the therapeutic effects of carvedilol and autophagy is still not well understood. The aim of the present study was to establish a rat model of AMI and observe changes in autophagy in different zones of the myocardium and the effects of carvedilol on autophagy in AMI rats. Methods The animals were randomly assigned to a sham group, an AMI group, a chloroquine intervention group and a carvedilol group. The AMI rat model was established by ligating the left anterior descending coronary artery. The hearts were harvested at 40 minutes, 2 hours, 24 hours and 2 weeks after ligation in the AMI group, at 40 minutes in the chloroquine intervention group and at 2 weeks in other groups. Presence of autophagic vacuoles （AV） in the myocytes was observed by electron microscopy. The expression of autophagy-, anti-apoptotic- and apoptotic-related proteins, MAPLC-3, Beclin-1, Bcl-xl and Bax, were detected by immunohistochemical staining and Western blotting. Results AVs were not observed in necrotic regions of the myocardium 40 minutes after ligation of the coronary artery. A large number of AVs were found in the region bordering the infarction. Compared with the infarction region and the normal region, the formation of AV was significantly increased in the region bordering the infarction （P 〈0.05）. The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the region bordering the infarction. Meanwhile, the expression of apoptotic-related proteins was significantly increased in the infarction region. In the chloroquine intervention group, a large number of initiated AVs （AVis） were found in the necrotic myocardial region. At 2 weeks after AMI, AVs were frequently observed in myocardial cells in the AMI group, the carvedilol group and the sham group, and the number of AVs was significantly increased in the carvedilol group compared with both the AMI group and the sham group （P 〈0.05）. The expression of autophagy- and anti-apoptotic-related proteins was significantly increased in the carvedilol group compared with that in the AMI group, and the positive expression located in the infarction region and the region bordering the infarction. Conclusions AMI induces the formation of AV in the myocardium. The expression of anti-apoptosis-related proteins increases in response to upregulation of autophagy. Carvedilol increases the formation of AVs and upregulates autophagy and anti-apoptosis of the cardiac myocytes after AMI.

Unconscious sedation/analgesia with propofol versus conscious sedation with fentanyl/midazolam for catheter ablation of atrial fibrillation:a prospective,randomized study

Catheter ablation of atrial fibrillation （AF） has been ,increased dramatically recently. However, it is an unpleasant procedure with intolerable pain without sedation. Propofol and fentanyl/midazolam have been widely used in painful clinical examination and cardiovascular procedures with established safety and efficacy. Propofol, alfentanyl and midazolam were administrated for catheter ablation in some electrophysiological labs for a less painful procedure. However, there is few published work on the sedation regimen for catheter ablation of AF.

Application of intraoperative arterial pressure-based cardiac output monitoring for patients undergoing coronary artery bypass grafting surgery

Background For patients undergoing off-pump coronary artery bypass grafting （OPCABG）, it is important to establish a hemodynamic monitoring system to obtain powerful parameters for better intraoperative treatment. This study aimed to observe the clinical feasibility of arterial pressure-based cardiac output （APCO） for cardiac output （CO） monitoring and to evaluate the correlation between APCO and pulmonary artery catheter （PAC） for CO measurement for patients undergoing OPCABG intraoperatively. Methods Fifty patients of American Society of Anaesthesiologists （ASA） classification Ⅱ-Ⅲ, undergoing elective OPCABG at Beijing Anzhen Hospital were randomly enrolled into this study. All patients were assigned to CO monitoring by PAC and APCO simultaneously. Patients with pacemaker, severe valvular heart disease, left ventricular ejection fraction （EF） 〈40%, cardiac arrhythmias, peripheral vascular disease, application of intra-aortic balloon pump （IABP） and emergent diversion to cardiac pulmonary bypass were excluded. The radial artery waveform was analyzed to estimate the stroke volume （SV） and heart rate （HR） continuously. CO was calculated as SV × HR; other derived parameters were cardiac index （CI）, stroke volume index （SVI）, systemic vascular resistance （SVR）, and systemic vascular resistance index （SVRI）. PAC was placed via right internal jugular vein and the correct position was confirmed by PAC waveforms. Continuous cardiac output （CCO）, CI and other hemodynamic parameters were monitored at following 5 time points： immediate after anesthesia induction （baseline value）, anastomosis of left internal mammary artery to left anterior descending artery （LAD）, anastomosis of left circumflex （LCX）, anastomosis of posterior descending artery （PDA） and immediate after sternal closure. Results In the 50 patients, preoperative echocardiography measured left ventricular EF was （52.8±11.5）%, and 35 patients （70%） showed regional wall motion abnormalities. The correlation coefficient of CO monitored by APCO and PAC were 0.70, 0.59, 0.78, 0.74 and 0.85 at each time point. The bias range of CI monitored from both APCO and PAC were （0.39±0.06） L.minl.m2, （0.48±0.12） L.min^-1.m2, （0.26±0.06） L.min1.m-2, （0.27±0.06） L.min-l.m2, （0.30＋0.05） L.min-l.m2 at each time point. The results of SVR by two hemodynamic monitoring techniques had good correlation during OPCABG. The variation trends of SVR were opposite comparing with the results of CO. SVR collected from PAC obtained the highest value of （1220.0±254.0） dyn.s.cm5 at PDA anastomosis, but the highest value obtained from APCO was （1206.0±226.5） dyn.s.cm-5 in LCX anastomosis. Conclusions APCO is feasible in hemodynamic monitoring for patients undergoing OPCABG The results of hemodynamic monitoring derived from APCO and PAC are closely correlated. Its characterizations of timely, accurate and continuous display of hemodynamic parameters are also obviously demonstrated in the present study.

High volume practice proved the safety of off-pump coronary artery bypass surgery in left main coronary artery lesions： a two-year single center experience

Background Left main coronary artery （LMCA） stenosis has been recognized as a risk factorfor early death among patients undergoing coronary artery bypass grafting （CABG）. This study aimed to assess if LMCA lesions pose an additional risk of early or mid-term mortality and/or a major adverse cardiac and cerebrovascular event （MACCE） after off-pump coronary artery bypass grafting （OPCABG）, compared with non-left main coronary artery stenosis （non-mainstem disease）.