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Objective:To evaluate the strategy and safety of the radiofrequency ablation (RFA) on ventricular arrhythmias (VAs) originating from the pulmonary sinus cusp (PSC) in pediatric patients.Methods:Retrospective study.Fifteen patients with VAs originating from the PSC who were intervened by RFA in the Department of Pediatric Cardiology, Guangdong Provincial People′s Hospital between March 2014 to July 2020 were enrolled.All the patients met the indication criteria for RFA in pediatric patients.The electrocardiogram, ablation method of ablation were analyzed.Different curved catheters were selected for RFA according to the age and weight of the patients.The catheter was then inserted in a " U" or inverted " P" shape to the PSC.The long-term effect of ablation were reviewed.Results:The mean age and body weight of 15 patients with VAs originating from the PSC were (11.6±2.6) (6-15) years and (39.9±12.2) (19-65) kg, respectively.The electrocardiogram recorded during VAs originating from the PSC showed left bundle branch block and inferior axis with monomorphic R pattern, as well as a QS-wave in aVR and aVL.The electrocardiogram characteristics varied in patients with VAs originating from the PSC.The ideal excitation point was not found in the right ventricular outflow tract or the ablation was unsuccessful in all patients, and the earliest target was mapped and RFA was successful.Among the 15 patients, the successful ablation site was in the lower regions of the PSC, involving the right cusp in 11 patients(73.3%), the anterior cusp in 3 patients(20.0%), and the left cusp in 1 patient(6.7%). The earliest potential recorded at the PSC ablation site preceded the QRS complex onset by (27.3±6.0) ms.During the follow-up period for (2.7±2.0) years, no recurrence of VAs or complications were recorded.Conclusions:Under the premise of gentle catheterization procedure and appropriate radiofrequency energy, ablation was effective, safe and with low recurrence rate to eradicate VAs originating from the PSC in children.
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<p><b>BACKGROUND</b>Autophagy has been found to be involved in animal and cell models of atherosclerosis, but to date, it lacks general observation in human atherosclerotic plaques. Here, we investigated autophagy in smooth muscle cells (SMCs), endothelial cells (ECs), and macrophages in human atherosclerotic plaques via transmission electron microscopy (TEM), western blotting, and immunohistochemistry analysis.</p><p><b>METHODS</b>The histopathologic morphology of these plaques was observed via hematoxylin and eosin staining. The ultrastructural morphology of the SMCs, ECs, and macrophages in these plaques was observed via TEM. The localization of microtubule-associated protein 1 light chain 3 (MAP1-LC3), a relatively special maker of autophagy, in plaques was observed by double fluorescent immunochemistry and western blotting.</p><p><b>RESULTS</b>All of these human atherosclerotic plaques were considered advanced and unstable in histologically observation. By double fluorescent immunochemistry, the expression of LC3-II increased in the SMCs of the fibrous cap, the macrophages, and the microvascular ECs of the plaque shoulders. The protein level of LC3-II by western blotting significantly increased in plaques compared with normal controls. In addition, TEM observation of plaques revealed certain features of autophagy in SMCs, ECs, and macrophages including the formation of myelin figures, vacuolization, and the accumulation of inclusions in the cytosol. These results indicate that autophagy is activated in SMCs, ECs, and macrophages in human advanced atherosclerotic plaques.</p><p><b>CONCLUSIONS</b>Our study is to demonstrate the existence of autophagy in human atherosclerotic plaques by different methods, which may contribute to the development of pharmacological approaches to stabilize vulnerable and rupture-prone lesions.</p>
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Humans , Atherosclerosis , Metabolism , Autophagy , Physiology , Endothelial Cells , Pathology , In Vitro Techniques , Microscopy, Electron, Transmission , Microtubule-Associated Proteins , Metabolism , Myocytes, Smooth Muscle , Pathology , Plaque, Atherosclerotic , MetabolismABSTRACT
Objective To analyze the causes of failed transcatheter closure for ventricular septal defects (VSD)in children. Methods One thousand two hundred and eighty children aged 13 to 141 months who underwent transcatheter closure from June 2009 to September 2013 in Guangdong General Hospital were selected. There were 43 failures(3. 36% ). The clinical data including transthoracic echocardiograph( TTE),radiography,interventional ap-proach and surgical findings were analyzed. Results Forty - three patients included 25 male and 18 female. The pa-tients' ages ranged from 13 to 141(43. 0 ± 31. 9)months and their weight ranged from 10 to 35(16. 3 ± 5. 59)kg. The causes of failure including doubly committed subarterial VSD misdiagnosed as perimembranous VSD(PMVSD)or intracristal VSD were in 6 patients. The size of occluder was too small in 13 cases,and there were statistical differences between three measurements of size of VSD(F = 19. 134,P = 0. 001). The size of VSD measured by left ventricular an-giography was significantly smaller than that measured by TTE,and there was statistical difference[(4. 78 ± 1. 11) mm vs(6. 48 ± 1. 43)mm,t = 4. 50,P = 0. 001]. The dimension of VSD measured by left ventricular angiography was significantly smaller than that measured by surgical findings,and there was statistical difference[(4. 78 ± 1. 11) mm vs(7. 02 ± 1. 08)mm,t = 5. 92,P = 0. 001]. But,the size of VSD measured by TTE had no significant difference compared with that measured by surgical findings(t = 1. 42,P = 0. 168). Aortic regurgitation occurred in 14 cases;atrioventricular block or left bundle branch block in 3 patients;tricuspid stenosis in 2 cases and residual shunt in 5 pa-tients. Conclusions Doubly committed subarterial VSD may be misdiagnosed as PMVSD or intracristal VSD. In the ca-ses of VSD concomitant with aortic valve prolapse,size of the occluders should be referred to VSD dimensions measured by TTE. In the cases of VSD adjacent to aortic valve,suitable occluders should be selected and operation technique should be improved to avoid aortic regurgitation.
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ObjectiveToanalyzetheclinicalandimagingcharacteristicsinpatientswithcarotidsteal syndrome ( CSS ) and to investigate its compensatory pathw ays, diagnosis, and treatment. Methods The medical history and imaging data of the patients with CSS were colected. Their vascular lesions, colateral circulation, treatment, and prognosis w ere analyzed. Results A total of 11 patients w ith CSS (8 males and 3 females, mean age 66.7 ±5.1 years) were enroled in the study. Their clinical manifestations were posterior circulation transient ischemic attack (TIA) ( n=9, 81.8%), posterior circulation infarction ( n=1, 9.1%), and anterior circulation TIA ( n=1, 9.1%). A total of 19 pathological arteries w ere found:12 (63.1%) w ith occlusion, 2 (10.5%) w ith subtotal occlusion, 4 (21.0%) w ith severe stenosis and 1 (5.2%) w ith artery dissection. Seven patients (63.6%) w ere bilateral internal carotid artery lesions, 3 (27.2%) w ere unilateral bilateral internal carotid artery lesions, and 1 (9.1%) w as bilateral common carotid artery occlusion. Eleven patients had primary col ateral circulation, including posterior communicating artery patency in 10 patients (90.9%) and anterior communicating artery patency in 1 patient (9.1%). Four patients (36.3%) had secondary col ateral circulation and 1 (9.1%) had tertiary col ateral circulation. Al patients w ere treated w ith medication on the basis of the management of risk factors. Three patients w ere treated w ith stenting and tw o were treated with carotid endarterectomy. No stroke occurred in al patients during folow -up til September 2014. Conclusions The vascular lesions of patients w ith CSS often occur in the extracranial segment of internal carotid artery. Usual y the compensatory blood is through the circle of Wil is. The presentation is ischemia in the stolen arteries. Its diagnosis needs to be examined by digital subtraction angiography. On the basis of medication therapy, some patients may be treated w ith surgery or endovascular intervention.
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Objective To evaluate the clinical effect for transcatheter closure of intracristal ventricular septal defects (IVSD) using duct occluder.Methods Between Jun.2012 and Sep.2013,implantaion of duct occluder was conducted in 27 IVSD pmients,which was compmed with acentric ventricular septal occluder attempted in 53 IVSD patients.The transthoracic echocardiography,electrocardiography,and clinical examination were observed at 24 hours,and after 1,3,6 and 12 months follows-up.Results Implantation of duct occluders were achieved in 26 (96.23 ％) patients and implantation of acentric ventricular septal occluder in 42 (79.25％) patients.The mean follow-up time was 6.78 months (1-17 months).The procedure time,fluoroscopic time and residual shunt were not statistically different between the 2 groups (all p ＞ 0.05).The size of VSD (t =-3.124,P =0.003) and occluder diameter (t =-4.285,P ＜0.001)were smaller and the procedure success rate was higher in the duct occluder group (x2 =9.099,P =0.011).Left ventricular end diastolic dimension,left atrial diameter,left ventricular end diastolic dimension,right ventricular end diastolic dimension and pulmonary artery diameter were decreased significantly (F =57.62,5.002,4.754,2.782,P =0.000,0.033,0.001,0.030) after surgical procedure compared with those before procedure,except for the right atrial diameter and left ventricular ejection fraction.No new serious aortic regurgitation or increased mitral regurgitation,tricuspid regurgitation was shown after procedure in 2 groups.Complete left bundle branch block occurred in 2 patients respectively,pericardial effusion and thromboembolism of right femoral artery occurred in 1 patient in the acentric ventricular septal occluder group.Conclusions The duct occluder for IVSD closure has presented a good result,without serious complications,which provides a new method for IVSD closure.Further studies are necessary to determine the long-term results in a larger population of patients.
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Objeetive To investigate the risk of hemorrhagic transformation (HT) and the outcome as well as its influencing factors at 3 months after thrombolytic therapy in acute ischemic stroke patients with non-valvular atrial fibrillation (NVAF).Methods Consecutive acute ischemic stroke patients with NVAF were enrolled retrospectively.Their demography,vascular risk factors and other clinical data were collected.The modified Rankin Scale (mRS) was used to evaluate the outcome at 3 months after symptom onset.The mRS score ≤ 2 was defined as good outcome,and ＞ 2 was defined as poor outcome.Results A total of 119 acute ischemic stroke patients with NVAF were enrolled,including 63 males (52.9％) and 56 females (47.1％); their mean age was 72.1± 10.0; 45 (37.81％) were treated with recombinant tissue type plasminogen activator (rtPA),55 (46.2％) had a good outcome and 27 (22.7％) combined with HT.Compared with the poor outcome group,the mean age was younger in the good outcome group (P =0.028).The proportions of the patients with ischemic heart disease and the time from onset to treatment ＞ 4.5 h were lower (P ＜0.05).The baseline systolic blood pressure and diastolic blood pressure,as well as the National Institutes of Health Stroke Scale (NIHSS) score were lower (P ＜0.05),while the proportion of patients receiving intravenous thrombolysis with rtPA was higher (P =0.019).Multivariate logistic regression analysis showed that the patients with ischemic heart disease (odds ratio [OR] 4.572,95％ confidence interval [CI] 1.392-15.014; P =0.012),systolic blood pressure before treatment (OR 1.028,95％ CI 1.007-1.049; P =0.009),baseline NIHSS score (OR 1.058,95％ CI 1.002-1.117; P =0.042) were the independent risk factors for poor outcome,while intravenous thrombolysis with rtPA (CI 0.264,95％ CI 0.102-0.683; P =0.006) was an independent protective factor for poor outcome.The proportions of the baseline systolic blood pressure,fasting blood glucose and NIHSS score,as well as the patients with a history of previous stroke or transient ischemic attack (TIA) in the HT group were significantly higher than those in the non-HT group (all P ＜ 0.05).Multivariate logistic regression analysis showed that the baseline NIHSS score (OR 1.147,95％ CI 1.068-1.231; P＜0.001),baseline systolic blood pressure (OR 1.951,95％ CI 1.921-1.982; P =0.002),and blood glucose level (OR 1.191,95％ CI 1.095-1.294; P ＜ 0.001) were the independent risk factors for HT.Compared with the non-thrombolysis group,the mean age of the thrombolysis group was younger (P =0.021),the baseline systolic blood pressure,fasting glucose and NIHSS scores,as well as the proportions of patients with hyperlipidemia,previous stroke or TIA history,and using antihypertensive drugs before admission were higher (all P ＜ 0.05).The proportion of patients with ischemic heart disease were lower (P =0.035),but the proportion of the patients with a good outcome was higher (P =0.019).Conclusions Patients with ischemic heart disease,systolic blood pressure and higher baseline NIHSS score before treatment were the independent risk factors for poor outcome,while intravenous thrombolytic therapy with rtPA was an independent protective factor for poor outcome; the high baseline NIHSS score,baseline systolic blood pressure and glucose level were the independent risk factors for HT.For acute ischemic stroke patients with NVAF,such as no obvious contraindications for thrombolytic therapy,might benefit from intravenous thrombolytic therapy,and it could not increase the risk of HT,but the blood pressure and glucose level of the patients should be controlled appropriately.
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Objective To explore the specific role of autophagy and ubiquitin-proteasome pathway in apoptosis, specific protease inhibitor and (or) macroautophagy inhibitors.Methods The stimulators were selected to work on the pheochromocytoma (PC12) cell lines transfected with human mutant α-synuclein (A53T).Cell activity and apeptosis rate were detected by MTT law and flow cytometry.NO energy, heat shock protein 70 (Hsp70) and Caspase-3 expression were determined in cell culture.Results A53T cell survival rate significantly decreased 24 hours after handling with the protease inhibitor (100 nmol/L) and (or) autophagy inhibitors 3-MA (10 mmol/L, A =0.23±0.01,0.19±0.01 and 0.17±0.01 respectively; P <0.05) compared with the control group (A =0.32±0.06).Cell survival rate was significantly higher than the other drug group after 24 hours handling with autophagy stimulators (A =0.44±0.08).Compared with the control group or autophagy stimulator of rapamycin (0.2 μg/ml) group (1.55%±1.15%), A53T cells apeptosis percentage rate was significantly higher after treated with proteasome inhibitor and macroautophagy inhibitors 24 hours (4.74%±0.91%, 4.59%±1.18% and 5.40%±1.75%respectively, P <0.05); and a slight decrease with stimulators.Protein Hsp70 and NO were significantly higher in proteasome inhibitor groups than the control group.But in antophagy inhibitor and stimulator group, NO and Hsp70 protein was similar to the control group.Conclusion The inhibition of macroautophagy and proteasome can promote apoptosis.Inhibiting or stimulating autophagy has less impact on Hsp70 and NO than proteasome pathway.
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AVNRT, (3)There was no evidence of new arrhythmia occurring for the late electrophysiologic sequelae of RFCA lesions. Conclusion The technique of RFCA is safe, it causes significant minor myocardial injury and takes 3 months to develop from initially resembling coagulation necrosis to fibrosis. There is no evidence of new arrhythmia occurring for late electrophysiologic sequelae of RFC lesions.