Risk Stratification and Prognosis of Pulmonary Arterial Hypertension Associated with Congenital Heart Disease

Background:Current guidelines for managing pulmonary arterial hypertension(PAH)recommend a risk strati-fication approach.However,the applicability and accuracy of these strategies for PAH associated with congenital heart disease(PAH-CHD)require further validation.This study aims to validate the reliability and predictive accuracy of a simplified stratification strategy for PAH-CHD patients over a three-year follow-up.Additionally,new prognostic variables are identified and novel risk stratification methods are developed for assessing and managing PAH-CHD patients.Methods:This retrospective study included 126 PAH-CHD patients.Clinical and biochemical variables across risk groups were assessed using Kruskal-Wallis and Fisher’s exact tests.Indepen-dent risk factors were identified using ordered logistic regression,while Kaplan-Meier and Cox proportional hazards regression analyses evaluated their impact on all-cause mortality.A new stratification model for the PAH-CHD population was constructed based on these analyses.Results:Significant survival differences across stratified risk groups were observed(p<0.001),validating the effectiveness of the simplified risk stratification method in PAH-CHD patients.Prothrombin activity was a strong independent predictor of adverse outcomes of PAH-CHD patients(Hazard ratio 0.95,p<0.001,C-index 0.70).A model combining N-terminal pro-brain natriuretic peptide,prothrombin activity,albumin,and right atrial area achieved an area under the curve of 0.89 and a C-index of 0.85.Conclusions:The simplified risk stratification method is applicable to PAH-CHD patients.Prothrombin activity is a strong independent predictor of adverse outcomes.A comprehensive risk stratification approach,incorporating both established and novel biomarkers,enhances accessibility and offers predictive efficacy during follow-up for PAH-CHD patients,comparable to established models.

Mufangji tang ameliorates pulmonary arterial hypertension through improving vascular remodeling,inhibiting inflammatory response and oxidative stress,and inducing apoptosis

Background:Mufangji tang(MFJT)is composed of Ramulus Cinnamomi,Radix Ginseng,Cocculus orbiculatus(Linn.)DC.,and Gypsum.In clinical settings,MFJT has been effectively employed in addressing a range of respiratory disorders,notably including pulmonary arterial hypertension(PAH).However,the mechanism of action of MFJT on PAH remains unknown.Methods:In this study,a monocrotaline-induced PAH rat model was established and treated with MFJT.The therapeutic effects of MFJT on PAH rat model were evaluated.Network pharmacology was conducted to screen the possible targets for MFJT on PAH,and the molecular docking between the main active components and the core targets was carried out.The key targets identified from network pharmacology were tested.Results:Results showed significant therapeutic effects of MFJT on PAH rat model.Analysis of network pharmacology revealed several potential targets related to apoptosis,inflammation,oxidative stress,and vascular remodeling.Molecular docking showed that the key components were well docked with the core targets.Further experimental validation results that MFJT treatment induced apoptosis(downregulated Bcl-2 levels and upregulated Bax levels in lung tissue),inhibited inflammatory response and oxdative stress(decreased the levels of IL-1β,TNF-α,inducible NOS,and malondialdehyde,and increased the levels of endothelial nitric oxide synthase,nitric oxide,glutathione and superoxide dismutase),reduced the proliferation of pulmonary arterial smooth muscle cells(downregulated ET-1 andβ-catenin levels and ERK1/2 phosphorylation,increased GSK3βlevels).Conclusion:Our study revealed MFJT treatment could alleviate PAH in rats via induction of apoptosis,inhibition of inflammation and oxidative stress,and the prevention of vascular remodeling.

Arterial Duct Stenting Versus Modified Blalock-Taussig Shunt in Patient with Ductal-Dependent Pulmonary Circulation: Systematic Review & Meta-Analysis

Objective:Patients with ductal-dependent pulmonary circulation require alternative bloodflow to provide and maintain adequate oxygenation.Modified Blalock-Taussig Shunt(MBTS)has been the standard for providing such a result.Currently,less invasive methods such as Arterial Duct(AD)stenting have been performed as alter-natives.This study aims to compare the outcome of AD stenting and MBTS.Method:Systematic research was performed in online databases using the PRISMA protocol.The outcomes measured were 30-day mortality,com-plication,unplanned intervention,oxygen saturation,duration of hospital,and ICU length of stay.Any compara-tive study provided with full text is included.The outcome of each study was analyzed using a trandom effects model with relative risk and mean difference as the effect size.Bias risk assessment was conducted using the New-castle-Ottawa Scale.All analyses were performed using Review Manager 5.4.1.Result:A total of 11 studies with 3154 samples included in this study.There is no significant difference in 30-day mortality between the two groups(p-value=0.10).However,there is significantly less complication(RR 0.53[0.35,0.82];p-value=0.004)and unplanned intervention(RR 0.59[0.38,0.92];p-value=0.02)in the AD stent group.Comparison of the Nakata index showed no significant difference(p-value=0.88).Post-operative oxygen saturation was measured signifi-cantly higher in the AD stenting(MD 1.80[0.85,2.74];p-value=0.0002).However,AD stent group shows sig-nificantly lower long-term oxygen saturation(MD-8.43[-14.38,-2.48];p-value=0.005).Both hospital and ICU length of stay was significantly shorter in the AD stent group(MD-8.30[-11.13,-5.48];p-value<0.00001;MD-5.09[-7.79,-2.38];p-value=0.0002).Conclusion:AD stenting provides comparable outcomes relative to MBTS as it provides less complication and unplanned intervention and higher post-procedural O2 saturation.However,MBTS proved its superiority in maintaining higher long-term oxygen saturation and still became the preferred option to manage complex cases where stenting is either challenging or unsuccessful.

Inhibitory Effect of PPARδAgonist GW501516 on Proliferation of Hypoxia-induced Pulmonary Arterial Smooth Muscle Cells by Regulating the mTOR Pathway

Objective This study aimed to investigate the effects of the peroxisome proliferator-activated receptorδ(PPARδ)agonist GW501516 on the proliferation of pulmonary artery smooth muscle cells(PASMCs)induced by hypoxia,in order to search for new drugs for the treatment and prevention of pulmonary vascular remodeling.Methods PASMCs were incubated with different concentrations of GW501516(10,30,100 nmol/L)under the hypoxic condition.The proliferation was determined by a CCK-8 assay.The cell cycle progression was analyzed by flow cytometry.The expression of PPARδ,S phase kinase-associated protein 2(Skp2),and cell cycle-dependent kinase inhibitor p27 was detected by Western blotting.Then PASMCs were treated with 100 nmol/L GW501516,100 nmol/L mammalian target of rapamycin(mTOR)inhibitor rapamycin and/or 2µmol/L mTOR activator MHY1485 to explore the molecular mechanisms by which GW501516 reduces the proliferation of PASMCs.Results The presented data demonstrated that hypoxia reduced the expression of PPARδin an oxygen concentration-and time-dependent manner,and GW501516 decreased the proliferation of PASMCs induced by hypoxia by blocking the progression through the G0/G1 to S phase of the cell cycle.In accordance with these findings,GW501516 downregulated Skp2 and upregulated p27 in hypoxia-exposed PASMCs.Further experiments showed that rapamycin had similar effects as GW501516 in inhibiting cell proliferation,arresting the cell cycle,regulating the expression of Skp2 and p27,and inactivating mTOR in hypoxia-exposed PASMCs.Moreover,MHY1485 reversed all the beneficial effects of GW501516 on hypoxia-stimulated PASMCs.Conclusion GW501516 inhibited the proliferation of PASMCs induced by hypoxia through blocking the mTOR/Skp2/p27 signaling pathway.

Changes of Protein Kinase Cα and Cyclin D1 Expressions in Pulmonary Arteries from Smokers with and without Chronic Obstructive Pulmonary Disease

The purpose of this study was to investigate the changes of protein kinase Ca （PKCα） and cyclin D1 expressions in pulmonary arteries from＇smokers with normal lung function and smokers with mild to moderate chronic obstructive pulmonary disease （COPD）. The peripheral lung tissues were obtained from 10 non-smokers with normal lung function （non-smoker group）, 14 smokers with normal lung function （smoker group）, 11 smokers with mild to moderate COPD （COPD group）. The morphological changes of pulmonary arteries were observed by HE-staining. The expressions of ct-smooth muscle actin （α-SMA）, proliferating cell nuclear antigen （PCNA）, PKCα and cyclin D1 proteins in pulmonary artery smooth muscle cells （PASMCs） were immunohistochemically determined. The percentages of PCNA-positive cells were taken as the smooth muscle cells proliferation index （PI）. The mRNA expressions of PKCα and cyclin D l in PASMCs were evaluated by real-time fluorescence PCR. Morphometrical analysis showed that the ratio of pulmonary artery wall area to total area （WA%） in smoker group and COPD group was significantly greater than that in non-smoker group （P〈0.01）. The PASMCs proliferation index in smoker group and COPD group was significantly higher than that in nonsmoker group （P〈0.01）. The protein levels of PKCct and cyclin D1 inPASMCs were significantly increased in smoker group and COPD group as compared with non-smoker group （P〈0.01）. The mRNA expressions of PKCα and cyclin D1 in PASMCs were significantly elevated in smoker group and COPD group as compared with non-smoker group （P〈0.01）. Significant correlations were found between PKCα protein and WA% or PI （P〈0.01）. Correlations between cyclin D1 protein and WA% or PI also existed （P〈0.01）. The expression of PKCa was positively correlated with the expression of cyclin D 1 at both protein and mRNA levels （P〈0.01）. In conclusion, increased expressions of PKCα and cyclin D1 might be involved in the pathogenesis of abnormal proliferation of PASMCs in smokers with normal lung function and smokers with mild to moderate COPD.

Rutaecarpine attenuates monocrotaline-induced pulmonary arterial hypertension in a Sprague-Dawley rat model

Background:Pulmonary arterial hypertension presents with obliterative remodeling of the pulmonary arteries and progressive elevation of pulmonary vascular resistance,which increase the risk of right ventricular failure and death.It has been reported in previous studies that rutaecarpine plays a crucial role in anti-inflammatory and antioxidant activities,which may help regulate cell apoptosis and cell proliferation.The purpose of this study was to determine the effects of rutaecarpine in the rat model of monocrotaline-induced pulmonary hypertension.Methods:We induced pulmonary arterial hypertension in adult Sprague-Dawley rats by injecting monocrotaline(60 mg/kg)and then treated with rutaecarpine(40 mg/kg·d)or sildenafil(30 mg/kg·d)(positive control).Subsequently,pulmonary function,inflammation,cytokines and pulmonary vascular remodeling or proliferation were assessed.Results:Rutaecarpine was found to improve monocrotaline-induced mean pulmonary artery pressure,cardiac index,right heart index,right ventricular hypertrophy index,pulmonary artery remodeling and pulmonary function.reverse transcription-quantitative polymerase chain reaction demonstrated a decrease in tumor necrosis factor-α,interleukin-6 and interleukin-1β,whereas western blots a significantly decrease in the expression of nuclear factor kappa-B,endothelin-1,extracellular signal-regulated kinases 1/2,B cell lymphoma-2,Beclin1 and microtubule-associated protein1 light chain 3-II protein,and increase in the expression of Bax,caspase-3 and p62 protein.Conclusion:Rutaecarpine attenuated pulmonary arterial hypertension by inhibiting inflammation,oxidative stress,cell proliferation and autophagy,while promoting apoptosis.

Pulmonary arterial hypertension confirmed by right heart catheterization following COVID-19 pneumonia: A case report and review of literature

BACKGROUND Pulmonary arterial hypertension(PAH)is a disease of the arterioles resulting in an increased resistance in pulmonary circulation with associated high pressures in the pulmonary arteries,causing irreversible remodeling of the pulmonary arterial walls.Coronavirus disease 2019(COVID-19)has been associated with development of new onset PAH in the literature leading to symptoms of dyspnea,cough and fatigue that persist in spite of resolution of acute COVID-19 infection.However,the majority of these cases of COVID related PAH were diagnosed using echocardiographic data or via right heart catheterization in mechanically ventilated patients.CASE SUMMARY Our case is the first reported case of COVID related PAH diagnosed by right heart catheterization in a non-mechanically ventilated patient.Right heart catheterization has been the gold standard for diagnosis of pulmonary hypertension.Our patient had right heart catheterization four months after her initial COVID-19 infection due to persistent dyspnea.CONCLUSION This revealed new onset PAH that developed following her infection with COVID-19,an emerging sequela of the infection.

Characterization of optimal resting tension in human pulmonary arteries

AIM To determine the optimum resting tension(ORT) for in vitro human pulmonary artery(PA) ring preparations.METHODS Pulmonary arteries were dissected from disease free sections of the resected lung in the operating theatre and tissue samples were directly sent to the laboratory in Krebs-Henseleit solution(Krebs).The pulmonary arteries were then cut into 2 mm long rings.PA rings were mounted in 25 m L organ baths or 8 m L myograph chambers containing Krebs compound(37 ℃,bubbled with 21% O_2:5% CO_2) to measure changes in isometric tension.The resting tension was set at 1-gram force(gf) with vessels being left static to equilibrate for duration of one hour.Baseline contractile reactions to 40 mmol/L KCl were obtained from a resting tension of 1 gf.Contractile reactions to 40 mmol/L KCl were then obtained from stepwise increases in resting tension(1.2,1.4,1.6,1.8 and 2.0 gf).RESULTS Twenty PA rings of internal diameter between 2-4 mmwere prepared from 4 patients.In human PA rings incrementing the tension during rest stance by 0.6 gf,up to 1.6 gf significantly augmented the 40 mmol/L KCl stimulated tension.Further enhancement of active tension by 0.4 gf,up to 2.0 gf mitigate the 40 mmol/L KCl stimulated reaction.Both Myograph and the organ bath demonstrated identical conclusions,supporting that the radial optimal resting tension for human PA ring was 1.61 g.CONCLUSION The radial optimal resting tension in our experiment is 1.61 gf(15.78 m N) for human PA rings.

Effects of Combined Inhalation of Budesonide,Formoterol,and Tiotropium Bromide on Arterial Blood Gas and Pulmonary Function Indexes in Patients with Chronic Obstructive Pulmonary Disease

Objective:To analyze the effect of combined inhalation of budesonide formoterol and tiotropium bromide on arterial blood gas and pulmonary function indexes in patients with chronic obstructive pulmonary disease(COPD).Methods:100 patients with COPD treated from January to December 2022 were selected as observation objects,and were divided into a control group(n=50,in which budesonide and formoterol were administered)and an experimental group(n=50,the treatment drug was budesonide formoterol combined with tiotropium bromide)according to the computer grouping method,and compared the treatment results.Results:(i)Before treatment,there was no difference in the partial pressure of carbon dioxide and partial pressure of oxygen between the control group and the experimental group(P>0.05);after treatment,the partial pressure of carbon dioxide and partial pressure of oxygen in the experimental group were higher than those in the control group,with significant differences(P<0.05).(ii)Before treatment,there was no difference in forced vital capacity(FVC),forced expiratory volume in one second(FEV1),FEV1/FVC between the control group and the experimental group(P>0.05);after treatment,the FVC,FEV1,and FEV1/FVC in the experimental group were significantly higher than those in the control group(P<0.05).(iii)There was no difference in the levels of CRP,IL-6,and TNF-αbetween the control group and the experimental group(P>0.05);after treatment,the levels of CRP,IL-6,and TNF-αin the experimental group were lower than those in the control group,with significant differences(P<0.05).(iv)Compared to the total incidence of adverse reactions in the control group(28.00%),the incidence of total adverse reactions in the experimental group was lower at 10.00%,and the difference was significant(P<0.05).Conclusion:The combined inhalation of budesonide and formoterol with tiotropium bromide has demonstrated a clear therapeutic efficacy and safety in treating chronic obstructive pulmonary disease.This treatment approach effectively enhances arterial blood gas levels and lung function,showing promising potential for widespread application.

Intervention control of aerobic exercise in maintaining quality of life and pulmonary hypertension in hemodialysis patients

BACKGROUND Pulmonary hypertension is a serious complication in the treatment of maintenance hemodialysis patients,which seriously affects the quality of life of patients and threatens their life safety.Prevention,treatment and improvement of pulmonary hypertension are of great significance to improve the quality of life of patients.AIM To investigate the intervention and control of pedal-powered bicycle in maintaining quality of life and pulmonary hypertension in hemodialysis patients.METHODS 73 patients with maintenance hemadialysis combined with pulmonary arterial hypertension at a hemodialysis center in a certain hospital from May 2021 to May 2022 are selected.Patients are divided into two groups,37 cases in the control group(group C)and 36 cases in the intervention group(group I).Patients are divided into two groups,group C is treated with oral administration of betaglandin sodium combined with routine nursing care.Based on group C,group I conducts power cycling exercises.RESULTS After treatment,group I patients had higher muscle strength,36-Item Short Form Health Survey scores,and Kidney Disease Targets Areas scores;The 6-minute walk distance test index level was higher and the Borg score was lower;The group I had lower systolic blood pressure,greater vital capacity,higher positive emotion,lower systolic pulmonary artery pressure index level,higher arterial partial oxygen pressure level,lower pulmonary vascular resistance index level,and higher blood oxygen saturation level[158.91±11.89 vs 152.56±12.81,1795.01±603.18 vs 1907.20±574.15,24.00(22.00,29.00)vs 24.00(22.00,28.00),P<0.001].CONCLUSION Aerobic exercise combined with Western medicine treatment can effectively improve patients'pulmonary hypertension,alleviate their negative emotions,and enable them to achieve a higher level of quality of life.

Migration of a Progestin Implant into a Pulmonary Artery: Observation of a Case at the Reference Health Center of Commune III of the District of Bamako in Mali

It was a 36-year-old patient, 5th Pregnancy, 5th Delivery, 4 live children, and I deceased, had a consultation in the department for the removal of implants. Questioning revealed that she had had the implant three years ago without medical follow-up. It was in view of the difficulties in extracting the capsule that the chest X-ray and CT scan carried out concluded that the implant had migrated into a branch of the left pulmonary artery. Therapeutic abstention has been the attitude of cardiovascular surgeons.

A Novel Perspective on Histopathology Provides Novel Insights into Surgical Effects in Pulmonary Atresia,Ventricular Septal Defect,and Major Aortopulmonary Collateral Arteries:A Case-Series Study

Background:Never had literatures characterized the relationship between the property of major aortopulmonary collateral arteries(MAPCAs)and outcomes of selective unifocalization of pulmonary atresia with ventricular septal defects and MAPCAs.Methods:This is a case-series study.Thirteen patients were included.Angiographybased assessment was conducted to determine whether collateral arteries should be unifocalized or treated with intraoperative ligature.Specimens were collected and stained by HE and ET+VG.Results:Twelve patients underwent one-stage unifocalization at a median age of 37 months(range:6–228 months)and a median weight of 14.0 kg(range:5.0–49.0 kg),which produced a favorable right ventricle to aortic systolic pressure ratio of no more than 0.5 except in one patient who died.Patients were divided into three groups:Group 1(n=6),had no native pulmonary arteries,and collateral arteries supplied all pulmonary blood;Group 2(n=6)presented dysplastic native pulmonary arteries on one or both sides,and in some lung lobes or segments,blood was supplied only by collateral arteries;Group 3(n=1)had well-developed left and right pulmonary arteries,and collateral arteries,and pulmonary arteries provided blood flow to the same segments.Pathological reports demonstrated two types of collateral arteries:Elastic arteries presented an arborization distribution similar to native pulmonary artery walls,while muscular arteries showed high resistance and distortion.We selectively unifocalized single-supply collateral arteries with morphologic features based on the arborization distribution.Conclusions:We found that there were two kinds of MAPCAs with different histology,and we performed selective UF for MAPCAs that might belong to the elastic artery.Selective unifocalization achieved a low right ventricle to aortic systolic pressure ratio and favorable surgical effects.

Contribution of oxidative stress to pulmonary arterial hypertension

Recent data implicate oxidative stress as a mediator of pulmonary hypertension (PH) and of the associated pathological changes to the pulmonary vasculature and right ventricle (RV). Increases in reactive oxygen species (ROS), altered redox state, and elevated oxidant stress have been demonstrated in the lungs and RV of several animal models of PH, including chronic hypoxia, monocrotaline toxicity, caveolin-1 knock-out mouse, and the transgenic Ren2 rat which overexpresses the mouse renin gene. Generation of ROS in these models is derived mostly from the activities of the nicotinamide adenine dinucleotide phosphate oxidases, xanthine oxidase, and uncoupled endothelial nitric oxide synthase. As disease progresses circulating monocytes and bone marrow-derived monocytic progenitor cells are attracted to and accumulate in the pulmonary vasculature. Once established, these inflammatory cells generate ROS and secrete mitogenic and fibrogenic cytokines that induce cell proliferation and fibrosis in the vascular wall resulting in progressive vascular remodeling. Deficiencies in antioxidant enzymes also contribute to pulmonary hypertensive states. Current therapies were developed to improve endothelial function, reduce pulmonary artery pressure, and slow the progression of vascular remodeling in the pulmonary vasculature by targeting deficiencies in either NO (PDE-type 5 inhibition) or PGI 2 (prostacyclin analogs), or excessive synthesis of ET-1 (ET receptor blockers) with the intent to improve patient clinical status and survival. New therapies may slow disease progression to some extent, but long term management has not been achieved and mortality is still high. Although little is known concerning the effects of current pulmonary arterial hypertension treatments on RV structure and function, interest in this area is increasing. Development of therapeutic strategies that simultaneously target pathology in the pulmonary vasculature and RV may be beneficial in reducing mortality associated with RV failure.

Iptakalim, a novel ATP-sensitive potassium channel opener, inhibits pulmonary arterial smooth muscle cell proliferation by downregulation of PKC-α

Iptakalim is a new ATP-sensitive potassium （KATp） channel opener, and it inhibits the proliferation of pulmonary arterial smooth muscle cells （PASMCs） and pulmonary vascular remodeling. However, the underlying mechanism remains unclear. In the present study, we found that iptakalim significantly decreased pulmonary artery pressure, inhibited pulmonary ariery remodeling and PKC-α overexpression in chronic hypoxia in a rat pulmonary hypertension model. Iptakalim reduced hypoxia-induced expression of PKC-α, and abolished the effect of hypoxia on PASMC proliferation significantly in a dose-dependent manner in vitro. Moreover, these effects were abol- ished by glibenclamide, a selective KArp channel antagonist. These results indicate that iptakalim inhibits PASMC proliferation and pulmonary vascular remodeling induced by hypoxia through downregulating the expression of PKC-α. Iptakalim can serve as a novel promising treatment for hypoxic pulmonary hypertension.

Transgelin as a potential target in the reversibility of pulmonary arterial hypertension second to congenital heart disease

Background The reversibility of pulmonary arterial hypertension(PAH)in congenital heart disease(CHD)is of great importance for the operability of CHD.Proteomics analysis found that transgelin was significantly upregulated in the lung tissue of CHD-PAH patients,especially in the irreversible group.However,how exactly it participated in CHD-PAH development is unknown.

Pulmonary and cerebral lipiodol embolism after transcatheter arterial hemoembolization in hepatocellular carcinoma

Pulmonary and cerebral lipiodol embolism after transcatheter arterial chemoembolization (TACE) of hepatocellular carcinoma is rare. To our knowledge, only 7 cases have been reported in the literature. We present a case of pulmonary and cerebral lipiodol embolism, and analyzed retrospectively the imaging and clinical data of the patient and conclude the most probable mechanism of pulmonary and cerebral lipiodol embolism, which is different from that of the cases reported previously.

Interventional treatment of pulmonary arteriovenous malformations

Pulmonary arteriovenous malformations(PAVM) are congenital vascular communications in the lungs.They act as right to left shunts so that the blood running through these malformations is not oxygenated or filtered.These patients are typically hypoxaemic with exercise intolerance and are at high risk of paradoxical emboli to the brain and other organs.These malformations are most commonly seen in hereditary haemorrhagic telangiectasia(HHT)(Mb.Osler-Weber-Rendu syndrome).Nowadays,the generally accepted treatment strategy of first choice is embolization of the afferent arteries to the arteriovenous malformations.It is a minimally invasive procedure and at the same time a lung preserving treatment with a very high technical success,high effectiveness and low morbidity and mortality.Embolization prevents cerebral stroke and abscess as well as pulmonary haemorrhage and further raises the functional level.Embolization is a well-established method of treating PAVM,with a significant effect on oxygenation of the blood.Screening for PAVM in patients at risk is recommended,especially in patients with HHT.

Prevalence of Anti-endothelial Cell Antibodies in Patients with Pulmonary Arterial Hypertension Associated with Connective Tissue Diseases

Objective To investigate the prevalence of anti-endothelial cell antibodies (AECAs) in the sera of connective tissue diseases (CTD) patients with pulmonary arterial hypertension (PAH) and its correlation with clinical manifestations. Methods AECAs in sera of 39 CTD patients with PAH,22 CTD patients without PAH,and 10 healthy donors as controls were detected with Western blotting. The prevalence of different AECAs in different groups was compared and its correlation with clinical manifestations was also investigated. Results The prevalence of AECAs was 82.1% in CTD patients with PAH,72.7% in CTD patients without PAH,and 20.0% in healthy donors. Anti-22 kD AECA was only detected in CTD patients with PAH (15.4%). Anti-75 kD AECA was more frequently detected in CTD patients with PAH than in those without PAH (51.3% vs. 22.7%,P<0.05). In CTD patients with PAH,anti-75 kD AECA was more frequently detected in those with Raynaud’s phenomenon or with positive anti-RNP antibody. Conclusion AECAs could be frequently detected in CTD patients with or without PAH,while anti-22 kD and anti-75 kD AECA might be specific in CTD patients with PAH.

Pulmonary complications of transcatheter arterial chemoembolization for hepatocellular carcinoma

Transcatheter arterial chemoembolization(TACE) is an effective palliative intervention that is widely accepted for the management of hepatocellular carcinoma(HCC). Post-TACE pulmonary complications resulting in acute lung injury(ALI) or acute respiratory distress syndrome(ARDS) are rare events. Pulmonary complications after TACE are thought to be related to chemical injury subsequent to the migration of the infused ethiodized oil or chemotherapeutic agent to the lung vasculature, facilitated by arteriovenous(AV) shunts within the hyper-vascular HCC. We review herein the literature on pulmonary complications related to TACE for HCC. Post-TACE pulmonary complications have included pulmonary oil embolism, interstitial pneumonitis, chemical pneumonitis, ALI, ARDS, lipoid pneumonia, acute eosinophilic and neutrophilic pneumonia, bilious pleuritis, pulmonary abscess, pulmonary tumor embolism, and possibly pulmonary metastasis with HCC. The risk factors associated with post-TACE pulmonary complications identified in the literature include large hyper-vascular HCC with AV shunts, large-volume Lipiodol infusion, and embolization via the right inferior phrenic artery. However, the absence of known risk factors is not a guarantee against serious complications. An astute awareness of the potential post-TACE pulmonary complications should expedite appropriate therapeutic interventions and increase potential for early recovery.

Proteomic analysis of the serum in patients with idiopathic pulmonary arterial hypertension

Idiopathic pulmonary arterial hypertension(IPAH) is a rare disease of unknown etiology.The exact pathogenesis of pulmonary arterial hypertension is still not well known.In the past decades,many protein molecules have been found to be in-volved in the development of IPAH.With proteomic techniques,profiling of human plasma proteome becomes more feasible in searching for disease-related markers.In present study,we showed the protein expression profiles of the serum of IPAH and healthy controls after depleting a few high-abundant proteins in serum.Thirteen spots had changed significantly in IPAH com-pared with healthy controls and were identified by LC-MS/MS.Alpha-1-antitrypsin and vitronectin were down-regulated in IPAH and may be valuable candidates for further explorations of their roles in the development of IPAH.