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.

THE ROLES OF bcl-2 GENE FAMILY IN THE PULMONARY ARTERY REMODELING OF HYPOXIA PULMONARY HYPERTENSION IN RATS

Objective. To investigate the roles of apoptosis in the pulmonary artery remodeling of pulmonary hypertension secondary to hypoxia and illustrate the relative genes expression. Methods. Thirty rats were divided into hypoxia group（ 10％ O2, 8h/d） and normal control group. On the 15th day of hypoxia, pulmonary artery pressure and right ventricular hypertrophy index were measured and pulmonary artery vessels were studied by light microscope. Then terminal deoxynucleotidyl transferase- mediated dUTP nick- end labeling（ TUNEL） technique was used to detect nucleosomal DNA fragmentation of apoptotic cells. In situ hybridization and RT- PCR were used to detect the expression level of bcl- 2 and bax. Results. The pulmonary artery pressure and right ventricular hypertrophy index of hypoxia group were increased significantly, the pulmonary artery wall of hypoxic group become incrassate than control group. Apoptotic cells can be found in lung with hypoxia or without hypoxia. Compared with control group, apoptotic index of hypoxic group decreased significantly. Through the methods of in situ hybridization and RT- PCR, we found the expression of bcl- 2 increased whereas bax decreased significantly in the hypoxic group. Conclusion. The alternation in bcl- 2 and bax expression induced by hypoxia play an important role in the pulmonary artery remodeling which is the main pathologic change of pulmonary hypertension secondary to hypoxia.

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.

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.

Compression of Left Main Coronary Artery in Patients with Pulmonary Artery Aneurysm and Pulmonary Hypertension

Background: Pulmonary artery aneurysm (PAA) is an unusual finding and its association with left main coronary (LMCA) compression is even more infrequent. Cardiac CT evaluates of presence and size of PAA and the degree of LMCA compression. The aim of this study is to describe two cases of adults with compression of LMCA with PAA associated with PDA and pulmonary hypertension. Case presentation: The first case is a 27-year-old man with PAA (78 mm diameter) and LMCA compression of 70% between the aortic sinus and the PAA. He presented angina as a manifestation of the LMCA compression. During follow-up the patient died. The second case is a 28-year-old man with PAA (110 mm diameter) that compresses LMCA in 55%, he rejected surgical treatment, but he is in close follow-up with medical treatment. Conclusion: Cardiac computed tomography played an important role both in the diagnosis and identification of high-risk PAA patients.

Early Results of Mitral Valve Replacement in Severe Pulmonary Artery Hypertension—An Institutional Prospective Study

Introduction: In patients undergoing surgery for mitral valve replacement (MVR) for valvular heart disease, pulmonary artery hypertension (PAH) has been considered a major risk factor. In this prospective study, we have studied the early hemodynamic changes and post-operative outcomes of MVR among patients with severe PAH. Methods: 68 consecutive patients who underwent mitral valve replacement for severe rheumatic mitral valve disease with severe PAH (pulmonary artery pressure (PAP) > 50 mmHg) were studied prospectively for immediate postoperative hemodynamics and outcomes. The mean age of the patients was 32.1 years. 32 (47.05%) patients had mitral stenosis, 13 (19.11%) had mitral regurgitation and 23 (33.82%) had mixed lesions. Patients were divided into two groups based on preoperative pulmonary artery pressures. In 56 patients (82.35%, group I) PAP was sub-systemic or systemic, with a mean of 58.4 mmHg. Twelve patients (17.65%, group II) had supra-systemic PAP with a mean of 82.4 mmHg. Results: After mitral valve replacement, the PAP and pulmonary vascular resistance (PVR) decreased significantly in group I to near normal levels. In group II also the PAP and PVR decreased significantly but significant residual PAH remained. Operative mortality was 3.5% in group I and 16.6% in group II. Conclusions: MVR is safe and effective at the presence of severe PAH as long as the PAP is below or equal to systemic pressures. With suprasystemic PAP, MVR carries a high risk of mortality and the patient continues to have severe PAH in the postoperative period.

Chronic thromboembolic pulmonary hypertension(CTEPH):outcomes of surgical effect in patients with unilateral main pulmonary artery occlusion

Objective To summarize the clinical characteristics and the effect of pulmonary endarterectomy(PEA)in CTEPH patients with unilateral main pulmonary artery occlusion.Methods Of 160 CTEPH patients operated between January2004 and March 2018 at our center,13(8.1%)had complete main pulmonary artery occlusion.Patients were included if the ventilation/perfusion(V/Q)scan revealed nonperfusion of an entire lung and the pathological examination showed chronic thromboembolic.

“Treat-Repair-Treat”:Management of Left Main Coronary Compression by a Pulmonary Artery Aneurysm in a Patient with Atrial Septal Defect and Significant Pulmonary Hypertension

Left main coronary compression syndrome(LMCS)may complicate pulmonary artery aneurysms(PAA),usually developed in the context of pulmonary arterial hypertension(PAH).We report the case of a 51-year-old female patient with an atrial septal defect(unsuitable for device closure)complicated by a PAA generating a 90%left main stenosis.The significant PAH held us back from immediate surgery.After specific dual PAH-targeted therapy(sildenafil and bosentan),the atrial septal defect could be closed with a unidirectional valved patch;the PAAinduced LMCS was treated by reductive arterioplasty.The postoperative course was uneventful.Follow-up showed clinical improvement,but PAH treatment was still needed.After three months,coronary angiography showed only an insignificant residual left main stenosis,proving that reductive pulmonary arterioplasty was effective in treating LMCS.Any PAA requires further evaluation for LMCS,a dangerous but treatable complication.The“treat-repair-treat”strategy and shunt-closure with a unidirectional valved patch can both improve surgical prospects of LMCS with shunt-related PAH.

Congenital coronary artery fistulas complicated with pulmonary hypertension: Analysis of 211 cases

AIM To compare the behavior of pulmonary hypertension(PHT) associated with coronary artery fistulas(CAFs) between the Asian and Caucasian subjects.METHODS CAFs may be complicated with PHT secondary to leftto-right shunt. Literature review limited to the English language. A total of 211 reviewed patients were collected. Of those, 111 were of Asian and 100 were of Caucasian ethnic origin. The mean age of the Asian and the Caucasian groups of patients were 48.9(range 19-83) and 49.9 years(range 16-85), respectively. In both groups, right heart catheterization was the most commonly(95%) used method for determining pulmonary artery pressure. RESULTS From all of the reviewed subjects, PHT was found in 49 patients(23%), of which 15 were Asian and 34 were Caucasian. In 75% of PHT subjects, mild to moderate PHT was reported and 76% of the fistulas had a vascular mode of termination. Treatment was surgical in 61%, followed by percutaneous therapeutic embolization(27%) and finally conservative medical management in 12% of PHT subjects. PHT was associated with a slight female gender predominance. The majority demonstrated mild to moderate PHT. PHT was reported more frequent in the Caucasian compared with the Asian ethnicity group. The majority of fistulas in patients with PHT had a vascular mode of termination. The results of this review are intended to be indicative and require cautious interpretation.CONCLUSION The likelihood for a CAF patient to develop PHT is presented when possessing the following features, with a Caucasian female having a fistula with a vascular mode of termination.

Plasma endothelin-1 and nitric oxide correlate with ligustrazine alleviation of pulmonary artery hypertension in patients of chronic cor pulmonale from high altitude plateau during acute exacerbation

Objective To explore the mechanisms involved in the ligustrazine alleviation of the pulmonary artery hypertension(PAH) in patients of chronic obstructive pulmonary disease(COPD) associated with chronic cor pulmonale(CCP) during exacerbation.Methods Seventy patients of COPD and CCP with acute exacerbation were randomly and equally divided into control group and treatment group.The control group received standard treatment with antibiotics,antiasthmatic and expectorant medications,and oxygenation;and the ligustrazine treatment group received ligustrazine treatment(80 mg/d;i.v.;for 2 weeks) in addition to the standard treatment.Before and at the end of 2 week treatment,the clinic responses of the two regimens were evaluated,plasma levels of endothelin-1(ET-1) and nitric oxide(NO) were determined;arterial oxygen partial pressure(PaO_2),mean pulmonary arterial pressure(mPAP),outflow tract of right ventricle(RVOT),and internal diameter of right ventricle(RV) were measured.Results Good clinic benefits were achieved in both the standard and ligustrazine regimens,plasma level of ET-1,values of mPAP,RV and RVOT decreased significantly,plasma level of NO and PaO_2 values decreased(all P<0.01 vs pretreatment to all parameters).Compared with the control group,ligustrazine greatly enhanced the clinic efficacy from 77.1%to 97.1%(P<0.05),and also resulted in more significant changes of all these parameters(P<0.01 vs control group for all parameters).For both groups,the levels of plasma ET-1 were positively correlated with values of mPAP,RVOT,and RV(r = 0.710,0.853,and 0.766,respectively,all P = 0.000),and negatively correlated with plasma NO and PaO_2(r =- 0.823,and- 0.752,respectively,all P = 0.000).Conclusion Ligustrazine is effective in treating pulmonary artery hypertension during acute exacerbation of COPD and CCP in patients from the plateau area.The observed changes in the plasma levels of NO and ET-1 in response to ligustrazine treatment suggest that ligustrazine may act through the selective effect on pulmonary blood vessels to enhance the synthesis and release of NO and suppress those of ET-1 from lung vascular endothelial cells,thus reducing pulmonary artery pressure and decreasing pulmonary arterial hypertension.

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.

Pulmonary hypertension secondary to seronegative rheumatoid arthritis overlapping antisynthetase syndrome:A case report

BACKGROUND Polyarthritis is the most frequent clinical manifestation in antisynthetase syndrome(ASS)forms of idiopathic inflammatory myositis and may be misdiagnosed as rheumatoid arthritis(RA),particularly in patients with seronegative RA(SNRA).It is unclear whether there is an overlap between ASS and RA,or if ASS sometimes mimics RA.Pulmonary hypertension(PAH)is common in connective tissue diseases(CTDs).However,published reports on CTD-PAH do not include overlapping CTDs,and its incidence and impact on patient prognosis are unclear.CASE SUMMARY We report the case of a 63-year-old woman who presented with a 3-mo history of symptom aggravation of recurrent symmetrical joint swelling and pain that had persisted for over 10 years.The patient was diagnosed with RA and interstitial lung disease.The patient repeatedly presented to the hospital’s respiratory and rhe-umatology departments with arthralgia,plus shortness of breath after activity.Relevant tests indicated that anti-CCP and RF remained negative,while anti-J0-1 and anti-Ro-52 were strongly positive.It was not until recently that we recognized that this could be an unusual case of SNRA with concurrent ASS.Joint pain was relieved after regular anti-rheumatic treatment.Chest computed tomography scans showed that pulmonary interstitial changes did not progress significantly over several years;however,they showed gradual widening of the pulmonary artery,and cardiac ultrasound indicated elevated pulmonary artery systolic pressure.The prescribed treatment of PAH was not effective in improving shortness of breath.CONCLUSION Overlap of RA and ASS may be missed.Further research is necessary to facilitate early diagnosis,effective evaluation,and prognosis.

Determination of the degree of pulmonary arteryhypertension by plasma atrial nateiuretic peptide levelsand pulmonary perfusion imaging

To evaluate the degree of pulmonary artery hypertension (PAH) and its significance, pulmonary perfusion tomographic imaging (PPTI) and radioimmunoassay of plasma atrial nateiuretic peptide (ANP) levels were examined in different stages of rabbit PAH models, controlled with cardiac catheterization. When the PAH was mild, ANP levels were not significantly changed (t= 1, p >0.05). The mean pulmonary artery pressures (mPAP) measured by catheterization had no significant change, but there was a significant increase of the ratio of dorsal/abdominal counts using pulmonary perfusion tomographic imaging (PPTI) (t=2.5, p <0.05). The ANP levels rose when PAH was moderate or severe, and the difference was significant compared with the control group (t=4 and 6.5, p <0.05). The other two methods also showed significant changes (p <0.01). There was positive correlation between the results of ANP/PPTI, ANP/catheterization, and PPTI/catheterizations (p <0.01). These results suggest that ANP levels can assess the degree of the PAH as a simple method, but it is not as sensitive as that of the PPTI in mild PAH.

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.

Pulmonary hypertension in hereditary haemorrhagic telangiectasia

Hereditary haemorrhagic telangiectasia(HHT) is an autosomal dominant inherited disorder characterised by vascular malformations in predominantly the brain,liverand lungs.Pulmonary hypertension(PH) is increasingly recognised as a severe complication of HHT.PH may be categorised into two distinct types in patients with HHT.Post-capillary PH most often results from a high pulmonary blood flow that accompanies the high cardiac output state associated with liver arteriovenous malformations.Less frequently,the HHT-related gene mutations in ENG or ACVRL1 appear to predispose patients with HHT to develop pre-capillary pulmonary arterial hypertension.Differentiation between both forms of PH by right heart catheterisation is essential,since both entities are associated with severe morbidity and mortality with different treatment options.Therefore all HHT patients should be referred to an HHT centre.

Role of ROS/Kv/HIF Axis in the Development of Hypoxia-Induced Pulmonary Hypertension

Hypoxic pulmonary hypertension (HPH) is a common complication in patients with chronic obstructive pulmonary disease (COPD), sleep-disordered breathing, or dwellers in high altitude. The exact mechanisms underlying the development of HPH still remain unclear. Reactive oxygen species (ROS),hypoxia inducible factors (HIF), and potassium channels (KV) are believed as the main factors during the development of HPH. We propose that the “ROS/Kv/HIF axis” may play an important initiating role in the development of HPH. Being formed under a hypoxic condition, ROS affects the expression and function of HIFs or KV, and consequently triggers multiple downstream signaling pathways and genes expression that participate in promoting pulmonary vasoconstriction and arterial remodeling. Thus, further study determining the initiating role of “ROS/Kv/HIF axis” in the development of HPH could provide theoretic evidences to better understand the underlying mechanisms of HPH, and help identify new potential targets in the treatment of HPH.

Hemodynamic assessment of pulmonary hypertension

There has been significant progress in our understanding of the pathobiology, epidemiology and prognosis of pulmonary vascular disease and, over the past few years, there has been an explosion of clinical therapeutic trials for pulmonary arterial hypertension (PAH). The increasing number of different conditions now associated with PAH and the appearance of new diagnostic techniques have led to a need for a systematic diagnostic approaches and a new disease classification, which has resulted in notable improvements in the quality and efficacy of clinical care. We appreciate traditional resting right heart catheterization techniques (which still remain the gold standard for diagnosing PAH and managing patients on therapy) and look forward to novel invasive techniques (e.g. intravascular ultrasound) that add greatly to our understanding of right ventricle and pulmonary circulation, and for the interpretation of data from clinical trials as well.

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.

Noninvasive model including right ventricular speckle tracking for the evaluation of pulmonary hypertension

AIM To find parameters from transthorathic echocardiography(TTE) including speckle-tracking(ST) analysis of the right ventricle(RV) to identify precapillary pulmonary hypertension(PH).METHODS Forty-four patients with suspected PH undergoing right heart catheterization(RHC) were consecutively included(mean age 63.1 ± 14 years, 61% male gender). All patients underwent standardized TTE including ST analysis of the RV. Based on the subsequent TTE-derived measurements, the presence of PH was assessed: Left ventricular ejection fraction(LVEF) was calculated by Simpsons rule from 4Ch. Systolic pulmonary artery pressure(s PAP) was assessed with continuous wave Doppler of systolic tricuspid regurgitant velocity and regarded raised with values ≥ 30 mmH g as a surrogate parameter for RA pressure. A concomitantly elevated PCWP was considered a means to discriminate between the precapillary and postcapillary form of PH. PCWP was considered elevated when the E/e' ratio was > 12 as a surrogate for LV diastolic pressure. E/e' ratio was measured by gauging systolic and diastolic velocities of the lateral and septal mitral valve annulus using TDI mode. The results were then averaged with conventional measurement of mitral valve inflow. Furthermore, functional testing with six minutes walking distance(6MWD), ECG-RV stress signs, NT pro-BNP and other laboratory values were assessed.RESULTS PH was confirmed in 34 patients(precapillary PH, n = 15, postcapillary PH, n = 19). TTE showed significant differences in E/e' ratio(precapillary PH: 12.3 ± 4.4, postcapillary PH: 17.3 ± 10.3, no PH: 12.1 ± 4.5, P = 0.02), LV volumes(ESV: 25.0 ± 15.0 mL, 49.9 ± 29.5 m L, 32.2 ± 13.6 m L, P = 0.027; EDV: 73.6 ± 24.0 mL, 110.6 ± 31.8 mL, 87.8 ± 33.0 mL, P = 0.021) and systolic pulmonary arterial pressure(sP AP: 61.2 ± 22.3 mm Hg, 53.6 ± 20.1 mm Hg, 31.2 ± 24.6 mm Hg, P = 0.001). STRV analysis showed significant differences for apical RV longitudinal strain(RVAS: -7.5% ± 5.6%, -13.3% ± 4.3%, -14.3% ± 6.3%, P = 0.03). NT pro-BNP was higher in patients with postcapillary PH(4677.0 ± 7764.1 pg/m L, precapillary PH: 1980.3 ± 3432.1 pg/mL, no PH: 367.5 ± 420.4 pg/mL, P = 0.03). Patients with precapillary PH presented significantly more often with ECG RV-stress signs(P = 0.001). Receiver operating characteristics curve analyses displayed the most significant area under the curve(AUC) for RVAS(cut-off < -6.5%, AUC 0.91, P < 0.001), sPAP(cut-off > 33 mmH g, AUC 0.86, P < 0.001) and ECG RV stress signs(AUC 0.83, P < 0.001). The combination of these parameters had a sensitivity of 82.8% and a specificity of 17.2% to detect precapillary PH. CONCLUSION The combination of non-invasive measurements allows feasible assessment of PH and seems beneficial for the differentiation between the pre- and postcapillary form of this disease.

Quercetin attenuates the progression of monocrotaline-induced pulmonary hypertension in rats

Pulmonary arterial hypertension （PAH） is a progressive disease associated with increased constriction and remodeling of the pulmonary vasculature. Quercetin is a natural fiavonoid and has a variety of pharmacological effects including improvement of endothelial cell function. However, its pharmacological effects on pulmonary hypertension have been rarely reported. We sought to observe the protective effect of quercetin in rats with monocrotaline induced PAH. We divided 30 male Sprague-Dawley rats randomly into three groups with ten rats in each group： the monocrotaline group, the quercetin group and the control group. We found that, compared with the controls, the mean pulmonary artery pressure （mPAP） and the right ventricular hypertrophy index in the monocrotaline group were significantly higher （P 〈 0.01）. Quercetin caused a significant reduction both in the mPAP and fight ventricular hypertrophy index compared with the monocrotaline group （P 〈 0.01） while no difference was found between the quercefin group and the control group （P 〉 0.05）. Monocrotaline induced a marked increase in the wall thickness （WT） in small and mid-sized pulmonary arteries compared with the controls （P 〈 0.01）. Monocrotaline also induced a marked increase in the wall area （WA） in small [（56.38 ±6.65）% in monocrotaline vs. （19.80±4.63）% in control] and mid-sized [（43.71± 5.38）% in monocrotaline vs. （14.24± 3.66）% in control] pulmonary arteries （P 〈 0.01）. Quercefin treatment markedly reduced monocrotaline induced increase in both WT and WA （P 〈 0.01）, which, however, still remained significantly elevated compared with those of the controls （P 〈 0.01）. Furthermore, compared with controls, proliferating cell nuclear antigen （PCNA） expression in the pulmonary artery tissues was markedly increased by monocrotaline [（45.59± 1.27） in monocrotaline vs. （9.64± 0.69） in controls], which was significantly attenuated by quercetin. Our animal experiment indicated that quercetin could have protective effects on monocrotaline-induced PAH.