Abstract： Right ventricular dysfunction or right heart failure is a complex clinical syndrome and often leads to a poor prognosis and high mortality. In order to detect right ventricular dysfunction at an early stage, provide a therapy guidance and evaluate treatment outcomes， right ventricular function evaluation has aroused more and more concern in clinical physicians. With the advantages of being non-invasive， accuracy and repetitiveness， echocardiography is used extensively in the assessment of heart function. In this review， we focus on how to use echocardiography to evaluate right ventricular function easily, efficiently， accurately and sensitively， and provide a good foundation for its further clinical application.
Pulmonary hypertension (PH), characterized by diverse etiologies and intricate pathological mechanisms, is a complex cardiopulmonary vascular disorder featuring high morbidity and mortality. Percutaneous pulmonary artery denervation (PADN) represents an emerging interventional treatment method, which shows good prospects in the clinical practice of PH. The PADN has attained preliminary achievements in terms of safety and efficacy. Nevertheless, its long-term prognosis, the characteristics of the appropriate patient populations, and the optimization strategies combined with targeted pharmacotherapy remain to be further explored. This article reviews the current clinical applications of PADN as well as the challenges it confronts.
The high incidence and mortality rates existed in chronic pulmonary thromboembolism(PTE), with considerable misdiagnosis and missed diagnosis rate. The prognosis for patients with chronic thromboembolic pulmonary hypertension was poor with medical therapy. But the pulmonary thromboendarterectomy was well established.The postoperative pulmonary hypertension and reperfusion pulmonary edema are main complications and death causes. The key management after pulmonary thromboendarterectomy is important which decreases pulmonary hypertension , and prevents reperfusion pulmonary edema and re thromboembolism.
Objective To systematically review whether the prevalence of left ventricular diastolic dysfunction was higher in systemic sclerosis (SSc) patients. Methods The Cochrane Library, PubMed, EMbase, CBM, CNKI and WanFang Data databases were electronically searched to collect the studies about comparing echocardiographic parameters in SSc patients and controls from January 1990 to June 2016. Two reviewers independently screened literature, extracted data and assessed the risk of bias of included studies, then, meta-analysis was performed by using RevMan 5.3 software. Results A total of 22 studies involving 1 146 patients were included. The results of meta-analysis showed that: compared to controls, patients with SSc had prolonged left isovolumetric relaxation time (MD=10.40, 95%CI 4.04 to 16.77, P=0.001), higher trans-mitral A-wave velocity (MD=0.11, 95%CI 0.07 to 0.15, P<0.000 01), prolonged mitral deceleration time (MD=8.04, 95%CI 2.66 to 13.42,P=0.003), larger mean left atrial dimension (MD=1.43, 95%CI 0.11 to 2.76, P=0.03), higher estimated pulmonary artery pressure (MD=11.35, 95%CI 6.08 to 16.6, P<0.001), higher E/E’ ratio (MD=2.08, 95%CI 0.19 to 3.96,P=0.03) and lower trans-mitral E-wave velocity (MD=–0.03, 95%CI –0.05 to –0.01, P=0.000 3), mitral E/A ratio (MD=–0.24, 95%CI –0.32 to –0.15, P<0.000 01) and trans-mitral E’-wave velocity (MD=–1.52, 95%CI –2.44 to –0.60,P=0.001). There were no differences in left ventricular ejection fraction, isovolumetric end-systolic dimension, septal end-diastolic thickness and posterior wall end-diastolic thickness, trans-mitral A’-wave velocity, E’/A’ ratio. Conclusion SSc patients are more likely to have echocardiographic parameters of LVDD. Due to limited quality and quantity of the included studies, more high quality studies are needed to verify above conclusion.
Objective To explore the relationship between thrombocytosis and all-cause in-hospital mortality in patients with chronic obstructive pulmonary disease (COPD) and low-risk pulmonary embolism (PE). Methods In a multicenter retrospective study on clinical characteristics, COPD patients with proven acute PE between October 2005 and February 2017 were enrolled. The patients in risk classes III-V on the basis of the PESI score were excluded. The patients with COPD and low-risk PE were divided into two groups of those with thrombocytosis and without thrombocytosis after extracting platelet count on admission. The clinical characteristics and prognosis of the two groups were compared. Multivariate logistic regression was performed to reveal an association between thrombocytosis and all-cause in-hospital mortality after confounding variables were adjusted. Results A total of 874 consecutive patients with COPD and PE at low risk were enrolled in which 191 (21.9%) with thrombocytosis. Compared with those without thrombocytosis, the thrombocytopenic group had significantly lower body mass index [(20.9±3.3) kg/m2 vs. (25.1±3.8) kg/m2, P=0.01], lower levels of forced expiratory volume in one second (FEV1) [(0.9±0.4) L vs. (1.3±0.3) L, P=0.001] and lower partial pressure of oxygen in the arterial blood (PaO2) [(7.8±1.2) kPa vs. (9.7±2.3) kPa, P=0.003]. The COPD patients with thrombocytosis had a higher proportion of cardiovascular complications as well as higher level of systolic pulmonary arterial pressure (sPAP) [(46.5±20.6) mm Hg vs. (34.1±12.6) mm Hg, P=0.001]. Multivariate logistic regression analysis after adjustment for confounders revealed that thrombocytosis was associated with all-cause mortality in hospitalized patients with COPD and low-risk PE (adjusted OR=1.53, 95%CI 1.03–2.29), and oral antiplatelet treatment was a protective factor (adjusted OR=0.71, 95%CI 0.31–0.84). Conclusions Thrombocytosis is an independent risk factor for all-cause in-hospital mortality in COPD patients with PE at low risk. Antiplatelet therapy may play a protective role in the high-risk cohort.
In left heart disease, pulmonary artery pressure would increase due to the elevated left atrial pressure. This type of pulmonary hypertension (PH) is belonged to type Ⅱ as a passive PH (pPH) in its classification. The essential cause of pPH is excessive blood volume. Recently, we have identified another type of pPH, which is induced by vasopressors. Vasopressor-induced pPH shares similar pathophysiological manifestations with left heart disease-induced pPH. pPH would, therefore, be aggressive if vasopressors were applied in patients with left heart disease, which may be common after cardiac surgery, because heart undergoing surgical trauma may require support of vasopressors. Unfortunately, pPH after cardiac surgery is often ignored because of the difficulty in diagnosis. To improve the understanding of pPH and its effect on outcomes, here we highlight the mechanisms of interaction between vasopressor-induced and left heart failure-induced pPH, and provide insights into its therapeutic options.
Objective To investigate the effect of prostaglandin E1 (PGE1) on serum vascular endothelial growth factor(VEGF) in patient with pulmonary hypertension secondary to congenital heart disease and its relation to different pathologic gradings of pulmonary arterioles. Methods Fifty three patients suffering from pulmonary hypertension secondary to congenital heart disease were chosen at random to undergo active tissue test of lung, including 6 patients suffering from severe cyanosis. All of them were intravenously dripped with PGE 1 for 15 days at the speed of 10 15 ng /kg·min, 12 hours a day. Venous blood was taken for study in the morning on the day before infusion, on the 5th day, the 10th day, and the 15th day after infusion. Then the concentration of VEGF was measured by enzyme linked immunosorbent assay (ELISA). Lung biopsy was taken from each patient and pathologic grading performed according to Heath and Edwards pathologic grading. Results Fifty three patients were classified into Grade Ⅴ:9 of them belonged to Grade Ⅰ, 14 to Grade Ⅱ, 19 to Grade Ⅲ, 5 to Grade Ⅳ, the other 6 with severe cyanosis belonged to Grade Ⅴ or even severe than Grade Ⅴ. Before administration of PGE 1, serum VEGF reached the peak while the pathologic grading of pulmonary arteriole was Grade Ⅲ, VEGF level markedly decreased in Grade Ⅳ and Ⅴ. After administration of PGE 1 serum VEGF in Grade Ⅰ showed no difference with that before administration of PGE 1( P gt;0.05), VEGF decreased in GradeⅡ and Ⅲ ( P lt;0.01), slightly decreased in Grade Ⅳ ( P lt; 0.05), while patients greater or equivalent to Grade Ⅴ showed no VEGF change during the course of PGE 1 administration ( P gt;0.05). Conclusions PGE 1 can lower the VEGF level, but the extent closely relates to the degree of pathologic change in pulmonary arteriole. It might be a pre operative parameter for pathologic grading of pulmonary arteriole.
ObjectiveBased on real-word data, and compared with two common chronic respiratory diseases, interstitial lung disease (ILD) and chronic obstructive pulmonary disease (COPD), this case-control study plans to investigate the risk factors and clinical characteristics of patients with combined pulmonary fibrosis and emphysema syndrome (CPFE).MethodsA retrospective case-control study was carried out to screen the clinical data of 96 patients with CPFE, 133 patients with COPD and 164 patients with ILD, analyze their demographics, clinical data, complications and related clinical indicators. Univariate analysis was used to compare the differences among the three groups, and multivariate logistic analysis was used to screen for risk factors.ResultsAll three groups were in old age with the average age of above 71 years. In terms of male ratio and smoking rate, the CPFE group (93.8%, 85.4%) was higher than the ILD group (75.0%, 64.0%), but there was no significant difference when compared with the COPD group (90.2%, 82.0%). Regarding comorbid disease, the proportion of connective tissue disease (CTD) in the CPFE group (10.4%) and the ILD group (13.4%) was higher than that in the COPD group (1.5%). The proportion of hyperlipidemia in the CPFE group (8.3%) was higher than that in the COPD group (1.5%) and the ILD group (1.2%). There were differences in the abnormal proportion of antinuclear antibody among the three groups, but no significant difference was found when compared with the CPFE group alone. The CPFE group (46.9%, 12.5%) and the ILD group (54.9%, 9.8%) were significantly higher than the COPD group (34.6%, 2.3%) in terms of carcinoembryonic antigen (CEA) abnormal proportion and cancer rate. In terms of the prevalence of pulmonary hypertension, the CPFE group (41.7%) > the COPD group (33.1%) > the ILD group (32.9%) was shown, but no statistical significance was found among the three groups.ConclusionsMale and smoking are not only risk factors for COPD but also for CPFE. At the same time, the suffering of CPFE may be affected by immune factors and hyperlipidemia. The proportion of CPFE patients complicated with cancer and CEA abnormalities is higher than COPD patients. The severity of pulmonary hypertension in CPFE patients is significantly higher than the other two diseases.
Pulmonary hypertension is a disease characterized by pulmonary artery pressure increased, with or without small artery pathological change, which ultimately leads to right heart failure or even death. Pulmonary hypertension seriously threatens to human health, however, the pathogenesis of pulmonary hypertension is unclear. Previous studies have found that bone morphogenetic protein (BMP) signaling system played an important role in the progress of pulmonary hypertension. In the current review, we describe the mechanism of BMP4 in the development of pulmonary hypertension.
ObjectiveTo observe the relationship of serum tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), and C-reactive protein (CRP) with obstructive sleep apnea hypopnea syndrome (OSAHS) associated pulmonary hypertension (OSAHS-PH). MethodsFrom September 2013 to October 2014, 38 OSAHS patients, 32 OSAHS-PH patients and 35 healthy subjects were enrolled from the General Hospital of Ningxia Medical University. OSAHS was diagnosed by polysomnography. The pulmonary artery systolic pressure (PASP) was measured by echocardiograph, and the diagnose criteria for pulmonary hypertension was PASP≥40 mm Hg. Serum TNF-α, IL-6, CRP and endothelin 1 (ET-1) were detected by enzyme-linked immunosorbent assay. The correlation between TNF-α, IL-6, CRP, ET-1 and PASP was analyzed. ResultsThe serum levels of TNF-α, IL-6, CRP and ET-1 were remarkably different among three groups (F=55.34, 25.05, 23.85, 34.06 respectively; all P < 0.05). The levels of TNF-α, IL-6, CRP and ET-1 in the OSAHS group were higher than those in the healthy group, and lower than those in the OSAHS-PH group (all P < 0.05). The PASP was positively correlated with the levels of the four factors (r=0.755, 0.762, 0.747, 0.759 respectively; all P < 0.01). ConclusionThe levels of serum TNF-α, IL-6 and CRP are correlated with pulmonary hypertension and they may be involved in the process of OSAHS-PH.