The fate and transport of neonicotinoid insecticides and their metabolites through municipal wastewater treatment plants in South China.

Neonicotinoid insecticides (NEOs) have gained widespread usage as the most prevalent class of insecticides globally and are frequently detected in the environment, posing potential risks to biodiversity and human health. Wastewater discharged from wastewater treatment plants (WWTPs) is a substantial source of environmental NEOs. However, research tracking NEO variations in different treatment units at the WWTPs after being treated by the treatment processes remains limited. Therefore, this study aimed to comprehensively investigate the fate of nine parent NEOs (p-NEOs) and five metabolites in two municipal WWTPs using distinct treatment processes. The mean concentrations of ∑NEOs in influent (effluent) for the UNITANK, anaerobic-anoxic-oxic (A2/O), and cyclic activated sludge system (CASS) processes were 189 ng/L (195 ng/L), 173 ng/L (177 ng/L), and 123 ng/L (138 ng/L), respectively. Dinotefuran, imidacloprid, thiamethoxam, acetamiprid, and clothianidin were the most abundant p-NEOs in the WWTPs. Conventional wastewater treatment processes were ineffective in removing NEOs from wastewater (-4.91% to -12.1%), particularly major p-NEOs. Moreover, the behavior of the NEOs in various treatment units was investigated. The results showed that biodegradation and sludge adsorption were the primary mechanisms responsible for eliminating NEO. An anoxic or anaerobic treatment unit can improve the removal efficiency of NEOs during biological treatment. However, the terminal treatment unit (chlorination disinfection tank) did not facilitate the removal of most of the NEOs. The estimated total amount of NEOs released from WWTPs to receiving waters in the Pearl River of South China totaled approximately 6.90-42.6 g/d. These findings provide new insights into the efficiency of different treatment processes for removing NEOs in current wastewater treatment systems.

Sub-2 nm IrRuNiMoCo High-Entropy Alloy with Iridium-Rich Medium-Entropy Oxide Shell to Boost Acidic Oxygen Evolution.

Ensuring high catalytic activity and durability at low iridium (Ir)usage is still a big challenge for the development of electrocatalysts toward oxygen evolution reaction (OER) in proton exchange membrane water electrolysis (PEMWE). Here, a rapid liquid-reduction combined with surface galvanic replacement strategy is reported to synthesize the sub 2 nm high-entropy alloy (HEA) nanoparticles featured with Ir-rich IrRuNiMo medium-entropy oxide shell (Ir-MEO) and a IrRuCoNiMo HEA core (HEA@Ir-MEO). Advanced spectroscopies reveal that the Ir-rich MEO shell inhibits the severe structural evolution of transition metals upon the OER, thus guaranteeing the structural stability. In situ differential electrochemical mass spectrometry, activation energy analysis and theoretical calculations unveil that the OER on HEA@Ir-MEO follows an adsorbate evolution mechanism pathway, where the energy barrier of rate-determining step is substantially lowered. The optimized catalyst delivers the excellent performance (1.85 V/3.0 A cm-2@80 °C), long-term stability (>500 h@1.0 Acm-2), and low energy consumption (3.98 kWh Nm-3 H2 @1.0 A cm-2) in PEMWE with low Ir usage of ≈0.4 mg cm-2, realizing the dramatical reduction of hydrogen (H2) production cost to 0.88 dollar per kg (H2).

Overall Design of Anode with Gradient Ordered Structure with Low Iridium Loading for Proton Exchange Membrane Water Electrolysis.

Insufficient catalyst utilization, limited mass transport, and high ohmic resistance of the conventional membrane electrode assembly (MEA) lead to significant performance losses of proton exchange membrane water electrolysis (PEMWE). Herein we propose a novel ordered MEA based on anode with a 3D membrane/catalytic layer (CL) interface and gradient tapered arrays by the nanoimprinting method, confirmed by energy dispersive spectroscopy. Benefiting from the maximized triple-phase interface, rapid mass transport, and gradient CL by overall design, such an ordered structure with Ir loading of 0.2 mg cm-2 not only greatly increases the electrochemical active area by 4.2 times but also decreases the overpotentials of both mass transport and ohmic polarization by 13.9% and 8.7%, respectively, compared with conventional MEA with an Ir loading of 2 mg cm-2, thus ensuring a superior performance (1.801 V at 2 A cm-2) and good stability. This work provides a new strategy of designing MEA for high-performance PEMWE.

Detecting Aflatoxin B1 in Peanuts by Fourier Transform Near-Infrared Transmission and Diffuse Reflection Spectroscopy.

Aflatioxin B1 (AFB1) has been recognized by the International Agency of Research on Cancer as a group 1 carcinogen in animals and humans. A fast, batch, and real-time control and no chemical pollution method was developed for the discrimination and quantification prediction of AFB1-infected peanuts by applying Fourier transform near-infrared (FT-NIR) coupled with chemometrics. Initially, the near-infrared transmission (NIRT) and diffuse reflection (NIRR) modules were applied to collect spectra of the samples. The principal component analysis (PCA) method was employed to extract the characteristic wavelength, followed by different preprocessing methods (seven methods) to build an effective linear discriminant analysis (LDA) classification and partial least squares (PLS) quantification models. The results showed that, for both the NIRT or NIRR modules, the LDA classification models satisfactorily distinguished peanuts infected with AFB1 or from those not infected, with external validation showing a 100% correct identification rate and a 0% misjudgment rate. In addition, combined with the concentration of AFB1 in peanuts determined by enzyme-linked immunoassay assay, the best partial least squares (PLS) models were established, with a combination of the first derivative and the Norris derivative filter smoothing pretreatment (Rc2 = 0.937 and 0.984, RMSECV = 3.92% and 2.22%, RPD = 3.98 and 7.91 for NIRR and NIRT, respectively). The correlation coefficient between the predicted value and the reference value in the external verification was 0.998 and 0.917, respectively. This study highlights that both spectral acquisition modules meet the requirements of online, rapid, and accurate identification of peanut AFB1 infection in the early stages.

Berberine Attenuates MPP+-Induced Neuronal Injury by Regulating LINC00943/miR-142-5p/KPNA4/NF-κB Pathway in SK-N-SH Cells.

Berberine plays a neuro-protective role in neurodegenerative diseases, including Parkinson's disease (PD). Long non-coding RNAs (lncRNAs) play critical roles in PD pathogenesis. The purpose of this study was to investigate whether LINC00943 was involved in the role of berberine in PD. 1-methyl-4-phenyl-1, 2, 3, 6-tetrahydropyridine (MPTP) or 1-methyl-4-phenyl pyridine (MPP+) were used to construct PD mouse and cell models, respectively. Cell proliferation was evaluated by Cell Counting Kit-8 (CCK-8) and 5-Ethynyl-2'-deoxyuridine (Edu) assays. Inflammation and cell apoptosis were assessed by enzyme-linked immunosorbent assay (ELISA) and flow cytometry, respectively. Quantitative real-time PCR (qRT-PCR) was employed to test the expression of LINC00943, microRNA (miR)-142-5p, and karyopherin subunit alpha 4 (KPNA4) mRNA. The protein levels of NF-κB pathway-related markers and KPNA4 were measured by western blot. Oxidative stress level was assessed by corresponding kits. The interaction between miR-142-5p and LINC00943 or KPNA4 was determined via dual-luciferase reporter and RNA immunoprecipitation (RIP) assays. Berberine inhibited MPP+-induced injury in SK-N-SH cells by promoting cell proliferation and suppressing inflammation, apoptosis, and oxidative injury. LINC00943 and KPNA4 were upregulated and miR-142-5p was downregulated in PD mouse and cell models. LINC00943 (or KPNA4) overexpression or miR-142-5p inhibition abated the neuro-protective role of berberine in PD cell model. Moreover, miR-142-5p was a target of LINC00943, and KPNA4 could specially bind to miR-142-5p. Additionally, berberine inhibited NF-κB pathway by regulating LINC00943/miR-142-5p/KPNA4 axis. Berberine protected SK-N-SH cell from MPP+-induced neuronal damage via regulating LINC00943/miR-142-5p/KPNA4/NF-κB pathway, highlighting novel evidence for the neuro-protective role of berberine in PD.

Qishen Yiqi dripping pills for chronic ischaemic heart failure: results of the CACT-IHF randomized clinical trial.

AIMS: Qishen Yiqi dripping pills (QSYQ) may be beneficial in patients with ischaemic heart failure (IHF). We aimed to assess the efficacy and safety of QSYQ administered together with guideline-directed medical therapy in patients with IHF. METHODS AND RESULTS: This prospective randomized, double-blind, multicentre placebo-controlled study enrolled 640 patients with IHF between March 2012 and August 2014. Patients were randomly assigned to receive 6 months of QSYQ or placebo in addition to standard treatment. The primary outcome was 6 min walking distance at 6 months. Among the 638 IHF patients (mean age 65 years, 72% men), the 6 min walking distance increased from 336.15 ± 100.84 to 374.47 ± 103.09 m at 6 months in the QSYQ group, compared with 334.40 ± 100.27 to 340.71 ± 104.57 m in the placebo group (mean change +38.32 vs. +6.31 m respectively; P < 0.001). The secondary outcomes in composite clinical events, including all-cause mortality and emergency treatment/hospitalization due to heart failure, were non-significantly lower at 6 months with QSYQ compared with placebo (13% vs. 17%; P = 0.45), and the change of brain natriuretic peptide was non-significantly greater with QSYQ compared with placebo (median change -14.55 vs. -12.30 pg/mL, respectively; P = 0.21). By contrast, the Minnesota Living with Heart Failure Questionnaire score significantly improved with QSYQ compared with placebo (-11.78 vs. -9.17; P = 0.004). Adverse events were minor and infrequent with QSYQ, similar to the placebo group. CONCLUSIONS: Treatment with QSYQ for 6 months in addition to standard therapy improved exercise tolerance of IHF patients and was well tolerated.

Clinical feasibility of a new method to identify chronotropic incompetence in heart failure patients.

Heart failure patients have a high incidence of chronotropic incompetence (CI) that receives less clinical attention. This study assessed a method using wearable devices to identify CI in heart failure patients. Twenty-six heart failure patients (LVEF: 43.9 ± 5.7% with LVEF ⩾40% in 19 patients; age: 52.8 ± 12.4 years, female patients = 6) were enrolled. Each patient underwent symptom-limited treadmill maximal exercise testing during which the simultaneous recording of ECG Holter and physical activity using Actigraph was conducted. The APMHR ratio, the maximal heart rate during peak exercise over the age-predicted maximal heart rate (APMHR, 220-age), was determined. CI was diagnosed in patients who failed to reach at least 0.70 APMHR ratio. Holter-Actigraph recording was also applied during a 6 min hall walk (6MHW) and for 24 h to validate the method to assess impaired chronotropic response. Based on the reports of exercise testing in 26 patients, 13 patients (50%) failed to reach at least 0.70 APMHR ratio while the remaining 13 patients achieved ⩾0.70 APMHR ratio. The APMHR ratio measured by Holter-Actigraph recording was significantly correlated with the APMHR ratio based on exercise test reports (R = 0.99, P < 0.001). The cut-off values of APMHR ratio (0.65) measured during 6MHW, APMHR ratio (0.69) measured during daily activities, and maximum Δ heart rate (37.8 bpm) measured during daily activities significantly predicted the results of exercise test reports with an area under the ROC curve of 0.7337, 0.7544 and 0.7870, respectively (all P values < 0.05). This pilot study found that the wearable device can potentially help in the identification of chronotropic incompetence in heart failure patients.

All-Trans Retinoic Acid Ameliorates Myocardial Ischemia/Reperfusion Injury by Reducing Cardiomyocyte Apoptosis.

Myocardial ischemia/reperfusion (I/R) injury interferes with the restoration of blood flow to ischemic myocardium. Oxidative stress-elicited apoptosis has been reported to contribute to I/R injury. All-trans retinoic acid (ATRA) has anti-apoptotic activity as previously reported. Here, we investigated the effects and the mechanism of action of ATRA on myocardial I/R injury both in vivo and in vitro. In vivo, ATRA reduced the size of the infarcted area (17.81±1.05% vs. 24.41±1.03%, P<0.05) and rescued cardiac function loss (ejection fraction 46.42±6.76% vs. 37.18±4.63%, P<0.05) after I/R injury. Flow-cytometric analysis and TUNEL assay demonstrated that the protective role of ATRA on myocardial I/R injury was related to its anti-apoptotic effects. The anti-apoptotic effects of ATRA were associated with partial inhibition of reactive oxygen species (ROS) production and significantly less phosphorylation of mitogen-activated protein kinases (MAPKs) including p38, JNK, and ERK. Western blot analysis also revealed that ATRA pre-treatment increased a disintegrin and metalloproteinase domain-containing protein 10 (ADAM10) expression (0.65 ± 0.20 vs. 0.41±0.02 in vivo) and reduced the level of receptor for advanced glycation end-products (RAGE) (0.38 ± 0.17 vs. 0.52 ± 0.11 in vivo). Concomitantly, the protective role of ATRA on I/R injury was not observed in RAGE-KO mice. The current results indicated that ATRA could prevent myocardial injury and reduced cardiomyocyte apoptosis after I/R effectively. One possible mechanism underlying these effects is that ATRA could increase ADAM10 expression and thus cleave RAGE, which is the main receptor up-stream of MAPKs in myocardial I/R injury, resulting in the down-regulation of MAPK signaling and protective role on myocardial I/R injury.

Valsartan decreases platelet activity and arterial thrombotic events in elderly patients with hypertension.

BACKGROUND: Angiotensin type 1 receptor (AT 1 R) antagonists are extensively used for blood pressure control in elderly patients with hypertension. This study aimed to investigate the inhibitory effects of AT 1 R antagonist valsartan on platelet aggregation and the occurrence of cardio-cerebral thrombotic events in elderly patients with hypertension. METHODS: Two-hundred and ten patients with hypertension and aged > 60 years were randomized to valsartan (n = 140) or amlodipine (n = 70) on admission. The primary endpoint was platelet aggregation rate (PAR) induced by arachidonic acid at discharge, and the secondary endpoint was the rate of thrombotic events including brain infarction and myocardial infarction during follow-up. Human aortic endothelial cells (HAECs) were stimulated by angiotensin II (Ang II, 100 nmol/L) with or without pretreatment of valsartan (100 nmol/L), and relative expression of cyclooxygenase-2 (COX-2) and thromboxane B 2 (TXB 2 ) and both p38 mitogen-activated protein kinase (p38MAPK) and nuclear factor-kB (NF-kB) activities were assessed. Statistical analyses were performed by GraphPad Prism 5.0 software (GraphPad Software, Inc., California, USA). RESULTS: PAR was lower after treatment with valsartan (11.49 ± 0.69% vs. 18.71 ± 2.47%, P < 0.001), associated with more reduced plasma levels of COX-2 (76.94 ± 7.07 U/L vs. 116.4 ± 15.89 U/L, P < 0.001) and TXB 2 (1667 ± 56.50 pg/ml vs. 2207 ± 180.20 pg/ml) (all P < 0.001). Plasma COX-2 and TXB 2 levels correlated significantly with PAR in overall patients (r = 0.109, P < 0.001). During follow-up (median, 18 months), there was a significantly lower thrombotic event rate in patients treated with valsartan (14.3% vs. 32.8%, P = 0.002). Relative expression of COX-2 and secretion of TXB 2 with concordant phosphorylation of p38MAPK and NF-kB were increased in HAECs when stimulated by Ang II (100 nmol/L) but were significantly decreased by valsartan pretreatment (100 nmol/L). CONCLUSIONS: AT 1 R antagonist valsartan decreases platelet activity by attenuating COX-2/TXA 2 expression through p38MAPK and NF-kB pathways and reduces the occurrence of cardio-cerebral thrombotic events in elderly patients with hypertension.

Clinical significance of pain in patients with chronic heart failure.

BACKGROUND: There is a paucity of studies investigating the clinical and biochemical characteristics of pain in chronic heart failure (CHF) patients. This study aimed to determine the clinical and biochemical characteristics and outcomes in Chinese patients with CHF and symptoms of pain. METHODS: Sociodemographics, serum levels of creatinine, NT-proBNP, high-sensitivity C-reactive protein (hs-CRP), tumor necrosis factor (TNF)-α, interleukin (IL)-6 and IL-10, and two-dimensional echocardiographic left ventricular ejection fraction (LVEF) were determined in 305 patients with CHF. A questionnaire packet including the Brief Pain Inventory (BPI) and the Minnesota Living with Heart Failure Questionnaire (MLHFQ) was used to assess the degree of pain rated on a 0 - 10 scale and the quality of life (QOL). A six-minute walking test was performed during routine clinic visits. Major adverse cardiac events (MACE) were recorded; including all-cause or cardiac mortality and rehospitalization because of myocardial infarction, worsening heart failure or stroke at follow-up. RESULTS: Pain occurred in 25.6% of CHF patients, and was more common when the New York Heart Association (NYHA) functional class was worse. More patients with pain were female in gender, and had more co-morbidities, lower LVEF, and shorter distance during the 6-minute walking test. Despite similar serum levels of creatinine, N-terminal prohormone of brain natriuretic peptide (NT-proBNP), IL-6 and IL-10, the TNF-α levels were higher and MLHFQ scores were greater in CHF patients with pain. At follow-up, CHF patients with moderate to severe pain (≥ 4 scale) had higher rates of all-cause and cardiac mortality and rehospitalization because of myocardial infarction, worsening heart failure or stroke. Multivariate regression analysis revealed that the presence of pain was an independent risk factor for MACE and reduced QOL in CHF patients. CONCLUSIONS: Pain occurs in all stages of the CHF trajectory, and its incidence increases as clinical functional status is worsened. The presence of pain exerts a negative impact on clinical outcome and QOL in patients with CHF.

Impact of potentially lethal ventricular arrhythmias on long-term outcome in patients with chronic heart failure.

BACKGROUND: Potentially lethal ventricular arrhythmias (PLVAs) occur frequently in survivors after acute myocardial infarction and are increasingly recognized in other forms of structural heart diseases. This study investigated the prevalence and prognostic significance of PLVAs in patients with chronic heart failure (CHF). METHODS: Data concerning demographics, etiology of heart failure, NYHA functional class, biochemical variables, electrocardiographic and echocardiographic findings, and medical treatments were collected by reviewing hospital medical records from 1080 patients with NYHA II-IV and a left ventricular (LV) ejection fraction ≤ 45%. PLVAs were defined as multi-focal ventricular ectopy (> 30 beats/h on Holter monitoring), bursts of ventricular premature beats, and nonsustained ventricular tachycardia. All-cause mortality, sudden death, and rehospitalization due to worsening heart failure, or cardiac transplantation during 5-year follow-up after discharge were recorded. RESULTS: The occurrence rate of PLVAs in CHF was 30.2%, and increased with age; 23.4% in patients < 45 years old, 27.8% in those between 45 - 65 years old, and 33.5% in patients > 65 years old (P = 0.033). Patients with PLVAs had larger LV size and lower ejection fraction (both P < 0.01) and higher all-cause mortality (P = 0.014) during 5-year follow-up than those without PLVAs. Age (OR 1.041, 95%CI 1.004 - 1.079, P = 0.03) and LV end-diastolic dimension (OR 1.068, 95%CI 1.013 - 1.126, P = 0.015) independently predicted the occurrence of PLVAs. And PLVA was an independent factor for all-cause mortality (RR 1.702, 95%CI 1.017 - 2.848, P = 0.031) and sudden death (RR 1.937, 95%CI 1.068 - 3.516, P = 0.030) in patients with CHF. CONCLUSION: PLVAs are common and exert a negative impact on long-term clinical outcome in patients with CHF.

[Recent advances in natriuretic peptide family genes and cardiovascular diseases].

Natriuretic peptide family consists of several hormones produced by cardiomyocyte, including atrial natriuretic peptide (ANP), brain natriuretic peptide (BNP) and C-type natriuretic peptide (CNP). They possess similar gene structures and protective effects of cardiovascular physiology, such as anti-hypertrophy, anti-fibrosis, myocardial relaxation and blood pressure regulation. The corresponding natriuretic peptide receptor A, B and C mediate multiple effects of natriuretic peptides to maintain cardiovascular homeostasis. Specially, natriuretic peptide receptor-A preferentially binds ANP and BNP, while natriuretic peptide receptor-B is more selective for C-type natriuretic peptides. Natriuretic peptide receptor-C(NPR-C), binding all kinds of natriuretic peptides, clears natriuretic peptides from the circulation through receptor-mediated internalization and degradation. BNP levels were reported to be a good predictor of left ventricular dysfunction and decompensated heart failure from a clinical standpoint. BNP infusion is an effective treatment for acute heart failure. Investigations on natriuretic peptides' single nucleotide polymorphisms and biological function suggested that they could be associated with several cardiovascular diseases, such as atrial fibrillation, cardiomyopathy, heart failure and so on. Transgenic mice with natriuretic peptides and their receptors gene deletion display myocardial hypertrophy and fibrosis, which are associated with the development of hypertension, cardiomyopathy and heart failure. Certain stimuli triggering cardiac hypertrophy and ischemic injuries may be involved in regulating gene expression of natriuretic peptides and their receptors. Therefore, advances in understanding of natriuretic peptide family genes and their regulatory mechanisms will lead to greater insight into the pathogenesis of cardiovascular diseases and blaze a new trail in clinical treatment.

Prevalence, clinical characteristics and outcome in patients with chronic heart failure and diabetes.

BACKGROUND: Chronic heart failure (CHF) and diabetes mellitus portend high morbidity and mortality because of an interrelated pathophysiologic process. This large cohort study aimed to analyze the prevalence, clinical characteristics and long-term outcome of patients with CHF and diabetes. METHODS: A total of 1119 patients with NYHA functional class II - IV and left ventricular ejection fraction (LVEF) < 45% between January 1995 and May 2009 were recruited. Clinical variables, biochemical and echocardiographic measurements were retrospectively reviewed, and composite major cardiac events (MCE) including death, heart transplantation, and refractory heart failure requiring multiple hospitalizations were recorded. RESULTS: The prevalence of CHF with diabetes was progressively increased with time (16.9% in 1995 - 1999; 20.4% in 2000 - 2004, and 29.1% in 2005 - 2009) and age (18.5% in < 60 years, 26.6% in 60 - 80 years, and 26.6% in > 80 years). Compared with CHF patients without diabetes, those with diabetes had worse cardiac function, more abnormal biochemical changes, and higher mortality. Treatment with glucose-lowering agents significantly improved LVEF and decreased MCE. An elevated serum HbA1c level was associated with large left ventricular end-systolic diameter (P < 0.05), decreased LVEF (P < 0.01) and reduced survival (P < 0.05). Multivariable Logistic regression analysis revealed that after adjustment for confounding factors, NYHA functional class (OR 2.65, 95%CI 1.14 - 6.16, P = 0.024) and HbA1c level >or= 7% (OR 2.78, 95%CI 1.00 - 7.68, P = 0.049) were independent risk factors for adverse outcomes in CHF patients with diabetes. CONCLUSIONS: Prevalence of CHF with diabetes was increasing during past decades, and patients with CHF and diabetes had worse clinical profiles and prognosis. Aggressive anti-CHF and diabetes therapies are needed to improve overall outcomes for these patients.

Polymorphisms of beta-adrenoceptor and natriuretic peptide receptor genes influence the susceptibility to and the severity of idiopathic dilated cardiomyopathy in a Chinese cohort.

BACKGROUND: This study evaluated the potential effects of beta-adrenoceptor (beta-AR) and natriuretic peptide receptor (NPR) gene polymorphisms on the susceptibility to and the severity of idiopathic dilated cardiomyopathy (IDCM) in a Chinese cohort. METHODS AND RESULTS: Ten polymorphisms in the coding regions of beta1-AR, beta2-AR, beta3-AR, NPR1, and NPR2 were genotyped in 430 IDCM patients and 468 healthy subjects. Patients with IDCM were followed for 2 years. In multi-loci combined subtype analysis, the combined profile of beta-AR and NPR was significantly different between IDCM patients and controls (P < .0001), mainly influenced by 2 loci beta1-Ser49Gly and NPR2-C2077T, which were also associated with the severity of IDCM. In single-loci analysis, allele frequencies of beta1-Gly49, NPR1-Glu939, and NPR2-T2077 were higher in patients with IDCM than in controls. Genotypes carrying NPR2-T2077 allele showed 1.94-fold independent risk for IDCM phenotype than C2077 homozygote (P < .001). Carriers of the NPR2-T2077 or beta1-Gly49 variant had worse New York Heart Association functional class or echocardiographic results and elevated serum brain natriuretic peptide, experienced severe symptoms, and required intensive medications and frequent hospitalization for heart failure. Furthermore, synergistic interactions between NPR2-C2077T and beta1-Ser49Gly were detected by multifactor-dimensionality reduction method. CONCLUSIONS: This study suggests that NPR2-T2077 and beta1-Gly49 polymorphisms may be genetically synergistic adverse factors for the susceptibility to or the severity of IDCM.

[Efficacy of shenfu injection as adjuvant therapy in treating patients of ischemic cardiomyopathy with heart insufficiency].

OBJECTIVE: To evaluate the clinical efficacy of Shenfu Injection (SFI), as a adjuvant therapy, in treating patients of ischemic cardiomyopathy with heart insufficiency (ICP-HI). METHODS: One hundred patients of ICP-HF were equally randomized into two groups, the SFI group and the control group. All received the conventional treatment, but to patients in the SFI group SFI was given additionally via intravenous injection, 60 mL once a day, 10 days each month, the treatment course was 6 months. Changes of cardial functional grading, 6-min walking distance, echocardiographic indices, plasma N terminal pro-brain natriuretic peptide (pro-BNP) level were observed before and after treatment, and the occurrence of major adverse cardiovascular events (MACE) and mortality in patients were observed as well. RESULTS: As compared with the conventional treatment alone, additional application of SFI showed a more significant efficacy in improving NYHA functional grade and 6-min walking distance, reducing the diameters of left ventricular at end diastole and systole, increasing left ventricular ejection fraction, and decreasing plasma N terminal pro-BNP level (P <0.05). The occurrence of MACE and the mortality in the SFI group were significantly lower than those in the control group respectively (P <0.05). CONCLUSIONS: Based on the conventional treatment, the adjuvant therapy of SFI could improve the cardiac function, improve the quality of life, ameliorate ventricular reconstruction, and decrease the occurrence of cardiovascular events in patients of ICP-HI.

[Left ventricular dyssynchrony evaluated by echocardiography in chronic heart failure patients with normal and wide QRS duration].

OBJECTIVE: The aim of the study is to evaluate the left ventricular (LV) dyssynchrony in chronic heart failure (HF) patients with normal and wide QRS duration. METHODS: Time to peak velocity at peak systolic and early diastolic phase (Ts and Te) were determined in 12 segments of LV by echocardiography (GE Vivid 7) in 54 HF patients (28 with wide and 26 with normal QRS duration) and 15 normal controls to evaluate LV systolic and diastolic dyssynchrony. The risk factors related to LV dyssynchrony were also evaluated. RESULTS: LV end systolic and diastolic volumes were significantly larger and 12 segmental mean Ts and maximal Te difference (Te-diff) were significantly higher in HF patients with wide QRS duration than HF patients with normal QRS duration. Using mean Ts >or= 182 ms as the cut-off value, systolic dyssynchrony was present in 46% HF patients with normal QRS and 71% HF patients with wide QRS. Using Te-diff >or= 79 ms as the cut-off value, diastolic dyssynchrony was seen in 58% HF patients with normal QRS and 89% HF patients with wide QRS. Combined systolic and diastolic dyssynchrony was seen in 31% HF patients with normal QRS and in 64% HF patients with wide QRS. Systolic dyssynchrony was significantly correlated to LV end systolic volume and diastolic dyssynchrony was correlated to end diastolic volume. CONCLUSION: Percentage of LV dyssynchrony was significantly higher in HF patients with wide QRS, especially in HF patients with increased LV end systolic and diastolic volume.

[Effects of antidepressant therapy in patients with suspected "angina pectoris" and negative coronary angiogram complicating comorbid depression].

OBJECTIVE: We observed the therapeutic effectiveness and safety of different antidepressants as well as the correlation between symptomatic improvement of depression and improvement of chest pain in patients with susceptible "angina pectoris" and negative coronary angiogram complicating comorbid depression. METHODS: In this double-blinded randomized study, a total of 123 eligible patients were allocated into three groups: (1) Group F: fluoxetine 20 mg QN (n = 41); (2) Group P: Placebo 1 tablet QN (n = 40); (3) Group F + O: fluoxetine 20 mg + olanzapine 2.5 mg QN for the former 2 weeks and only fluoxetine 20 mg QN for the latter 2 weeks (n = 42). The total therapy duration was 4 weeks. HAMD, HAMA and self-evaluation table of chest pain were obtained before therapy, at the end of 1 and 2 weeks after therapy. RESULTS: Baseline HAMD and HAMA scores and self-evaluation score of chest pain were similar among 3 groups and all scores were significantly improved post various therapies in the order of group F + O > group F > group P. The rate of score decrease were seen after 1 week treatment in group F + O and after 2 week treatment in group F. There was a significant positive correlation between the rates of self-evaluation chest pain score decrease and HAMD (r = 0.867, P < 0.001) and HAMA (r = 0.854, P < 0.001) score decreases after 4 weeks therapies (P < 0.05). During the whole course of treatment, no serious adverse reaction was found in all patients. CONCLUSION: In patients with suspected "angina pectoris" and negative coronary angiogram complicating comorbid depression, the antidepressants were safe and significantly improved the symptoms of depression and anxiety and chest pain. Low dose fluoxetine plus short term olanzapine regimen was superior to fluoxetine alone regimen in terms of stronger and quicker symptom improvement.

[Changes in Macruz index of patients with coronary artery diseases and their clinical implications].

OBJECTIVE: To study the association of Macruz index with left ventricular diastolic function of patients with coronary artery disease (CAD). METHODS: The ratio of P/P-R segment (Macruz index) was measured using regular 12-lead electrocardiography in 90 CAD patients, whose mitral E/A wave ratios were determined by means of Doppler echocardiography. The measurements were also performed in 85 patients with non-coronary artery diseases for comparison. RESULTS: The mitral E/A ratio of the CAD patients with 1 or 3 branches involved was lower than 1, while in patients with two branches involved, the E/A ratio exceeded 1. The P/P-R segment ratio of the 3 CAD groups was all over 1.6. CONCLUSION: The Macruz index is more helpful than E/A ratio to some extent in estimating the left ventricular diastolic function of CAD patients.