Atorvastatin ameliorated myocardial fibrosis by inhibiting oxidative stress and modulating macrophage polarization in diabetic cardiomyopathy

In this editorial,we commented on the article published in the recent issue of the World Journal of Diabetes.Diabetic cardiomyopathy(DCM)is characterized by myocardial fibrosis,ventricular hypertrophy and diastolic dysfunction in diabetic patients,which can cause heart failure and threaten the life of patients.The pathogenesis of DCM has not been fully clarified,and it may involve oxidative stress,inflammatory stimulation,apoptosis,and autophagy.There is lack of effective therapies for DCM in the clinical practice.Statins have been widely used in the clinical practice for years mainly to reduce cholesterol and stabilize arterial plaques,and exhibit definite cardiovascular protective effects.Studies have shown that statins also have anti-inflammatory and antioxidant effects.We were particularly concerned about the recent findings that atorvastatin alleviated myocardial fibrosis in db/db mice by regulating the antioxidant stress and antiinflammatory effects of macrophage polarization on diabetic myocardium,and thereby improving DCM.

Isolated Hyperacute T-Waves in West Nile Encephalitis Indicating Atypical Variant of Stress-Induced Cardiomyopathy

Several cardiac outcomes have been reported with West Nile-encephalitis;however, the underlying pathophysiology remains complex. We present a 42-year-old female, with multiple sclerosis, whose neurological symptoms and respiratory decline were finally explained by the diagnosis of West Nile-encephalitis. During her admission, the isolated peaked T-waves indicated the underlying stress-induced cardiomyopathy. The absence of all other causes of hyperacute T-waves, their subsequent resolution with the resolution of infection and improvement in wall motion abnormalities, further supported the association. This case highlights the importance of considering hyperacute T-waves in an approach towards the diagnosis of WNV-encephalitis related atypical variant of stress-induced cardiomyopathy.

Cirrhotic cardiomyopathy:Isn't stress evaluation alwaysrequired for the diagnosis?

AIM:To describe the proportion of patients with cirrhotic cardiomyopathy(CCM) evaluated by stress echocardiography and investigating its association with the severity of liver disease.METHODS:A cross-sectional study was conducted.Cirrhotic patients without risk factors for cardiovascular disease were included.Data regarding etiology and severity of liver disease(Child-Pugh score and model for end-stage liver disease),presence of ascites and gastroesophageal varices,pro-brain natriuretic peptide(proBNP) and corrected QT(QTc) interval were collected.Dobutamine stress echocardiography(conventional and tissue Doppler imaging) was performed.CCM was considered present when diastolic and/or systolic dysfunction was diagnosed at rest or after pharmacological stress.Therapy interfering with cardiovascular system was suspended 24 h before the examination.RESULTS:Twenty-six patients were analyzed,17(65.4%) Child-Pugh A,mean model for end-stage liver disease(MELD) score of 8.7.The global proportion of patients with CCM was 61.5%.At rest,only 2(7.7%)patients had diastolic dysfunction and none of the patients had systolic dysfunction.Dobutamine stress echocardiography revealed the presence of diastolic dysfunction in more 6(23.1%) patients and of systolic dysfunction in 10(38.5%) patients.QTc interval prolongation was observed in 68.8%of the patients and increased pro-BNP levels in 31.2%of them.There was no association between the presence of CCM and liver impairment assessed by Child-Pugh score or MELD(P= 0.775,P= 0.532,respectively).Patients with QTc interval prolongation had a significant higher rate of gastroesophageal varices comparing with those without QTc interval prolongation(95.0%vs 50.0%,P= 0.028).CONCLUSION:CCM is a frequent complication of cirrhosis that is independent of liver impairment.Stress evaluation should always be performed,otherwise it will remain an underdiagnosed condition.

Takotsubo syndrome:Advances in the understanding and management of an enigmatic stress cardiomyopathy

Takotsubo cardiomyopathy is a syndrome mimicking an acute myocardial infarction in absence of obstructive epicardial coronary artery disease to explain the degree of the wall motion abnormalities. Typically more common in the elderly women, this condition is usually triggered by unexpected emotional or physical stress situations, and is associated with electrocardiogram abnormalities and slight elevation of cardiac biomarkers. The pathophysiological mechanism is not clear yet, but it is believed that a high circulating concentration of catecholamines causes an acute dysfunction of the coronary microcirculation and metabolism of cardiomyocytes, leading to a transient myocardial stunning. Typically, it presents with acute left ventricular systolic dysfunction that in most cases is completely resolved at short term. Recurrences are rare and it is thought that the long-term prognosis is good. We present here a review of the clinical features, pathophysiology and management of this enigmatic condition.

Stress cardiomyopathy: clinical features and outcomes

Objectives: To establish the prevalence, clinical features, and outcomes of the recently recog- nized stress cardiomyopathy whose physiopathology is still not completely clarified. Material and methods: The prevalence and clinical findings of stress cardiomyopathy were assessed in a group of 378 patients undergoing cinecoronariography for acute coronary syndromes dur- ing a 7-year period. The inclusion criteria were severe chest pain, ischemic electrocardiogra- phic changes, reversible left ventricular dys- hypokinesia, and normal coronary arteries. Eight patients, 7 female (2.1% of all patients and 5.0% of the women), with a mean age of 65.3 ± 8.5 years fulfilled the requirements. Results: The precipitating factor was severe stress in all of them. Cardiac enzymes were slightly raised. There was apical left ventricular dyskinesia in 6 patients, midventricular in another, and diffuse hypokinesia in the remaining. One patient showed moderate mitral regurgitation. The response to con- ventional treatment and patient outcomes were favorable in all cases with prompt reversal of the left ventricular dyskinesia as assessed by echocardiography. There were 4 recurrences, 2 requiring readmission to hospital, despite continuous treatment with combined alfa and beta adrenergic blockers and calcium antagonists. Conclusions: In our hospital, stress cardiomyo- pathy had a prevalence of 2.1% in all patients with acute coronary syndromes and 5.1% in women and should be considered in their differential diagnosis, especially in middle aged female patients with a history of severe previous stress. There was a favorable outcome but recurrences may occur despite uninterrupted me- dical treatment following discharge.

Transient stress cardiomyopathies in the elderly： Clinical ＆ Pathophysiologic considerations

短暂导致压力的心肌症逐渐地被认出了并且当时稀罕，他们趋于多于另外的人口统计的组影响老女人。一种类型，经常叫的 tako-tsubo 心肌症(TTC ) ，被重要感情或物理的应力典型地触发并且与胸疼痛，心电图(ECG ) 变化和反常的心脏的酶被联系。重要的左室的地区性的墙运动畸形通常包括运动不能的 &#x0201c； ballooning&#x0201d；有正常或底的 hyperdynamic 功能的顶。第二种类型，经常叫的神经原的震惊的心肌层，典型地与 subarachnoid 出血联系了，通常也与 ECG 介绍变化和积极的酶，而是典型的墙打手势看见的畸形包括正常有 akinesis 的基础、顶端的左室的收缩以一种环绕的方式中间洞。pathophysiology，临床的照顾和典型功课，被考察。

Pheochromocytoma and stress cardiomyopathy:Insight into pathogenesis

AIM To investigate the occurrence of cardiomyopathy(CMP)in a cohort of patients with histologically proven pheochromocytoma(pheo),and to determine if catecholamine excess was causative of the left ventricular(LV)dysfunction.METHODS A retrospective chart review spanning years 1998through 2014 was undertaken and patients with a diagnosis of pheo confirmed with histopathologic examination were included.Presenting electrocardiograms and cardiac imaging studies were reviewed.Transthoracic echocardiography(TTE),ventriculography or single positron emission computed tomography imaging was evaluated and if significant abnormalities[left ventricular hypertrophy(LVH)or LV dysfunction]were noted in the pre operative period a follow up post-operative study was also analyzed.Multivariate analysis using logistic regression was used to investigate independent predictors for outcomes of interest,LV dysfunction and LVH.RESULTS We identified 18 patients with diagnosis of pheo confirmed on pathology.Mean age was 54.3±19.3years and 11(61.1%)patients were females.50%of such patients had either resistant hypertension or labile blood pressures during hospitalization,which had raised suspicion for a pheo.Cardiac imaging studies were available for 12(66.7%)patients at the time of inclusion into study and preceding the adrenalectomy.7(58.3%)patients with a TTE available for review had mild or more severe LVH while 3(25%)patients had LV dysfunction of presumably acute onset.In a multivariate analysis,elevated catecholamine levels as assessed by urinary excretion of metabolites was not an independent predictor of development of LV systolic dysfunction or of presence of LVH on TTE.Two female patients with a preceding history of hypertension had marked LV hypertrophy and systolic anterior motion of the mitral valve.Prolongation of the QTc interval was noted in 5(27.8%)patients but no acute arrhythmias were observed in any patient.CONCLUSION This study adds to the growing body of literature on the predilection of patients with pheochromocytomas to develop non-ischemic CMP.Degree of catecholamine excess as measured by urinary secretion of metabolites did not predict the development of CMP but 2 of 3patients developed CMP in the setting of significant acute physiologic stress.Our findings provide support to the proposed etiologic role of elevated catecholamines in TC and other stress induced forms of CMP,however,activation of a brain-neural-cardiac axis from acute stress and local release of catecholamines but not chronic catecholamine elevations are likely to be responsible in pheo related CMP.

Flow stress behavior of Al-Cu-Li-Zr alloy containing Sc during hot compression deformation

The flow stress behavior of Al-3.5Cu-1.5Li-0.25(Sc+Zr) alloy during hot compression deformation was studied by isothermal compression test using Gleeble-1500 thermal-mechanical simulator. Compression tests were preformed in the temperature range of 653-773 K and in the strain rate range of 0.001-10 s-1 up to a true plastic strain of 0.7. The results indicate that the flow stress of the alloy increases with increasing strain rate at a given temperature,and decreases with increasing temperature at a given imposed strain rate. The relationship between the flow stress and the strain rate and the temperature was derived by analyzing the experimental data. The flow stress is in a hyperbolic sine relationship with the strain rate,and in an Arrhenius relationship with the temperature,which imply that the process of plastic deformation at an elevated temperature for this material is thermally activated. The flow stress of the alloy during the elevated temperature deformation can be represented by a Zener-Hollomon parameter with the inclusion of the Arrhenius term. The values of n,α and A in the analytical expressions of flow stress σ are fitted to be 5.62,0.019 MPa-1 and 1.51×1016 s-1,respectively. The hot deformation activation energy is 240.85 kJ/mol.

Empagliflozin ameliorates diabetic cardiomyopathy probably via activating AMPK/PGC-1αand inhibiting the RhoA/ROCK pathway

BACKGROUND Diabetic cardiomyopathy(DCM)increases the risk of hospitalization for heart failure(HF)and mortality in patients with diabetes mellitus.However,no specific therapy to delay the progression of DCM has been identified.Mitochondrial dysfunction,oxidative stress,inflammation,and calcium handling imbalance play a crucial role in the pathological processes of DCM,ultimately leading to cardiomyocyte apoptosis and cardiac dysfunctions.Empagliflozin,a novel glucoselowering agent,has been confirmed to reduce the risk of hospitalization for HF in diabetic patients.Nevertheless,the molecular mechanisms by which this agent provides cardioprotection remain unclear.AIM To investigate the effects of empagliflozin on high glucose(HG)-induced oxidative stress and cardiomyocyte apoptosis and the underlying molecular mechanism.METHODS Twelve-week-old db/db mice and primary cardiomyocytes from neonatal rats stimulated with HG(30 mmol/L)were separately employed as in vivo and in vitro models.Echocardiography was used to evaluate cardiac function.Flow cytometry and TdT-mediated dUTP-biotin nick end labeling staining were used to assess apoptosis in myocardial cells.Mitochondrial function was assessed by cellular ATP levels and changes in mitochondrial membrane potential.Furthermore,intracellular reactive oxygen species production and superoxide dismutase activity were analyzed.Real-time quantitative PCR was used to analyze Bax and Bcl-2 mRNA expression.Western blot analysis was used to measure the phosphorylation of AMP-activated protein kinase(AMPK)and myosin phosphatase target subunit 1(MYPT1),as well as the peroxisome proliferator-activated receptor-γcoactivator-1α(PGC-1α)and active caspase-3 protein levels.RESULTSIn the in vivo experiment, db/db mice developed DCM. However, the treatment of db/db mice with empagliflozin(10 mg/kg/d) for 8 wk substantially enhanced cardiac function and significantly reduced myocardial apoptosis,accompanied by an increase in the phosphorylation of AMPK and PGC-1α protein levels, as well as a decrease inthe phosphorylation of MYPT1 in the heart. In the in vitro experiment, the findings indicate that treatment ofcardiomyocytes with empagliflozin (10 μM) or fasudil (FA) (a ROCK inhibitor, 100 μM) or overexpression of PGC-1α significantly attenuated HG-induced mitochondrial injury, oxidative stress, and cardiomyocyte apoptosis.However, the above effects were partly reversed by the addition of compound C (CC). In cells exposed to HG,empagliflozin treatment increased the protein levels of p-AMPK and PGC-1α protein while decreasing phosphorylatedMYPT1 levels, and these changes were mitigated by the addition of CC. Adding FA and overexpressingPGC-1α in cells exposed to HG substantially increased PGC-1α protein levels. In addition, no sodium-glucosecotransporter (SGLT)2 protein expression was detected in cardiomyocytes.CONCLUSION Empagliflozin partially achieves anti-oxidative stress and anti-apoptotic effects on cardiomyocytes under HGconditions by activating AMPK/PGC-1α and suppressing of the RhoA/ROCK pathway independent of SGLT2.

Atorvastatin ameliorated myocardial fibrosis in db/db mice by inhibiting oxidative stress and modulating macrophage polarization

BACKGROUND People with diabetes mellitus(DM)suffer from multiple chronic complications due to sustained hyperglycemia,especially diabetic cardiomyopathy(DCM).Oxidative stress and inflammatory cells play crucial roles in the occurrence and progression of myocardial remodeling.Macrophages polarize to two distinct phenotypes:M1 and M2,and such plasticity in phenotypes provide macrophages various biological functions.AIM To investigate the effect of atorvastatin on cardiac function of DCM in db/db mice and its underlying mechanisms.METHODS DCM mouse models were established and randomly divided into DM,atorvastatin,and metformin groups.C57BL/6 mice were used as the control.Cardiac function was evaluated by echocardiography.Hematoxylin and eosin and Masson staining was used to examine the morphology and collagen fibers in myocardial tissues.The expression of transforming growth factor-β1(TGF-β1),tumor necrosis factor-α(TNF-α),interleukin-1β(IL-1β),M1 macrophages(iNOS^(+)),and M2 macrophages(CD206^(+))were demonstrated by immunohistochemistry and immunofluorescence staining.The levels of TGF-β1,IL-1β,and TNF-αwere detected by ELISA and real-time quantitative polymerase chain reaction.Malondialdehyde(MDA)concentrations and superoxide dismutase(SOD)activities were also measured.RESULTS Treatment with atorvastatin alleviated cardiac dysfunction and decreased db/db mice. The broken myocardialfibers and deposition of collagen in the myocardial interstitium were relieved especially by atorvastatin treatment.Atorvastatin also reduced the levels of serum lactate dehydrogenase, creatine kinase isoenzyme, and troponin;lowered the levels of TGF-β1, TNF-α and IL-1β in serum and myocardium;decreased the concentration of MDAand increased SOD activity in myocardium of db/db mice;inhibited M1 macrophages;and promoted M2macrophages.CONCLUSION Administration of atorvastatin attenuates myocardial fibrosis in db/db mice, which may be associated with theantioxidative stress and anti-inflammatory effects of atorvastatin on diabetic myocardium through modulatingmacrophage polarization.

Role of Neuropeptide Y and Peroxisome Proliferator-activated Receptor γ Coactivator-1α in Stress Cardiomyopathy

Death following situations of intense emotional stress has been linked to the cardiac pathology described as stress cardiomyopathy, whose pathomechanism is still not clear. In this study, we sought to determine, via an animal model, whether the transcriptional coactivator peroxisome proliferator-activated receptor γ coactivator-1alpha (PGC-1α) and the amino peptide neuropeptide Y (NPY) play a role in the pathogenesis of this cardiac entity. Male Sprague-Dawley rats in the experimental group were subjected to immobilization in a plexy glass box for 1 h, which was followed by low voltage elec-tric foot shock for about 1h at 10s intervals in a cage fitted with metallic rods. After 25 days the rats were sacrificed and sections of their hearts were processed. Hematoxylin-eosin staining of cardiac tissues revealed the characteristic cardiac lesions of stress cardiomyopathy such as contraction band necrosis, inflammatory cell infiltration and fibrosis. The semi-quantitative RT-PCR analysis for PGC-1α mRNA expression showed significant overexpression of PGC1-α in the stress-subjected rats (P<0.05). Fluorescence immunohistochemistry revealed a higher production of NPY in the stress-subjected rats as compared to the control rats (P=0.0027). Thus, we are led to conclude that following periods of intense stress, an increased expression of PGC1-α in the heart and an overflow of NPY may lead to stress car-diomyopathy and even death in susceptible victims. Moreover, these markers can be used to identify stress cardiomyopathy as the cause of sudden death in specific cases.

A Case Series and Review of Takotsubo Cardiomyopathy: Does Stress Really Cause the Stress Cardiomyopathy?

Objective: We sought to describe clinical characteristics of emergency department patients ultimately diagnosed with Takotsubo Cardiomyopathy (TCM) and to explore the causal role that stress may play in its pathogenesis. Methods: We performed a retrospective chart review analyzing all myocardial infarction patients with non-obstructive coronary artery disease on cardiac catheterization to assess for the presence of TCM. Various clinical data, including the pres-ence of stressors, from emergency department records were reported. We also analyzed factors from several studies (including ours) to assess the true causality of stress in the development of TCM. Results: Twelve ED patients out of 2,179 charts reviewed were identified as having TCM. Most were female, post-menopausal, and had chest pain, but only half had a specific stressful event identified in the ED. One-third of patients had no stressful event identified during their hospital stay. Several other studies suggest that stressful events are associated with increased diagnoses of TCM, but we found that causality of stress cannot be substantiated. Conclusion: Stressful events are often not identified in emergency department patients ultimately diagnosed with TCM. The causative nature of stress in the development of TCM cannot be firmly established from any existing data.

Recurrent Takotsubo cardiomyopathy triggered by emotionally stressful events: A case report

BACKGROUND Takotsubo cardiomyopathy(TCM)is characterized by reversible left ventricular dysfunction triggered by emotional or physical stress.Only 1%-2%of patients with acute coronary syndrome are diagnosed with TCM.Although obstructive coronary artery disease is frequently considered to be the cause of chest pain,TCM should be considered in some clinical settings.In this case,clinicians did not make a timely and accurate diagnosis for TCM due to a lack of knowledge until the third hospitalization with a left ventriculogram.CASE SUMMARY A 55-year-old postmenopausal woman had intermittent chest pain following emotionally stressful events three times in the past 3 years.Cardiac troponin levels increased after each instance of symptom onset.A transthoracic echocardiogram showed reversible left ventricular dysfunction.The patient underwent three coronary angiograms without evidence of coronary artery disease.A left ventriculogram was first performed at the third hospitalization and revealed apical akinesia with ballooning of the apical region and consistent hypercontractile basal segments.The diagnosis of TCM was confirmed.The patient was treated with an angiotensin-converting-enzyme inhibitor(perindopril)and aβ-blocker(metoprolol).No complications occurred during the patient’s hospitalization.The patient was told to avoid stressful events.During the 9-mo follow-up visit,the patient was asymptomatic with an ejection fraction of 55%.CONCLUSION Clinicians should be conscious of the possibility of TCM,especially in postmenopausal women presenting with clinical manifestations similar to acute coronary syndrome without coronary occlusion.

Simultaneous Multimode Oscillation of Stress-Compensated Cut Quartz Resonator with Narrow-Band Wide Variable-Range Quartz Crystal Oscillator

A multimode-quartz-crystal oscillator was developed to excite stable dual-mode resonance at different frequencies: The oscillation of the 3rd harmonic resonance of the principle C-mode and an additional resonance B-mode of SC-cut crystal. Harmonic combinations of the 3rd and fundamental mode of B-mode with the 3rd harmonics of C-mode are demonstrated. The measurement of the temperature dependence of the oscillation frequency is demonstrated along with the stability determined by root Allan variance. Dependence on the open conductance of the active circuit and the dependence on the coupling capacitors are discussed.

Stress cardiomyopathy in critical care:A case series of 109 patients

BACKGROUND Critically ill patients are at risk of developing stress cardiomyopathy(SC)but can be under-recognized.AIM To describe a case series of patients with SC admitted to critical care units.METHODS We conducted a retrospective observational study at a tertiary care teaching hospital.All adult(≥18 years old)patients admitted to the critical care units with stress cardiomyopathy over 5 years were included.RESULTS Of 24279 admissions to the critical care units[19139 to medical-surgical intensive care units(MSICUs)and 5140 in coronary care units(CCUs)],109 patients with SC were identified.Sixty(55%)were admitted to the coronary care units(CCUs)and forty-nine(45%)to the medical-surgical units(MSICUs).The overall incidence of SC was 0.44%,incidence in CCU and MSICU was 1.16%and 0.25%respectively.Sixty-two(57%)had confirmed SC and underwent cardiac catheterization whereas 47(43%)had clinical SC,and did not undergo cardiac catheterization.Forty-three(72%)patients in the CCUs were diagnosed with primary SC,whereas all(100%)patients in MSICUs developed secondary SC.Acute respiratory failure that required invasive mechanical ventilation and shock developed in twenty-nine(59%)MSICU patients.There were no statistically significant differences in intensive care unit(ICU)mortality,in-hospital mortality,use of inotropic or mechanical circulatory support based on type of unit or anatomical variant.CONCLUSION Stress cardiomyopathy can be under-recognized in the critical care setting.Intensivists should have a high index of suspicion for SC in patients who develop sudden or worsening unexplained hemodynamic instability,arrhythmias or respiratory failure in ICU.

Correlation of the electrical remodeling of myocardial cells with oxidative stress and inflammatory injury in animal models with dilated cardiomyopathy

Objective:To study the correlation of the electrical remodeling of myocardial cells with oxidative stress and inflammatory injury in animal models with dilated cardiomyopathy. Methods: Male New Zealand white rabbits were selected as experimental animals and divided into model group and control group, model group were made into animal models with dilated cardiomyopathy through ear intravenous injection of adriamycin, and the control group received ear intravenous injection of same dose of saline. 8 weeks later, the myocardial tissue was collected to detect the myocardial cell delay after depolarization (DADs) through the technique of unicell patch clamp, and radioimmunoprecipitation kits and enzyme-linked immunosorbent assay kits were used to determine oxidative stress indexes and inflammatory reaction indexes.Results:The incidence of myocardial cell DADs of animal model group was significantly higher than that of control group, and ROS, MDA, AOPP, CHOP, GRP78, TLR4, NF-kB, IL-1β, IL-6 and TNF-α levels in myocardial tissue were significantly higher than those of control group;ROS, MDA, AOPP, CHOP, GRP78, TLR4, NF-kB, IL-1β, IL-6 and TNF-α levels in myocardial tissue of DADs animals in model group were significantly higher than those of non-DADs animals.Conclusion:Adriamycin-induced dilated cardiomyopathy can lead to myocardial cell delay after depolarization through oxidative stress and inflammatory injury.

Cardiovascular complications following medical termination of pregnancy: An updated review

BACKGROUND Around 1 million cases of medical termination of pregnancy(MTP)take place yearly in the United States of America with around 2 percent of this population developing complications.The cardiovascular(CVD)complications occurring post MTP or after stillbirth is not very well described.AIM To help the reader better understand,prepare,and manage these complications by reviewing various cardiac comorbidities seen after MTP.METHODS We performed a literature search in PubMed,Medline,RCA,and google scholar,using the search terms“abortions”or“medical/legal termination of pregnancy”and“cardiac complications”or“cardiovascular complications”.RESULTS The most common complications described in the literature following MTP were infective endocarditis(IE)(n=16),takotsubo cardiomyopathy(TTC)(n=7),arrhythmias(n=5),and sudden coronary artery dissection(SCAD)(n=4).The most common valve involved in IE was the tricuspid valve in 69%(n=10).The most observed causative organism was group B Streptococcus in 81%(n=12).The most common type of TTC was apical type in 57%(n=4).Out of five patients de veloping arrhythmia,bradycardia was the most common and was seen in 60%(3/5)of the patients.All four cases of SCAD-P type presented as acute coronary syndrome 10-14 d post termination of pregnancy with predominant involvement of the right coronary artery.Mortality was only reported following IE in 6.25%.Clinical recovery was reported consistently after optimal medical management following all these complications.CONCLUSION In conclusion,the occurrence of CVD complications following pregnancy termination is infrequently documented in the existing literature.In this review,the most common CVD complication following MTP was noted to be IE and TTC.

应激性高血糖比值对围产期心肌病患者预后的预测价值

目的探讨应激性高血糖比值(SHR)对围产期心肌病(PPCM)患者预后的预测价值。方法连续性收集2007年1月至2023年3月于首都医科大学附属北京安贞医院住院治疗诊断为PPCM的78例患者的临床资料进行回顾性分析。根据心功能是否改善分为无改善组(37例)和改善组(41例)。使用受试者工作特征(ROC)曲线分析SHR对患者不良预后的预测效能,采用Logistic回归分析方法评估心功能无改善的影响因素。结果无改善组患者年龄、经产妇比例、PPCM病史比例、左心室舒张末期内径、血肌酐、血糖、B型脑钠肽水平、SHR均大于/高于改善组,收缩压、左心室射血分数(LVEF)均低于改善组(均P<0.05)。ROC曲线分析结果显示,SHR预测PPCM患者出现不良预后的最佳截断值为1.079,敏感度为81.1%,特异度为90.2%,曲线下面积为0.880(95%置信区间:0.800~0.961)(P=0.041)。多因素Logistic回归分析结果显示SHR≥1.079、血肌酐及LVEF<35%为PPCM患者不良预后的独立危险因素(均P<0.05)。结论SHR≥1.079是PPCM患者预后不良的危险因素,使用SHR可以协助识别PPCM高危人群。

降糖舒心方抑制内质网应激-过度自噬对糖尿病大鼠心肌病变的影响

目的:探讨降糖舒心方对自噬通路过度激活反应的影响及其防止糖尿病合并心力衰竭心肌重构的机制。方法:100只大鼠按随机数字表法分成模型组、西药组、降糖舒心方低剂量组、降糖舒心方高剂量组、假手术组,每组20只。先对大鼠腹腔单次注射链脲佐菌素(STZ)进行糖尿病造模,再采用腹主动脉缩窄手术方法建立慢性心力衰竭动物模型。各给药组分别灌胃给予相应药物,假手术组和模型组大鼠灌胃给予等容积蒸馏水,1次/d,连续2个月。检测心脏左室射血分数(LVEF)、舒张末期室间隔厚度(IVSd)、收缩末期室间隔厚度(IVSs)、收缩末期左心室后壁厚度(LVPWs)与舒张末期左心室后壁厚度(LVPWd);HE染色检测大鼠心肌组织病理学改变情况;透射电镜观察心肌组织自噬超微结构变化;RT-PCR检测内质网应激信号分子GRP78 mRNA、IRE-1 mRNA、TRAF2 mRNA相对表达量;Western blotting检测心肌组织中自噬蛋白LC3-Ⅱ、Beclin 1表达情况。结果:与模型组比较,各给药组大鼠LVPWs、LVPWd、IVSs、IVSd均明显降低(P<0.05),LVEF均明显升高(P<0.05);心肌组织病理学积分均明显降低(P<0.05);大鼠心肌细胞损害程度有所减轻,自噬小体和空泡有所减少,纤体化程度减轻;心肌组织GRP78 mRNA、IRE-1 mRNA、TRAF2 mRNA相对表达量均明显降低(P<0.05);LC3-Ⅱ、Beclin 1蛋白相对表达量均明显降低(P<0.05)。与西药组比较,降糖舒心方高剂量组大鼠LVEF明显升高(P<0.05);降糖舒心方低、高剂量组大鼠心肌组织病理学积分均明显降低(P<0.05);大鼠心肌细胞数量较多,自噬小体和空泡减少,纤体增生减轻;心肌组织GRP78 mRNA、IRE-1 mRNA、TRAF2 mRNA相对表达量均明显降低(P<0.05);LC3-Ⅱ、Beclin 1蛋白相对表达量均明显降低(P<0.05)。与降糖舒心方低剂量组比较,降糖舒心方高剂量组大鼠心肌肌原纤维排列整齐,间质增生少,胞体大部分光滑完整,胞内有少量自噬小体和空泡,各项指标均有剂量依赖性。结论:内质网应激-自噬在心力衰竭的发生发展过程中发挥了重要的作用。糖尿病状态过度自噬可导致心肌细胞数量降低,使心室壁变薄。降糖舒心方能减轻过度自噬对心肌的损害,抑制心肌重构,改善心功能。

Al-Mg-Sc合金热压缩变形的流变应力行为

采用热模拟试验对1种Al-Mg-Sc合金进行等温热压缩实验,研究该合金在变形温度为300～450℃,应变速率0.001～1s-1条件下的热压缩变形流变应力行为。结果表明:该Al-Mg-Sc合金在变形温度为300℃,应变速率0.01～1s-1的条件下,流变应力开始随应变增加而增大,达到峰值后趋于平稳,表现出动态回复特征;而在其他条件下,应力达到峰值后随应变的增加而逐渐下降,表现出动态再结晶特征。应变速率和流变应力之间满足指数关系,温度和流变应力之间满足Arrhenius关系,通过线性回归分析计算出该材料的应变硬化指数n以及变形激活能Q,获得该铝合金高温条件下的流变应力本构方程。