L-carvone attenuates myocardial injury and dyslipidemia in rats with isoproterenol-induced cardiac hypertrophy

Objective:To explore the therapeutic efficacy of L-carvone from Mentha spicata L.leaf extracts against isoproterenol-induced cardiac hypertrophy in rats.Methods:Isoproterenol(5 mg/kg)was injected intraperitoneally into rats for one month to induce cardiac hypertrophy.L-carvone(25 and 100 mg/kg)was administered orally to treat cardiac hypertrophy.The cardioprotective activity of L-carvone was evaluated by electrocardiogram,histopathological analysis as well as determination of biochemical parameters and enzymatic markers.Results:L-carvone from Mentha spicata L.at 25 and 100 mg/kg ameliorated isoproterenol-induced cardiac hypertrophy,as evidenced by reduced QRS interval on electrocardiogram,and decreased heart weight and heart index.In addition,both doses of L-carvone markedly lowered the levels of glucose,total protein,low-density lipoprotein cholesterol,aspartate transaminase,alanine transaminase,lactate dehydrogenase,creatine kinase MB,troponin-Ⅰ,N-terminal pro-B type natriuretic peptide and triglycerides while increasing high-density lipoprotein cholesterol and lipase level(P<0.05).Moreover,L-carvone alleviated contraction band necrosis,and reorganized the myofibrils with normal striations and myocytes as well as normal nuclei in cardiac histoarchitecture of rats with isoproterenol-induced cardiac hypertrophy.Conclusions:L-carvone from Mentha spicata L.leaf extract can restore abnormal cardiac function and may be further explored as a therapeutic agent against the deleterious effects of cardiac hypertrophy after further evaluation.

Effect of Zhenwu Tang Granule on pressure-overloaded left ventricular myocardial hypertrophy in rats

BACKGROUND： In the perspective of traditional Chinese medicine, few studies have focused on the compound preparations though there are many investigations. The present study was undertaken to investigate the effect of Zhenwu Tang Granule on chronic pressure-overloaded left ventricular hypertrophy in rats.METHODS： The study was performed at the laboratory of Guangzhou Institute of Respiratory Disease. Male SD rats were divided randomly into 3 groups： sham operation group （n=8）, operation group （n=15） and traditional Chinese medicine （TCM） group （n=15）.The model of myocardial hypertrophy was made by gradually constricting the abdominal aorta. Sixteen weeks later, cardiac ultrasonography was performed in all groups in order to ascertain post-operational left ventricular （LV） hypertrophy. And Zhenwu Tang Granule was added at a dose of 12 g/kg in the mixed feedstuff for 8 weeks in the TCM group. In the 24th week, weight, structure as well as function of the heart in each group were measured by high-frequency ultrasonography, and Masson＇s staining was performed on the cardiac muscles. Meanwhile, total collagen volume fraction （CVF-T） and non-coronary vessel collagen volume fraction （CVF-NV） were analyzed.RESULTS： There was an increase in the weight of the heart in the operation group, with the left ventricule dominated （P〈0.05）. The heart was enlarged, with diastolic interventricular septal distance （IVSd） and left ventricular posterior wall distance （LVPWd） dominated （P〈0.01）.There was a significant decrease in the cardiac function （P〈0.05）. The weight （P〈0.01） and volume of the heart decreased in the TCM group compared with the operation group, with IVSd and systolic left ventricular posterior wall dominated （P〈0.01）. And the cardiac function was improved （P〈0.05）. Significant interstitial and collagen hyperplasia was shown in the operation group based on pathological analysis, and various improvements were proved in the TCM group, i.e. there was a significant decrease in CVF-T and CVF-NV （P〈0.01） compared with the operation group; but no difference （P〉0.05） was found when compared with the pseudo-operation group.CONCLUSION： Zhenwu Tang Granule could reduce the weight and volume of the heart, improve the cardiac function, inhibit hyperplasia of collagen, and reverse myocardial hypertrophy in rats with pressure-overloaded left ventricular hypertrophy.

Expression of Wnt and NCX1 and its correlation with cardiomyocyte apoptosis in mouse with myocardial hypertrophy

Objective:To study the correlation between expression of Wnt and NCXl and cardiomyocyte apoptosis in mouse with myocardial hypertrophy.Methods:C57B/16 male mice were given the subcutaneous injection of 1 mg/kg isoprenaline to build the myocardial hypertrophy model.After 14 d of model building,mice were executed by cervical vertebra luxation.The ratio of heart weight/body weight(HW/BW) and heart weight/tibia length(HW/TL) was observed and proved using HE staining mat detected the size of eaidiomyocytes.40 male C57B/16 mice were randomly divided into the sham group(normal saline) and model group(isoprenaline),with 20 mice in each group.The terminal deoxynucleotidyl transferase-mediated dUTP nick end labeling was applied to detect the cardiomyocyte apoptosis;while Western blot and immunohistochemistry were employed to detect the expression of Wnt and NCX1.Meanwhile,the correlation between these two proteins and cardiomyocyte apoptosis was explored.Results:Compared with the sham group,the ratio of HW/BW and HW/TL was increased in the model group,as well as the bigger and hypertrophied cardiomyocytes,decreased number and increased apoptosis of eaidiomyocytes,and increased positive expression of Wnt3 a,WntSa and NCXl in the cardiac muscle tissue.Besides,there was positive correlation between the expression of Wnt and NCXl and the cardiomyocyte apoptosis.Conclusions:The expression of Wnt3 a,Wnt5a and NCXl in mouse with myocardial hypertrophy is increased and positively correlated with the cardiomyocyte apoptosis.

Alterations in Cardiac Structure and Function in a Modified Rat Model of Myocardial Hypertrophy

This study was aimed to establish a stable animal model of left ventricular hypertrophy （LVH） to provide theoretical and experimental basis for understanding the development of LVH. The abdominal aorta of male Wistar rats （80-100 g） was constricted to a diameter of 0.55 mm between the branches of the celiac and anterior mesenteric arteries. Echocardiography using a linear phased array probe was performed as well as pathological examination and plasma B-type natriuretic peptide （BNP） measurement at 3, 4 and 6 weeks after abdominal aortic constriction （AAC）. The results showed that the acute mortality rate （within 24 h） of this modified rat model was 8%. Animals who underwent AAC demonstrated significantly increased interventricular septal （IVS）, LV posterior wall （LVPWd）, LV mass index （LVMI）, cross-sectional area （CSA） of myocytes, and perivascular fibrosis; the ejection fraction （EF）, fractional shortening （FS）, and cardiac output （CO） were consistently lower at each time point after AAC. Notably, differences in these parameters between AAC group and sham group were significant by 3 weeks and reached peaks at 4th week. Following AAC, the plasma BNP was gradually elevated compared with the sham group at 3rd and 6th week. It was concluded that this modified AAC model can develop LVH, both stably and safely, by week four post-surgery; echocardiography is able to assess changes in chamber dimensions and systolic properties accurately in rats with LVH.

Icariin ameliorate diabetic myocardial hypertrophy by inhibiting autophagy via the AMPK/mTOR pathway

Objective:To observe the effect of Icariin on diabetic myocardial hypertrophy and explore its molecular mechanism.Methods:C57BL/6 mice were randomly divided into Ctrl group(normal control group),DM group(STZ intraperitoneal injection model),and DM+ICA group(diabetic C57BL/6 mice by intragastric Icariin solution 80mg/kg/d,for 3 consecutive weeks).Real-time quantitative PCR was used to detect myocardial hypertrophy markers BNP andβ-MHC.Western blotting was used to detect myocardial AMPK,p-AMPK,mTOR,p-mTOR,LC3B and Beclin1 protein expression.Echocardiogram was used to detect left ventricular mass and ejection fraction.Results:Compared with the normal control group,the expression of myocardial hypertrophy markers BNP andβ-MHC mRNA in diabetic mice were significantly increased;the expression of phosphorylated AMPK protein,autophagy-related protein LC3B and Beclin1 were significantly increased,and the expression of phosphorylated mTOR protein is significantly reduced;the left ventricular mass is significantly increased.The above changes can be reversed after treatment with Icariin,but the effect of Icariin is blocked by the autophagy inhibitor rapamycin.Conclusion:Icariin may inhibit autophagy and reduce diabetic myocardial hypertrophy through AMPK-mTOR signaling pathway.

The Effect of TanshinoneⅡ A upon the TGF-beta1/Smads Signaling Pathway in Hypertrophic Myocardium of Hypertensive Rats

To investigate the molecular mechanism by which Tanshinone Ⅱ A （TSN Ⅱ A） prevents left ventricular hypertrophy （LVH）, we examined the expression of AT1R, TGF-β1 and Smads gene in the hypertrophic myocardium of hypertensive rats with abdominal aorta constriction. LVH model was established by creating abdominal aorta constriction. Four weeks later, animals were randomly divided into 4 groups with 8 animals in each. One group was used as model control, the other three groups were treated with TSN ⅡA （20 mg/kg）, TSN ⅡA （10 mg/kg） and valsartan （10 mg/kg）, respectively. Another 8 SD rats were subjected to sham surgery and served as blank control. After 8- week treatment, the caudal artery pressure of the animals was measured. The tissues of left ventricle were taken for the measurement of the left ventricular mass index （LVMI） and pathological sectioning and HE-staining were used for determining the myocardial fiber dimension （MFD）. The mRNA expression of AT1R, protein expression of TGF-betal and activity of Smad-2, 4, 7 were detected by RT-PCR and Western blotting, respectively. Our results showed that （1） the blood pressure of rats treated with TSN Ⅱ A, either at high or low dose, was significantly higher than those in the control and valsartan-treated group （P〈0.01, P〈0.05）; （2） LVMI and MFD in TSN Ⅱ A and valsartan-treated rats were higher than those in the control group （P〈0.05） but significantly lower than those in the model control （P〈0.01）; （3） the high doses of TSN Ⅱ A and valsartan significantly down-regulated the mRNA expression of AT 1R and protein expression of TGF-beta l and Smad-3 in the hypertrophic myocardium （P〈0.01）, and TGF-betal in valsartan-treated animals was more significantly lower than that in rats treated with TSN Ⅱ A; （4） the two doses of TSN Ⅱ A and valsartan significantly up-regulated the protein expression of Smad-7 in the hypertrophic myocardium （P〈0.01）, and Smad-7 in the animals treated with high-dose TSN Ⅱ A was significantly higher than that in rats treated with valsartan. It is concluded that inhibition of myocardial hypertrophy induced by TSN ⅡA independent of blood pressure. The underlying mechanism might be the down-regulated expression of AT1R mRNA and Smad-3, increased production of Smad-7, and blocking effect of TSN Ⅱ A on TGF betal/Smads signal pathway in local myocardium.

Vaspin alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence

Background:Visceral adipose tissue-derived serine protease inhibitor(vaspin),a secretory adipokine,protects against insulin resistance.Recent studies have demonstrated that serum vaspin levels are decreased in patients with coronary artery disease and that vaspin protects against myocardial ischemia-reperfusion injury and atherosclerosis.However,it remains unclear whether vaspin exerts specific effects on pathological cardiac hypertrophy.Methods:An in vivo study was conducted using a cardiac hypertrophy model established by subcutaneous injection of isoproterenol(ISO)in C57BL/6 and vaspin-ko mice.Rapamycin was administered intraperitoneally to mice,for further study.H9c2 cells and neonatal rat ventricular myocytes(NRVMs)were treated with ISO to induce hypertrophy.Human vaspin fusion protein,the proteasome inhibitor MG132,and chloroquine diphosphate were used for further mechanistic studies.Results:Here,we provide the first evidence that vaspin knockdown results in markedly exaggerated cardiac hypertrophy,fibrosis,and cardiomyocyte senescence in mice treated with ISO.Conversely,the administration of exogenous recombinant human vaspin protected NRVMs in vitro against ISO-induced hypertrophy and senescence.Furthermore,vaspin significantly potentiated the ISO-induced decrease in autophagy.Both rapamycin and chloroquine diphosphate regulated autophagy in vivo and in vitro,respectively,and participated in vaspin-mediated cardioprotection.Moreover,the PI3K-AKT-mTOR pathway plays a critical role in vaspin-mediated autophagy in cardiac tissues and NRVMs.Our data showed that vaspin downregulated the p85 and p110 subunits of PI3K by linking p85 and p110 to NEDD4L-mediated ubiquitination degradation.Conclusion:Our results show,for the first time,that vaspin functions as a critical regulator that alleviates pathological cardiac hypertrophy by regulating autophagy-dependent myocardial senescence,providing potential preventive and therapeutic targets for pathological cardiac hypertrophy.

Effect of matrine and carvedilol on collagen and MMPs activity of hypertrophy myocardium induced by pressure overload

Objective： To explore the effect and mechanism of matrine （Mt.） on myocardial interstitial fibrosis induced by pressure overload. Methods： Pressure overloaded myocardial hypertrophy was produced by banding of aorta abdominalis in 67 male Sprague-Dawley rats weighing （200±15） g. The rats were assigned into one of the following groups： sham-operation control, operation control, operation group treated with matrine （15 mg/（kg·d）） and treated with carvedilol （Car.） （3.6 mg/（kg·d）） group. The rats were given drugs one day after operation. Five weeks after treatment, the left ventricular weight （LVW） was measured and the volume of myocardial cells was detected with Hematoxylin-Eosin （H-E） stain and Masson stain was used to assess the level of fibrosis of the myocardial matrix. Myocardial metalloproteinase activity was quantified with zymography, and survival rate was calculated. Results： Survival rate significantly decreased （P〈0.05）, LVW/BW （body weight）, MMP-2 （matrix metalloproteinase-2） activity （P〈0.05）, size of cardiomyocytes and interstitial fibrosis obviously increased in the operation group compared with sham control group. Mr. and Car. treatment can significantly increase survival rate （P〈0.05）, decrease LVW/BW （P〈0.05） and MMP-2 activity （P〈0.05）, decrease size of cardiomyocytes and interstitial fibrosis compared with operation group. But there was difference compared with sham group. Conclusion： Matrine was shown to be able to prevent cardiac remodelling of bypertrophy cardium induced by pressure overload including myocardial hypertrophy and fibrosis which may be associated with the decrease in MMP-2 activity of heart.

EXPERIMENTAL STUDY ON THE BIOCHEMICAL REMODELING OF VENTRICULAR COLLAGEN MATRIX FOLLOWING MYOCARDIAL INFARCTION IN RATS

The present study is to characterize the biochemicai remodeling of ventricular collagen matrix and its natural history following myocardial infarction(MI)in rats.Collagen concentration,the total collagen content and the ratio of types Ⅰ,Ⅲ collagen (Ⅰ/Ⅲ) were measured at 3,15 and 42 days after MI.The results showed:1)The total collagen content of non-infarcted area (NIA) and right ventricle (RV) foliowing the development of ventricular hypertrophy increased progressively. Although the collagen concentration had no difference in RV, it showed dynamic changes in NIA. Both the collagen concentration and the total collagen content in infarcted area (IA) increased rapidly following reparative fibrosis.2)At the early stage or MI,type Ⅲ collagen in NIA increased significantly;later,type collagen was remarkedly higher in NIA and RV.Ⅰ/Ⅲ of IA showed difrerent patterns than that of NIA.The results suggest:(1) the blochemical remodeling or collagen matrix in NIA, IA and RV occurred following MI and its time courses were different;(2)the mechanism of the biochemlcal remodeling of collagen matrix in ventricles may be different.

Cardioprotective effect of Danshen injectable powder on pressure overloadinduced ventricular remodeling in rats and isoproterenol induced myocardial injury in mice

OBJECTIVE To determine the effects of Danshen injectable powder on myocardial remodeling in pressure overload rats and isoproterenol(ISO) injection mice.METHODS SD Rats were subject to abdominal aortic constriction(AAC) surgery to develop pressure overload.Therapeutic effect of Danshen injectable powder was assessed six weeks after AAC surgery.The lactic dehydrogenase(LDH) and creatine kinase(CK) levels in serum,biometric,echocardiographic parameters,interstitial fibrosis,the expression of DJ-1 and SOD2 were then measured.The myocardial impairment in mice was induced by ISO injection.LDH and CK in serum,biometric,interstitial fibrosis were measured to investigate the cardioprotective effect of Danshen injectable powder.Matrix-assisted laser desorption mass spectrometry imaging(MALDI-MSI) was used to detect the changes of 60-1000 Da molecules in mice heart tissue.RESULTS In AAC rats,we observed compensatory hypertrophy and perivascular fibrosis,however cardiac function had not progressed to deterioration.The levels of LDH and CK were decreased significantly in the Danshen injectable powder groups(P<0.05,P<0.05).Danshen injectable powder could alleviate the perivascular collagen deposits but not cardiac hypertrophy in AAC rats.Furthermore,Danshen injectable powder enhanced the expression levels of SOD2 and DJ-1 in cardio.myocytes(P<0.05,P<0.01).In ISO injection mice,the levels of HWI and LDH were decreased signifi.cantly in drug treatment group compared with model group(P<0.01,P<0.01).In the MALDI-MSI of mice heart section,Danshen injectable powder can improve the reduction of energy metabolism-related substances including adenosine,creatine and ADP induced by ISO impairment.CONCLUSION Danshen injectable powder can attenuate perivascular fibrosis and improve the expression of antioxidative stress-related proteins SOD2,DJ-1 in the rats with pressure overload-induced left ventricular remodeling.Danshen injectable powder has cardioprotective effect on ISO impairment in mice which is probably related to improvement of energy metabolism.

Total flavonoids of bugloss limits left ventricular remodeling after myocardial infarction in mice

OBJECTIVE To investigate the effects of total flavonoids of bugloss(TFB) on left ventricular(LV) remodeling after myocardial infarction(MI),LV size and function was compared in mice subjected to left anterior descending coronary artery ligation.METHODS 28 d after MI,the infarcted fraction of the LV and LV mass,systolic and diastolic function were measured.Capillary density and myocyte width in the nonischemic portion of the LV were also determined.RESULTS 28 d after MI,both groups had dilated LVs with decreased fractional shortening and lower ejection fractions.Although the infarcted size of the LV was similar in both groups,LV end-diastolic internal diameter,end-diastolic volume,and mass were lower,but fractional shortening,ejection fraction,and the maximum rate of developed LV pressure(dp/dtmax) were greater in TFB treated mice than in control mice.Impairment of diastolic func.tion,as measured by the time constant of isovolumic relaxation(t) and the maximum rate of LV pres.sure decay(dp/dtmin),was more marked in control mice than in TFB treated mice.Mortality after MI was greater in control mice than in TFB treated mice.In control mice,capillary density and myocyte width in the nonischemic portion of the LV did not differ before and 28 days after MI,whereas in TFB treated mice,capillary density increased and myocyte width declined after MI.CONCLUSION These results suggest that the presence of TFB limits LV dysfunction and remodeling in a murine model of MI in part by decreasing myocyte hypertrophy in the remote myocardium.

Hypertrophic cardiomyopathy secondary to deficiency in lysosomeassociated membrane protein-2: A case report

BACKGROUND Danon disease(DD),in which mutations in the X-linked lysosome-associated membrane protein-2(LAMP-2)gene result in hypertrophic cardiomyopathy,is a rare disease,reported primarily in small samples or cases.However,with the development of cardiac magnetic resonance imaging and genetic technology in recent years,the number of reports has increased.CASE SUMMARY We report a case of DD in an adolescent male patient,confirmed by genetic testing.The patient was admitted to our hospital with complaints of a three-year history of chest tightness and shortness of breath.His preliminary clinical diagnosis is hypertrophic cardiomyopathy.Our report includes the patient’s clinical course from hospital admission to death,step-by-step diagnosis,treatment course,and noninvasive imaging features.We highlight how a noninvasive diagnostic approach,based solely on clinical and imaging“red flags”for DD,can be used to achieve a diagnosis of DD with a high degree of confidence.CONCLUSION DD is a very dangerous cardiomyopathy,and it is necessary to achieve early diagnosis and treatment.

不典型急性心肌梗死心电图误诊分析

目的探讨不典型急性心肌梗死(AMI)早期心电图误诊原因及防范措施。方法回顾分析2022年1月—2023年2月收治的曾误诊的不典型AMI 2例的临床资料。结果1例因发热、胸闷、心悸、咳嗽和全身乏力1 d就诊,心电图检查示Ⅱ、Ⅲ、aVF导联ST段压低,T波低平,窦性心律不齐,误诊为心肌炎,予对症治疗无好转,复查心电图及心肌酶等后诊断为AMI。1例因胸痛、晕厥倒地2 h入院,心电图无ST-T及异常Q波改变,提示右心室肥大,诊断为右心室肥大,后经心肌酶、心脏超声及冠状动脉造影检查明确诊断AMI。误诊时间3 d和6 h。1例行药物保守治疗,1例行经皮冠状动脉介入术治疗,随访均预后良好。结论不典型AMI患者或因无明显胸痛症状,或因早期心电图表现不典型或正常,导致初期极易误诊。加强对不典型AMI认识,对伴有高危因素者提高警惕性,熟知其心电图动态变化特点,注重动态心电图监测,并结合临床症状及心肌酶情况综合分析病情,有助于早期确诊并治疗。

急性脑卒中患者心脏电学改变研究

目的通过分析急性脑卒中患者心脏电学变化,探讨心电图评估急性脑卒中患者血压控制效果的临床价值。方法选取2023-06—2024-01郑州大学第二附属医院收治入院的急性脑卒中患者103例(脑出血50例,脑梗死53例)为研究组,原发性高血压患者61例为对照组,分析研究组临床资料和心电图特点,比较研究组和对照组的心电图改变。将研究组分为血压异常组和血压正常组,比较不同血压状态下脑出血和脑梗死患者心电图改变。结果急性脑卒中患者中脑出血患者年龄偏小,糖尿病占比高,入院收缩压/舒张压、血糖较高,差异有统计学意义(P<0.05)。脑卒中患者心电图异常率高于原发性高血压患者,以P波时限≥120 ms、P波双峰(峰间距>40 ms)、Macrua指数、左心室高电压、左心室肥大、快速性心律失常检出率较高,差异有统计学意义(P<0.05)。脑出血患者心电图异常率高于脑梗死患者,左心房/左心室肥大、心肌缺血比较差异有统计学意义(P<0.05)。血压异常的脑出血患者心电图异常率高于血压正常者,左心房/左心室肥大、心肌缺血比较差异有统计学意义(P<0.05)。血压异常的脑梗死患者快速性心律失常检出率高于血压正常者,差异有统计学意义(P<0.05)。结论急性脑卒中患者心电图异常率高,尤其高血压合并脑卒中患者心电图异常表现更加明显,心电图检查可作为诊断和评估急性脑卒中患者血压控制效果的重要依据。

血清miR-31在主动脉狭窄致心肌肥厚患者中的作用价值

目的探究血清microRNA-31(miR-31)在主动脉狭窄致心肌肥厚患者中的作用。方法选取2020年1月至2020年10月就诊于新疆医科大学第一附属医院的主动脉狭窄致心肌肥厚患者150例为观察组,并选取同期健康志愿者150例为对照组,比较两组患者miR-31、舒张末期左心室后壁厚度(LVPWTd)、室间隔舒张末期厚度(IVSTd)、左心室舒张末期内径(LVEDD)、左心室射血分数(LVEF)和左心室重量指数(LVMI)。同时对150例主动脉狭窄致心肌肥厚患者进行随访3年,观察其是否发生不良心血管事件,分析miR-31对不良心血管事件的预测价值。结果与对照组比较,观察组miR-31显著增加(1.25±0.26 vs.0.71±0.23,P<0.001)。血清miR-31与主动脉狭窄致心肌肥厚患者LVPWTd、IVSTd、LVEDD、LVMI均呈显著正相关(r=0.372、0.401、0.362和0.452,P<0.05),而与LVEF呈显著负相关(r=-0.317,P=0.010)。对150例主动脉狭窄致心肌肥厚患者随访3年发现,与未发生不良心血管事件的患者相比,发生不良心血管事件的患者血清miR-31显著增加(1.44±0.17 vs.1.21±0.26,P<0.001)。血清miR-31对主动脉狭窄致心肌肥厚患者不良心血管事件具有较好的预测价值,曲线下面积0.752(95%CI:0.668~0.837,P<0.001)。结论血清miR-31在主动脉狭窄致心肌肥厚患者中可能具有重要潜力,是主动脉狭窄致心肌肥厚的潜在生物学指标。

经胸超声心动图联合超声造影检测冠状动脉血流储备对高血压患者冠状动脉病变的预测价值

目的 探讨经胸超声心动图联合超声造影检测冠状动脉血流储备(CFR)对高血压患者冠状动脉病变的预测价值。方法 纳入伴有左心室肥厚(LVH)的高血压患者45例作为观察组,另纳入45例单纯高血压患者作为对照组。对所有患者开展经胸超声心动图联合超声造影检查,比较两组经胸超声心动图检查结果及造影检查结果。结果 两组患者的静息舒张期峰值血流速度(PDV)比较无差异(P>0.05);观察组的负荷PDV(47.34±14.98)cm/s及CFR(1.94±0.78)低于对照组的(67.78±15.57)cm/s、(2.83±1.82)(P<0.05)。观察组灌注量(7.02±2.91)L/min、曲线峰值强度(9.46±7.62)dB、曲线斜率(1.23±1.03)dB/s低于对照组的(9.64±3.34)L/min、(16.78±8.43)dB、(1.78±1.22)dB/s,灌注阳性率71.11%高于对照组的22.22%(P<0.05)。结论 经胸超声心动图联合超声造影可实现对CFR的评估,帮助了解高血压患者的冠状动脉病变情况,为冠状动脉病变的防治提供依据。

心脏磁共振评价慢性肾脏病患者不同左心室构型的心肌组织特征

目的通过心脏磁共振(cardiac magnetic resonance,CMR)分析慢性肾脏病(chronic kidney disease,CKD)患者不同左心室构型的心肌应变、native T1值及T2值,研究CKD患者不同左心室构型的心肌组织特征。材料与方法前瞻性纳入CKD患者114例和年龄性别匹配的健康对照(对照组)30例。扫描序列包括心脏电影序列、T1 mapping及T2 mapping序列。根据左心室重构指数(left ventricular remodeling index,LVRI)和左心室质量指数(left ventricular mass index,LVMI)将患者分为左心室正常几何构型(n=43)、向心性重构(n=22)、向心性左心室肥厚(left ventricular hypertrophy,LVH)(n=20)和离心性LVH(n=29)共四组。利用心脏后处理软件CVI 42测量受试者的左心室心肌应变及应变率,包括周向、径向和纵向的整体应变、收缩期整体应变率、舒张期整体应变率,以及native T1值和T2值。分析不同左心室构型患者的心肌组织特征。采用单因素和多因素线性回归分析探讨左心室心肌应变参数、native T1值及T2值与生理变量的关系。结果除左心室正常构型组的整体周向应变[-18.40%(3.30%)vs.-19.71%±1.66%,P=0.063]、整体径向应变(30.63%±7.03%vs.34.07%±4.61%,P=0.324)与对照组差异无统计学意义,CKD患者的其余心肌应变参数显著低于对照组(P均<0.05)。应变分析结果显示离心性LVH组的整体径向应变(22.02%±8.31%)最低;向心性LVH组的整体周向应变(-14.42%±3.24%)和整体纵向应变(-9.55%±2.79%)最低。应变率分析结果显示离心性LVH组的收缩期整体周向应变率[(-0.84±0.25)s^(-1)]、舒张期整体周向应变率[(0.73±0.29)s^(-1)]、收缩期整体径向应变率[(1.25±0.46)s^(-1)]和舒张期整体径向应变率[(-1.18±0.50)s^(-1)]最低;向心性LVH组的收缩期整体纵向应变率[(-0.62±0.16)s^(-1)]和舒张期整体纵向应变率[(0.53±0.14)s^(-1)]最低。向心性重构组的native T1值与对照组差异无统计学意义[1285.50(85.25)ms vs.(1262.53±38.18)ms,P=0.083];离心性LVH组的native T1值最大,显著高于对照组[(1351.10±58.49)ms vs.(1262.53±38.18)ms,P<0.001]。与对照组相比,四个患者组的T2值均显著升高(P均<0.05),离心性LVH组的T2值[(54.86±8.71)ms]最大。不同组CKD患者的T2值差异无统计学意义(P均>0.05)。Native T1值的独立决定因素是血红蛋白含量(校正的R^(2)=0.216,β=-0.442,P<0.001)和血清肌酐(校正的R^(2)=0.216,β=-0.220,P=0.010)。结论CKD患者的心肌应变降低、native T1值及T2值增加,离心性LVH患者的心肌组织特征改变最明显。

m6A甲基化修饰非编码RNA调控病理性心脏重塑的作用

背景:m6A甲基化修饰非编码RNA是病理性心脏重塑形成机制的研究热点,在心血管疾病的发生发展中起着重要作用。目的:总结m6A甲基化修饰非编码RNA对调控病理性心肌肥大、心肌细胞死亡、心肌纤维化与血管重塑等病理性心脏重塑主要过程的可能作用机制。方法:以“m6A甲基化修饰,非编码RNA,病理性心肌肥大,心肌细胞凋亡,心肌细胞焦亡,心肌细胞铁死亡,心肌纤维化,血管重塑”为中文主题词,以“m6A、non-coding RNA,pathological cardiac hypertrophy,cardiomyocyte apoptosis,cardiomyocyte pyroptosis,cardiomyocyte ferroptosis,myocardial fibrosis,vascular remodeling”为英文主题词,检索中国知网、PubMed、Web of Science数据库1974年1月至2023年4月发表的相关文献,对符合筛选标准的86篇文献进行综述。结果与结论:①m6A甲基化修饰是一种动态可逆的表观遗传修饰方式;②病理性心脏重塑主要包括病理性心肌肥大、心肌细胞死亡、心肌纤维化、血管重塑,m6A相关酶可调控病理性心脏重塑相关进程;③m6A甲基化修饰相关酶可通过多种非编码RNA与不同信号通路参与调控病理性心脏重塑过程,可作为心血管疾病新的潜在干预方式;④在病理性心脏重塑中,m6A甲基化修饰与非编码RNA之间的调控关系仍处于起步阶段,随着表观遗传学的发展,m6A甲基化修饰非编码RNA来调控病理性心脏重塑有望有新的发展。

甲状腺功能亢进激活心肌细胞β-catenin/FoxO1诱导大鼠心室重构的作用

【目的】探究甲亢激活心肌细胞β-catenin/FoxO1诱导大鼠心室重构的作用和机制。【方法】通过甲状腺激素(T40.1 mg/kg/day;腹腔注射)连续给药30 d构建甲亢诱导心室重构大鼠体内模型。利用β-catenin抑制剂MSAB(14 mg/kg)同时给药30 d,通过Western-blot检测心肌肥厚主要标志物ANP以及β-catenin、FoxO1等蛋白的表达情况;免疫荧光检测β-catenin、FoxO1的核内外表达及分布情况。利用原代培养的乳鼠心肌细胞,使用甲状腺激素(T320 nmol/L)处理心肌细胞24 h构建体外甲亢诱导心肌细胞肥厚模型,利用β-cateninsiRNA(30 nmol/L)转染心肌细胞敲低β-catenin,Western-blot和免疫荧光检测抑制β-catenin对甲亢诱导乳鼠心肌细胞肥厚的影响。【结果】Wnt/β-catenin通路激活后β-catenin入核增多并于细胞核内的转录因子结合发挥转录调控作用。β-catenin在甲亢诱导的大鼠心室重构模型心肌细胞核内表达显著增加,而其经典下游转录因子TCF7l2表达无显著差异。我们的结果显示,MSAB抑制β-catenin明显改善甲亢诱导的大鼠心室重构。进一步研究表明甲亢诱导大鼠心肌肥厚过程中心肌细胞β-catenin/FoxO1表达明显增强,抑制心肌细胞β-catenin/FoxO1改善甲亢诱导大鼠心肌肥厚。【结论】甲亢性心肌肥厚心肌细胞β-catenin/FoxO1活化,抑制β-catenin/FoxO1改善甲状腺激素诱导的心肌细胞肥大。

慢性心力衰竭动物模型的研究趋势与热点可视化分析

目的 基于可视化软件和文献计量学方法,了解慢性心力衰竭(简称慢性心衰)动物模型研究情况,探索慢性心衰动物模型的研究热点,指导动物实验和科研设计。方法 检索Web of Science核心合集从2001年1月1日至2022年10月10日收录的慢性心衰动物模型相关文献,通过阅读全文得到最终纳入文献后,以VOSviewer与CiteSpace程序软件分析机构、期刊和共被引期刊、作者和共被引作者、关键词等内容。结果 共纳入961篇文献,年发文量稳中有升;美国和中国等是主要研究国家;约翰·霍普金斯大学和哈佛大学等是主要研究机构;出版和被引用次数较多的期刊为AM J PHYSIOL-HEART C和CIRCULATION等;Schultz Harold D和Sabbah Hani N是较有影响力的作者;myocardial infarction(心肌梗死)、cardiac hypertrophy(心脏肥大)和rat(大鼠)等是频数较高的关键词,生成10个聚类与18个突现词。结论 该领域研究众多、质量较高但分散。常用动物模型为鼠类和犬类;造模方法主要为手术和药物;病理机制以心肌肥厚、氧化应激和心肌纤维化为主。