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 int...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.展开更多
OBJECTIVE To determine the role of ascending aorta dilatation in the relationship between pulse pressure(PP)and left ventricular(LV)hypertrophy.METHODS A total of 1556 Chinese elderly hypertensive patients were retros...OBJECTIVE To determine the role of ascending aorta dilatation in the relationship between pulse pressure(PP)and left ventricular(LV)hypertrophy.METHODS A total of 1556 Chinese elderly hypertensive patients were retrospectively studied.Transthoracic echocardiography was used to obtain the aortic and cardiac structure measurements.In addition,brachial blood pressure was measured,and total arterial compliance,systemic vascular resistance,arterial elastance,and end-systolic LV elastance were calculated.The participants were divided into four groups according to the status of ascending aortic diameter and PP.RESULTS LV mass index increased in succession in the four groups,i.e.,the group with the normal aorta and lower PP,with the normal aorta and higher PP,with aortic dilatation and lower PP,and with aortic dilatation and higher PP(Ptrend<0.001).Total arterial compliance−1,arterial elastance,and end-systolic LV elastance were slightly higher in the individuals with normal aorta compared to those with aortic dilatation,regardless of PP being lower or higher(P<0.01).Compared to the group with the normal aorta and lower PP,individuals with aortic dilatation had a significantly increased multivariable adjusted risk of LV hypertrophy,and higher PP further exacerbated this risk[aortic dilatation with lower PP(OR=1.75,95%CI:1.01–3.04)and aortic dilatation with higher PP(OR=3.42,95%CI:2.03–5.77)].In the relation between PP and LV mass index(β=0.095,P<0.001),-41.3%of the total effect was attributable to mediation by ascending aortic diameter(P<0.0001).CONCLUSIONS In Chinese elderly patients with hypertension,ascending aorta dilatation could reduce the influence of elevated PP on LV hypertrophy.展开更多
Due to its prevalence of 0.5%to 2%in the general population,with a 75%predominance among men,bicuspid aortic valve is the most common congenital heart defect.It is frequently accompanied by other cardiac congenital an...Due to its prevalence of 0.5%to 2%in the general population,with a 75%predominance among men,bicuspid aortic valve is the most common congenital heart defect.It is frequently accompanied by other cardiac congenital anomalies,and clinical presentation can vary significantly,with stenosis being the most common manifestation,often resulting in mild to moderate concentric hypertrophy of the left ventricle.Echocardiography is the primary diagnostic modality utilized for establishing the diagnosis,and it is often the sole diagnostic tool relied upon by clinicians.However,due to the heterogeneous clinical presentation and possible associated anomalies(which are often overlooked in clinical practice),it is necessary to employ various diagnostic methods and persist in finding the accurate diagnosis if multiple inconsistencies exist.By employing this approach,we can effectively manage these patients and provide them with appropriate treatment.Through a clinical case from our practice,we provide an overview of the literature on bicuspid aortic valve with aortophaty and the possible association with hypertrophic cardiomyopathy,diagnostic methods,and treatment options.This review article highlights the critical significance of achieving an accurate diagnosis in patients with bicuspid aortic valve and significant left ventricular hypertrophy.It is crucial to exclude other possible causes of left ventricular outflow tract obstruction,such as sub-or supra-aortic obstructions,and hypertrophic cardiomyopathy.展开更多
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 isopren...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.展开更多
During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteoc...During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization,but its effects in CKD are unknown.We tested the hypothesis that DMP1 supplementation in CKD would improve bone health,prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes.We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3^-/- mouse model of CKD.Col4a3^-/- mice demonstrated impaired kidney function,reduced bone DMP1 expression,reduced bone mass,altered osteocyte morphology and connectivity,increased osteocyte apoptosis,increased serum FGF23,hyperphosphatemia,left ventricular hypertrophy (LVH),and reduced survival.Genetic or pharmacological supplementation of DMP1 in Col4a3^-/- mice prevented osteocyte apoptosis,preserved osteocyte networks,corrected bone mass,partially lowered FGF23 levels by attenuating NFAT-induced FGF23 transcription,and further increased serum phosphate.Despite impaired kidney function and worsened hyperphosphatemia,DMP1 prevented development of LVH and improved Col4a3^-/- survival.Our data suggest that CKD reduces DMP1 expression,whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD.展开更多
Objective: Clinical symptoms of otitis media with effusion are rarely brought forward to the guardians of young children who the disease is most prevalent in. This often leads to poor scholastic performances and diffi...Objective: Clinical symptoms of otitis media with effusion are rarely brought forward to the guardians of young children who the disease is most prevalent in. This often leads to poor scholastic performances and difficult social interactions. The objective of this study was to identify asymptomatic cases of otitis media with effusion present in individuals with adenoid hypertrophy. Material and Methods: In a cross sectional study advocated in Justice K.S.Hegde Hospital, Karnataka India we evaluated one hundred patients above the age of three from August 2016 to December 2017. Candidates who presented with an adenoid nasopharyngeal ratio of more than 0.5 were selected for the study. Individuals who complained of otological symptoms were not considered for the study. Patients cleared of other pathological otological conditions were underwent audiological evaluation with pure tone audiometry and tympanometry for evaluating the middle ear status and hearing loss. Results: The study showed a total of 36% of patients evaluated presented with asymptomatic otitis media with effusion. In candidates who presented with a bilateral B tympanogram, 40% had significant conductive hearing loss of more than 25dB. Conclusion: An objective test such as impedance audiometry in all patients with adenoid hypertrophy would aid in the diagnosis of fluid in the middle ear, so that timely intervention can be done and possible complications be averted.展开更多
OBJECTIVE Right ventricular(RV)remodeling is one of the essential pathological features in pulmonary arterial hypertension(PAH).RV hypertrophy or fibrosis are the leading causes of RV remodeling.Magnolol is a compound...OBJECTIVE Right ventricular(RV)remodeling is one of the essential pathological features in pulmonary arterial hypertension(PAH).RV hypertrophy or fibrosis are the leading causes of RV remodeling.Magnolol is a compound isolated from Magnolia officinalis.It possesses multiple pharmacological activities,such as anti-oxidation and anti-inflammation.This study aims to evaluate the effects and underlying mechanisms of magnolol on RV remodeling in hypoxia-induced PAH.METHODS①Male SD rats(220 g)were randomly divided into 5 groups(n=10):the normoxia group,the hypoxia group,the hypoxia plus Magnolol(10 and 20 mg·kg^(-1)·d-1)group,and the vehicle group.Rats in the normoxia group were kept in a normoxia environment for 4 weeks,while rats in the hypoxia group were kept in a hypoxic chamber(10%O2).The rats in the hypoxia plus magnolol groups were administered with magnolol at 10 or 20 mg·kg^(-1)(ip)once a day for 4 weeks.At the end of 4 weeks,the heart function was assessed by Doppler echocardiography,and then the rats were anesthetized with sodium pentobarbital(30 mg·kg^(-1),ip).The RVSP was measured by the right heart catheterization method.The heart tissues were collected and dissected to calculate the index of RV remodeling(RV/LV+IVS,RV/tibial length,or RV/body weight).Part of the RV samples was fixed with 4%paraformaldehyde for morphological analysis,while other samples were frozen at-80℃for molecular studies(measurements of ANP,BNP,α-SMA,and collagenⅠ/ⅢmRNA expression as well as p-JAK2/JAK2 and p-STAT3/STAT3 protein levels).②To evaluate the effect of magnolol on hypoxia-induced myocardial hypertrophy and fibrosis,H9c2 or cardiac fibroblasts were divided into 7 groups:the control group,cells were cultured under normal conditions;the hypoxia group,cells were cultured under hypoxic condition(3%O2);the hypoxia plus magnolol 10 mg·kg^(-1) group,magnolol10μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus magnolol 30 mg·kg^(-1) group,magnolol 20μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus TG-101348 group,TG-101348(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus JSI-124 group,JSI-124(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;and the hypoxia plus vehicle group,an equal volume of vehicle(DMSO)was added to the culture medium before the hypoxia treatment.At the end of the experiments,the cells were collected for morphological and molecular analysis.RESULTS In vivo,male Sprang-Daley rats were exposed to 10%O2 for 4 weeks to establish an RV remodeling model,which showed hypertrophic and fibrotic features(increases of RV remodeling index,cellular size,hypertrophic and fibrotic marker expression),accompanied by an elevation in phosphorylation levels of JAK2 and STAT3;these changes were attenuated by treating rats with magnolol.In vitro,the cultured H9c2 cells or cardiac fibroblasts were exposed to 3%O2 for 48 h to induce hypertrophy or fibrosis,which showed hypertrophic(increases in cellular size as well as the expression of ANP and BNP)or fibrotic features(increases in the expression of collagenⅠ,collagenⅢandα-SMA).Administration of magnolol and TG-101348 or JSI-124 (JAK2 selective inhibitors) could prevent the process of myocardial hypertrophy and fibrosis, accompanied by the decrease in the phosphorylation level of JAK2 and STAT3. CONCLUSION Magnolol can attenuate RV hypertrophy and fibrosis in hypoxia-induced PAH rats through a mechanism involving inhibition of the JAK2/STAT3 signaling pathway.展开更多
The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechan...The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechanism were investigated. Normal Wistar-kyoto (WKY) rats were used as negative control, and spontaneously hypertensive rats (SHR) were randomly assigned to receive pla- cebo or SMB. SMB (1 g/kg·d) was injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction (CVF), perivascular circumferential area (PVCA), and tumor necrosis factor-α (TNF-α) expression in the left ventricular tissue. The results showed, as compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression were increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI (P<0.01), size of cardiomyocytes (P<0.01), collagen volume fraction (P<0.01), perivascular circum- ferential area (P<0.01), and TNF-α expression (P<0.01), but had no effect on SBP (P>0.05). It was suggested that chronic administration of SMB could inhibit and reverse the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mecha- nism of LVH by SMB.展开更多
BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing l...BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing liver segments.This study aimed to determine the effects of transcatheter arterial embolization(TAE)on tumor volume and liver regeneration in a rabbit VX2 tumor model.METHODS:Twenty-three rabbits underwent subcapsular tumor implantation with a VX2 tumor.Two weeks after implantation,18 rabbits were used for TAE experiments,5were for sham controls.Tumor response and liver regeneration response of the embolized cranial and non-embolized caudal liver lobes were assessed by CT volumetry,liver to body weight index,and the amount of proliferating hepatocytes.RESULTS:All super-selective arterial tumor embolization procedures were performed successfully.Despite embolization,the tumor volume increased after an initial steady state.The tumor volume after embolization was smaller than that of the sham group,but this difference was not significant.Massive necrosis of the tumor,however,was seen after embolization,without damage of the surrounding liver parenchyma.There was a significant atrophy response of the tumor bearing cranial lobe after super-selective arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized,caudal lobe.This regeneration response was confirmed histologically by a significantly higher number of proliferating hepatocytes on the Ki-67 stained slides.CONCLUSIONS:Super-selective,bland arterial coil embolization causes massive necrosis of the tumor,despite increase of volume on CT scan.Atrophy of the tumor bearing liver lobe is seen after arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized lobe,despite absence of histological damage of the tumor-surrounding liver parenchyma.展开更多
Liver resection(LR) with negative margins confers survival advantage in many patients with hepatic malignancies.However,an adequate future liver remnant(FLR) is imperative for safe LR.Presently,in patients with an ina...Liver resection(LR) with negative margins confers survival advantage in many patients with hepatic malignancies.However,an adequate future liver remnant(FLR) is imperative for safe LR.Presently,in patients with an inadequate FLR; the 2 most established clinical techniques performed to induce liver hypertrophy are portal vein embolization(PVE) and portal vein ligation.More recently,it has been observed that patients who undergo treatment via Y90 radioembolization experience hypertrophy of the contra-lateral untreated liver lobe.Based on these observations,several investigators have proposed the potential use of this modality as an alternative technique for increasing the FLR prior to liver resection.Y90 radioembolization induces hypertrophy at a slower rate than PVE but has the added advantage of concomitant local disease control and tumour downstaging.展开更多
BACKGROUND Left ventricular hypertrophy(LVH) is a common manifestation of cardiovascular disease and a risk factor for cardiovascular morbidity and mortality, but available methods for its electrocardiographic(ECG) di...BACKGROUND Left ventricular hypertrophy(LVH) is a common manifestation of cardiovascular disease and a risk factor for cardiovascular morbidity and mortality, but available methods for its electrocardiographic(ECG) diagnosis have limited accuracy.AIM To investigate findings associated with LVH on ECG and developed an improved system for the diagnosis of LVH.METHODS A cohort study comparing ECG data acquired within 30 days of transthoracic echocardiography(TTE) was performed. Multivariate regression analysis identified ECG findings associated with increased LV mass and mass index. A scoring system was derived and performance compared to established criteria for LVH.RESULTS Data from 5486 outpatients with TTEs and corresponding ECGs were included in the derivation cohort, 333(6.1%) of whom had LVH by TTE. In the primary regression analysis, findings associated with LVH were amplitudes of Q in V3, R in V6, S in V3, T in V6, P' in V1, P in V6, as well as R and T-axis discordance, R peak time in V6, QRS duration, weight, height, sex, and age. From this we derived a score consisting of 5 criteria, and validated it in an independent cohort of 910 patients. With a threshold of 1.5 points, sensitivity and specificity were67.9% and 81.4%, and 62.5% and 83.2% in the derivation and validation cohorts,respectively. With a threshold of 2 points, sensitivity and specificity were 42.3% and 93.0%, and 37.5% and 93.4% in these cohorts.CONCLUSIONS This score had superior sensitivity for detection of LVH by ECG while making a modest sacrifice in specificity compared to conventional criteria.展开更多
Objective:To investigate the effects of Xinjikang on the left ventricular hypertrophy remodeling and myocardial activity in hypertension.Methods:Sixty Wistar rats were randomly divided into four groups.The pressure-lo...Objective:To investigate the effects of Xinjikang on the left ventricular hypertrophy remodeling and myocardial activity in hypertension.Methods:Sixty Wistar rats were randomly divided into four groups.The pressure-loaded left ventricular hypertrophy model was established with abdominal aorta ligation method.Rats in A and B groups were intragastrically administered with physiological saline,while C and D groups were administered with Xinjikang and metoprolol,respectively.The changes in blood pressure.E/A ratio,myocardial pathological morphology,myocardial lipoperoxides and superoxide dismustase activity in four groups were observed and compared before and after treatment.Results:There were statistically significant differences in E/A ratio between C group after treatment and model group(P<0.05).while no difference was observed between A and D groups(P>0.05);after treatment the myocardial lipoperoxides and superoxide dismustase contents in C and D groups were improved significantly compared with model group(P<0.05).Conclusions:Xinjikang can improve myocardial injury,restore myocardial parenchyma and myocardial interstitial remodeling functions in hypertensive rats with the left ventricular hypertrophy.展开更多
Myostatin, a member of the transforming growth factor beta(TGF-β) superfamily, is a dominant inhibitor that acts to limit skeletal muscle growth and development. In this study, we generated transgenic mice that expre...Myostatin, a member of the transforming growth factor beta(TGF-β) superfamily, is a dominant inhibitor that acts to limit skeletal muscle growth and development. In this study, we generated transgenic mice that express porcine myostatin containg mutations at its cleavage site(RSRR) to evaluate its effect on muscle mass. Results showed that the weight of four skeletal muscles including gastrocnemius, rectus femoris, tibialis anterior, and pectoralis increased by 17.83 and 28.39%, 21.76 and 28.70%, 34.31 and 41.62%, 53.21 and 27.54% in transgenic male and female mice, respectively, compared to their corresponding non-transgenic control mice. Measurement of muscle fiber size and number indicated that the mean myofiber size increased by 50.73 and 61.30% in transgenic male and female mice respectively compared to the non-transgenic controls. However, there was no difference in the number of myofiber between transgenic and non-transgenic male mice. These results clearly demonstrated that the increase in skeletal muscle mass in transgenic mice is caused by hypertrophy instead of hyperplasia.展开更多
Introduction
Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension.It contributes a lot to high mortality of essential hypertension due to sudden cardiac death,ventr... Introduction
Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension.It contributes a lot to high mortality of essential hypertension due to sudden cardiac death,ventricular arrhythmia and heart failure.Many factors involve in the pathogenesis of hypertension-induced LVH including inherited variants as well as environmental factors.……展开更多
Background: Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumf...Background: Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumferential shortening (MWCS). Depressed MWCS is an adverse prognostic indicator, but whether this finding reflects reduced global or regional LV myocardial function, as assessed by three-dimensional (3D) myocardial strain, is unknown. Methods and Results: Cardiac Magnetic Resonance (CMR) tissue tagging permits direct evaluation of regional 3D intramyocardial strain, independent of LV geometry. We evaluated 21 hypertensive patients with electrocardiographic LVH in the LIFE study and 8 normal controls using 3D MR tagging and echocardiography. Patients had higher MR LV mass than normals (116 ± 40 versus 63 ± 6 g/m2, P = 0.002). Neither echocardiographic fractional shortening (32 ± 6 versus 33% ± 3%), LVEF (63% versus 64%) or mean end-systolic stress (175 ± 27 versus 146 ± 28 g/cm2) were significantly different, yet global MWCS was decreased by both echocardiography (13.4 ± 2.8 versus 18.2% ± 1.5%, P P P = 0.002) in LVH and greater in lateral and anterior regions versus septal and posterior regions ( P P P 0.60, P = 0.001 for both). Conclusions: In patients with hypertensive LVH, despite normal LV function via echocardiography or CMR, CMR intramyocardial tagging show depressed global MWCS while 3D MR strain revealed marked underlying regional heterogeneity of LV dysfunction.展开更多
Objective To explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population.Methods We conducted a retrospective observational study to investigate the relationship bet...Objective To explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population.Methods We conducted a retrospective observational study to investigate the relationship between lipid markers[including triglycerides,total cholesterol,low-density lipoprotein cholesterol,high-density lipoprotein(HDL)cholesterol,non-HDL-cholesterol,apolipoprotein A-I,apolipoprotein B,lipoprotein[a],and composite lipid profiles]and left ventricular hypertrophy.A total of 309,400 participants of two populations(one from Beijing and another from nationwide)who underwent physical examinations at different health management centers between 2009 and 2018 in China were included in the cross-sectional study.7,475 participants who had multiple physical examinations and initially did not have left ventricular hypertrophy constituted a longitudinal cohort to analyze the association between lipid markers and the new-onset of left ventricular hypertrophy.Left ventricular hypertrophy was measured by echocardiography and defined as an end-diastolic thickness of the mterventricular septum or left ventricle posterior wall>11 mm.The Logistic regression model was used in the cross-sectional study.Cox model and Cox model with restricted cubic splines were used in the longitudinal cohort.Results In the cross-sectional study for participants in the highest tertile of each lipid marker compared to the respective lowest,triglycerides[odds ratio(OR):1.2S0,95%CI:1.060 to 1.474],HDL-cholesterol(OR:0.780,95%CI:0.662 to 0.918),and lipoprotein(a)(OR:1.311,95%C7:1.115 to 1.541)had an association with left ventricular hypertrophy.In the longitudinal cohort,for participants in the highest tertile of each lipid marker at the baseline compared to the respective lowest,triglycerides[hazard ratio(HR):3.277,95%C/:1.720 to 6.244],HDL-cholesterol(HR:0.516,95%C7:0.283 to 0.940),non-HDL-cholesterol(HR:2.309,95%C/:1.296 to 4.112),apolipoprotein B(HR:2.244,95%CI:1.251 to 4.032)showed an association with new-onset left ventricular hypertrophy.In the Cox model with forward stepwise selection,triglycerides were the only lipid markers entered into the final model.Conclusion Lipids levels,especially triglycerides,are associated with left ventricular hypertrophy.Controlling triglycerides level potentiate to be a strategy in harnessing cardiac remodeling but deserve to be furdier investigated.展开更多
Objective:Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading,but continuous cardiac hypertrophy can lead to cardiac remodeling and heart failure.Cardiac hypertrophy is mostly consider...Objective:Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading,but continuous cardiac hypertrophy can lead to cardiac remodeling and heart failure.Cardiac hypertrophy is mostly considered reversible,and recent studies have indicated that decorin not only prevents cardiac fibrosis associated with hypertension,but also achieves therapeutic effects by blocking fibrosis-related signaling pathways.However,the mechanism of action of decorin remains unknown and unconfirmed.Methods:We determined the degree of myocardial hypertrophy by measuring the ratios of the heart weight/body weight and left ventricular weight/body weight,histological analysis and immunohistochemistry.Western blotting was performed to detect the expression levels of CaMKⅡ,p-CaMKⅡ and MEF-2 in the heart.Results:Our results confirmed that decorin can regulate the CaMKⅡ/MEF-2 signaling pathway,with inhibition thereof being similar to that of decorin in reducing cardiac hypertrophy.Conclusion:Taken together,the results of the present study showed that decorin induced cardiac hypertrophy by regulating the CaMKⅡ/MEF-2 signaling pathway in vivo,revealing a new therapeutic approach for the prevention of cardiac hypertrophy.展开更多
Background : Hypertension and dyslipidemia are considered reversible risk factors for cardiovascular disease. The purpose of this study was to explore the impact of traditional and nontraditional blood lipid profiles ...Background : Hypertension and dyslipidemia are considered reversible risk factors for cardiovascular disease. The purpose of this study was to explore the impact of traditional and nontraditional blood lipid profiles on the risk of left ventricular hypertrophy(LVH) and to explore the superposition effect of dyslipidemia combined with hypertension.Methods : Data on 9134 participants(53.5 ±10.3 years old) from the Northeast China Rural Cardiovascular Health Study(NCRCHS) were statistically analyzed. The blood lipid profile was measured by total cholesterol(TC), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol(HDL-C), total glyceride(TG), and calculated nontraditional blood lipid indices including non-HDL-C, atherosclerosis index(AI), TC/HDL-C, and residual cholesterol(RC).Results : After the adjustment of age and gender, the odds ratios(ORs) of LVH in patients with hypertension, high LDL-C, high non-HDL-C, high AI, and high TC/HDL-C were 3.97(3.31– 4.76), 1.27(1.02– 1.59), 1.21(1.04– 1.39), 1.33(1.15– 1.53), and 1.42(1.22– 1.65), respectively. After full adjustment of potential confounding factors, high AI and TC/HDL-C were associated with LVH rather than traditional blood lipid indices.The combination of hypertension and nontraditional dyslipidemia(defined by high AI and TC/HDL-C) was associated with the highest risk of LVH, especially in participants under 45 years of age. The risk was more significant in men, 5.09-fold and 6.24-fold,respectively, compared with 3.66-fold and 4.01-fold in women.Conclusions : People with dyslipidemia defined by nontraditional blood lipid indices(high AI and high TC/HDL-C) and hypertension were more likely to develop LVH.展开更多
Free fatty acids(FFAs)play important roles in cardiovascular disease.Studies have shown that it is an important way for FAs to exert biological effects through their own receptors besides directly participating bioche...Free fatty acids(FFAs)play important roles in cardiovascular disease.Studies have shown that it is an important way for FAs to exert biological effects through their own receptors besides directly participating biochemical reaction in body.Free fatty acid receptor 2(FFA2)can be activated by short-chain FAs and is involved in inflammatory reactions and lipid accumulation.Since the known pathological changes caused by FFA2 are also implicated in cardiac hypertrophy,we hypothesized that FFA2 might be pathogenic in cardiac hypertrophy.This paper showed that FFA2 expression significantly increased in cardiac hypertrophy in vivo and in vitro.FFA2 agonist 4-CMTB or TUG-1375 promoted the expression of the hypertrophy markers ANF and BNP and increased cell surface area in vitro,which was further strengthened by FFA2 overexpression,suggesting that FFA2 might contribute to cardiomyocyte hypertrophy.Furthermore,4-CMTB treatment or FFA2 overexpression combined with 4-CMTB treatment elevated the phosphorylation and transcriptional activity of GATA4 and STAT3,which were inhibited by an ERK1/2 inhibitor,and GATA4 and STAT3 knockdown inhibited the elevation of hypertrophy biomarkers in cardiomyocytes treated with 4-CMTB.Taken together,these data indicate that FFA2 can enhance cardiomyocyte hypertrophy by activating STAT3 and GATA4 via ERK1/2,providing a potential new target for therapy.展开更多
Proline contents of parotid glands (PG) in pigs constantly increase after the inclusion of different amounts of ripe hulled acorns in the diet providing high polyphenols levels. The dose-response relationship was esti...Proline contents of parotid glands (PG) in pigs constantly increase after the inclusion of different amounts of ripe hulled acorns in the diet providing high polyphenols levels. The dose-response relationship was estimated on natural hydrolizable tannins (expressed as tannic acid equivalent TAE) amounts of 25.8 to 36.1 g TAE/kg DM in experimental diets. Macroscopic and histological morphometry of parotid glands greatly varied according to feed intake and dosages of TAE ingested. The PG response (hypertrophy grade) on acorns’ tannins content in the diet was positively correlated (R2 = 0.748): the response to the protein precipitating activity (PPA) of tannins consisted of a functional parotidomegaly (hypertrophy), 1.34 up to 3.55 folds than control PGs, following an oral dosage 0.596 up 1.72 TAE g·kg body weight·d-1 respectively, after one week exposure.展开更多
文摘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.
基金the National Key Research and Development Program of China(No.2018 YFC2000301)。
文摘OBJECTIVE To determine the role of ascending aorta dilatation in the relationship between pulse pressure(PP)and left ventricular(LV)hypertrophy.METHODS A total of 1556 Chinese elderly hypertensive patients were retrospectively studied.Transthoracic echocardiography was used to obtain the aortic and cardiac structure measurements.In addition,brachial blood pressure was measured,and total arterial compliance,systemic vascular resistance,arterial elastance,and end-systolic LV elastance were calculated.The participants were divided into four groups according to the status of ascending aortic diameter and PP.RESULTS LV mass index increased in succession in the four groups,i.e.,the group with the normal aorta and lower PP,with the normal aorta and higher PP,with aortic dilatation and lower PP,and with aortic dilatation and higher PP(Ptrend<0.001).Total arterial compliance−1,arterial elastance,and end-systolic LV elastance were slightly higher in the individuals with normal aorta compared to those with aortic dilatation,regardless of PP being lower or higher(P<0.01).Compared to the group with the normal aorta and lower PP,individuals with aortic dilatation had a significantly increased multivariable adjusted risk of LV hypertrophy,and higher PP further exacerbated this risk[aortic dilatation with lower PP(OR=1.75,95%CI:1.01–3.04)and aortic dilatation with higher PP(OR=3.42,95%CI:2.03–5.77)].In the relation between PP and LV mass index(β=0.095,P<0.001),-41.3%of the total effect was attributable to mediation by ascending aortic diameter(P<0.0001).CONCLUSIONS In Chinese elderly patients with hypertension,ascending aorta dilatation could reduce the influence of elevated PP on LV hypertrophy.
文摘Due to its prevalence of 0.5%to 2%in the general population,with a 75%predominance among men,bicuspid aortic valve is the most common congenital heart defect.It is frequently accompanied by other cardiac congenital anomalies,and clinical presentation can vary significantly,with stenosis being the most common manifestation,often resulting in mild to moderate concentric hypertrophy of the left ventricle.Echocardiography is the primary diagnostic modality utilized for establishing the diagnosis,and it is often the sole diagnostic tool relied upon by clinicians.However,due to the heterogeneous clinical presentation and possible associated anomalies(which are often overlooked in clinical practice),it is necessary to employ various diagnostic methods and persist in finding the accurate diagnosis if multiple inconsistencies exist.By employing this approach,we can effectively manage these patients and provide them with appropriate treatment.Through a clinical case from our practice,we provide an overview of the literature on bicuspid aortic valve with aortophaty and the possible association with hypertrophic cardiomyopathy,diagnostic methods,and treatment options.This review article highlights the critical significance of achieving an accurate diagnosis in patients with bicuspid aortic valve and significant left ventricular hypertrophy.It is crucial to exclude other possible causes of left ventricular outflow tract obstruction,such as sub-or supra-aortic obstructions,and hypertrophic cardiomyopathy.
基金supported by National Natural Science Foundation of China(81070655)
文摘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.
基金supported by grants to A.M.(R01DK101730),V.D.(R01DK102815,R01DK114158),and M.W.(R01DK076116)from National Institute of Health
文摘During chronic kidney disease (CKD),alterations in bone and mineral metabolism include increased production of the hormone fibroblast growth factor 23 (FGF23) that may contribute to cardiovascular mortality.The osteocyte protein dentin matrix protein 1 (DMP1) reduces FGF23 and enhances bone mineralization,but its effects in CKD are unknown.We tested the hypothesis that DMP1 supplementation in CKD would improve bone health,prevent FGF23 elevations and minimize consequent adverse cardiovascular outcomes.We investigated DMP1 regulation and effects in wild-type (WT) mice and the Col4a3^-/- mouse model of CKD.Col4a3^-/- mice demonstrated impaired kidney function,reduced bone DMP1 expression,reduced bone mass,altered osteocyte morphology and connectivity,increased osteocyte apoptosis,increased serum FGF23,hyperphosphatemia,left ventricular hypertrophy (LVH),and reduced survival.Genetic or pharmacological supplementation of DMP1 in Col4a3^-/- mice prevented osteocyte apoptosis,preserved osteocyte networks,corrected bone mass,partially lowered FGF23 levels by attenuating NFAT-induced FGF23 transcription,and further increased serum phosphate.Despite impaired kidney function and worsened hyperphosphatemia,DMP1 prevented development of LVH and improved Col4a3^-/- survival.Our data suggest that CKD reduces DMP1 expression,whereas its restoration represents a potential therapeutic approach to lower FGF23 and improve bone and cardiac health in CKD.
文摘Objective: Clinical symptoms of otitis media with effusion are rarely brought forward to the guardians of young children who the disease is most prevalent in. This often leads to poor scholastic performances and difficult social interactions. The objective of this study was to identify asymptomatic cases of otitis media with effusion present in individuals with adenoid hypertrophy. Material and Methods: In a cross sectional study advocated in Justice K.S.Hegde Hospital, Karnataka India we evaluated one hundred patients above the age of three from August 2016 to December 2017. Candidates who presented with an adenoid nasopharyngeal ratio of more than 0.5 were selected for the study. Individuals who complained of otological symptoms were not considered for the study. Patients cleared of other pathological otological conditions were underwent audiological evaluation with pure tone audiometry and tympanometry for evaluating the middle ear status and hearing loss. Results: The study showed a total of 36% of patients evaluated presented with asymptomatic otitis media with effusion. In candidates who presented with a bilateral B tympanogram, 40% had significant conductive hearing loss of more than 25dB. Conclusion: An objective test such as impedance audiometry in all patients with adenoid hypertrophy would aid in the diagnosis of fluid in the middle ear, so that timely intervention can be done and possible complications be averted.
文摘OBJECTIVE Right ventricular(RV)remodeling is one of the essential pathological features in pulmonary arterial hypertension(PAH).RV hypertrophy or fibrosis are the leading causes of RV remodeling.Magnolol is a compound isolated from Magnolia officinalis.It possesses multiple pharmacological activities,such as anti-oxidation and anti-inflammation.This study aims to evaluate the effects and underlying mechanisms of magnolol on RV remodeling in hypoxia-induced PAH.METHODS①Male SD rats(220 g)were randomly divided into 5 groups(n=10):the normoxia group,the hypoxia group,the hypoxia plus Magnolol(10 and 20 mg·kg^(-1)·d-1)group,and the vehicle group.Rats in the normoxia group were kept in a normoxia environment for 4 weeks,while rats in the hypoxia group were kept in a hypoxic chamber(10%O2).The rats in the hypoxia plus magnolol groups were administered with magnolol at 10 or 20 mg·kg^(-1)(ip)once a day for 4 weeks.At the end of 4 weeks,the heart function was assessed by Doppler echocardiography,and then the rats were anesthetized with sodium pentobarbital(30 mg·kg^(-1),ip).The RVSP was measured by the right heart catheterization method.The heart tissues were collected and dissected to calculate the index of RV remodeling(RV/LV+IVS,RV/tibial length,or RV/body weight).Part of the RV samples was fixed with 4%paraformaldehyde for morphological analysis,while other samples were frozen at-80℃for molecular studies(measurements of ANP,BNP,α-SMA,and collagenⅠ/ⅢmRNA expression as well as p-JAK2/JAK2 and p-STAT3/STAT3 protein levels).②To evaluate the effect of magnolol on hypoxia-induced myocardial hypertrophy and fibrosis,H9c2 or cardiac fibroblasts were divided into 7 groups:the control group,cells were cultured under normal conditions;the hypoxia group,cells were cultured under hypoxic condition(3%O2);the hypoxia plus magnolol 10 mg·kg^(-1) group,magnolol10μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus magnolol 30 mg·kg^(-1) group,magnolol 20μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus TG-101348 group,TG-101348(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;the hypoxia plus JSI-124 group,JSI-124(a specific inhibitor of JAK2)1μmol·L^(-1) was added to the culture medium before the hypoxia treatment;and the hypoxia plus vehicle group,an equal volume of vehicle(DMSO)was added to the culture medium before the hypoxia treatment.At the end of the experiments,the cells were collected for morphological and molecular analysis.RESULTS In vivo,male Sprang-Daley rats were exposed to 10%O2 for 4 weeks to establish an RV remodeling model,which showed hypertrophic and fibrotic features(increases of RV remodeling index,cellular size,hypertrophic and fibrotic marker expression),accompanied by an elevation in phosphorylation levels of JAK2 and STAT3;these changes were attenuated by treating rats with magnolol.In vitro,the cultured H9c2 cells or cardiac fibroblasts were exposed to 3%O2 for 48 h to induce hypertrophy or fibrosis,which showed hypertrophic(increases in cellular size as well as the expression of ANP and BNP)or fibrotic features(increases in the expression of collagenⅠ,collagenⅢandα-SMA).Administration of magnolol and TG-101348 or JSI-124 (JAK2 selective inhibitors) could prevent the process of myocardial hypertrophy and fibrosis, accompanied by the decrease in the phosphorylation level of JAK2 and STAT3. CONCLUSION Magnolol can attenuate RV hypertrophy and fibrosis in hypoxia-induced PAH rats through a mechanism involving inhibition of the JAK2/STAT3 signaling pathway.
文摘The effects of salvia miltiorrhiza Bge (SMB) on left ventricular hypertrophy (LVH) and the expression of tumor necrosis factor-α (TNF-α) in the left ventricle of spontaneously hypertensive rats and the action mechanism were investigated. Normal Wistar-kyoto (WKY) rats were used as negative control, and spontaneously hypertensive rats (SHR) were randomly assigned to receive pla- cebo or SMB. SMB (1 g/kg·d) was injected intraperitoneally for 12 weeks. Systolic blood pressure (SBP) and left ventricular mass index (LVMI) were measured. HE, VG and immunohistochemical staining combined with computed morphometry were employed to evaluate the cardiomyocyte size, diameter, the collagen volume fraction (CVF), perivascular circumferential area (PVCA), and tumor necrosis factor-α (TNF-α) expression in the left ventricular tissue. The results showed, as compared with WKY rats, the SBP, LVMI, cardiomyocyte size, diameter, CVF, PCVA, and TNF-α expression were increased markedly in the 20-week-old spontaneously hypertensive rats. SMB decreased LVMI (P<0.01), size of cardiomyocytes (P<0.01), collagen volume fraction (P<0.01), perivascular circum- ferential area (P<0.01), and TNF-α expression (P<0.01), but had no effect on SBP (P>0.05). It was suggested that chronic administration of SMB could inhibit and reverse the development of LVH in spontaneously hypertensive rats independent of BP. TNF-α may be involved in the reversal mecha- nism of LVH by SMB.
文摘BACKGROUND:Portal vein embolization not only induces hypertrophy of the non-embolized liver,but also enhances tumor growth.The latter could be prevented by embolizing the hepatic arteries supplying the tumor-bearing liver segments.This study aimed to determine the effects of transcatheter arterial embolization(TAE)on tumor volume and liver regeneration in a rabbit VX2 tumor model.METHODS:Twenty-three rabbits underwent subcapsular tumor implantation with a VX2 tumor.Two weeks after implantation,18 rabbits were used for TAE experiments,5were for sham controls.Tumor response and liver regeneration response of the embolized cranial and non-embolized caudal liver lobes were assessed by CT volumetry,liver to body weight index,and the amount of proliferating hepatocytes.RESULTS:All super-selective arterial tumor embolization procedures were performed successfully.Despite embolization,the tumor volume increased after an initial steady state.The tumor volume after embolization was smaller than that of the sham group,but this difference was not significant.Massive necrosis of the tumor,however,was seen after embolization,without damage of the surrounding liver parenchyma.There was a significant atrophy response of the tumor bearing cranial lobe after super-selective arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized,caudal lobe.This regeneration response was confirmed histologically by a significantly higher number of proliferating hepatocytes on the Ki-67 stained slides.CONCLUSIONS:Super-selective,bland arterial coil embolization causes massive necrosis of the tumor,despite increase of volume on CT scan.Atrophy of the tumor bearing liver lobe is seen after arterial embolization of the tumor with a concomitant hypertrophy response of the non-embolized lobe,despite absence of histological damage of the tumor-surrounding liver parenchyma.
文摘Liver resection(LR) with negative margins confers survival advantage in many patients with hepatic malignancies.However,an adequate future liver remnant(FLR) is imperative for safe LR.Presently,in patients with an inadequate FLR; the 2 most established clinical techniques performed to induce liver hypertrophy are portal vein embolization(PVE) and portal vein ligation.More recently,it has been observed that patients who undergo treatment via Y90 radioembolization experience hypertrophy of the contra-lateral untreated liver lobe.Based on these observations,several investigators have proposed the potential use of this modality as an alternative technique for increasing the FLR prior to liver resection.Y90 radioembolization induces hypertrophy at a slower rate than PVE but has the added advantage of concomitant local disease control and tumour downstaging.
文摘BACKGROUND Left ventricular hypertrophy(LVH) is a common manifestation of cardiovascular disease and a risk factor for cardiovascular morbidity and mortality, but available methods for its electrocardiographic(ECG) diagnosis have limited accuracy.AIM To investigate findings associated with LVH on ECG and developed an improved system for the diagnosis of LVH.METHODS A cohort study comparing ECG data acquired within 30 days of transthoracic echocardiography(TTE) was performed. Multivariate regression analysis identified ECG findings associated with increased LV mass and mass index. A scoring system was derived and performance compared to established criteria for LVH.RESULTS Data from 5486 outpatients with TTEs and corresponding ECGs were included in the derivation cohort, 333(6.1%) of whom had LVH by TTE. In the primary regression analysis, findings associated with LVH were amplitudes of Q in V3, R in V6, S in V3, T in V6, P' in V1, P in V6, as well as R and T-axis discordance, R peak time in V6, QRS duration, weight, height, sex, and age. From this we derived a score consisting of 5 criteria, and validated it in an independent cohort of 910 patients. With a threshold of 1.5 points, sensitivity and specificity were67.9% and 81.4%, and 62.5% and 83.2% in the derivation and validation cohorts,respectively. With a threshold of 2 points, sensitivity and specificity were 42.3% and 93.0%, and 37.5% and 93.4% in these cohorts.CONCLUSIONS This score had superior sensitivity for detection of LVH by ECG while making a modest sacrifice in specificity compared to conventional criteria.
文摘Objective:To investigate the effects of Xinjikang on the left ventricular hypertrophy remodeling and myocardial activity in hypertension.Methods:Sixty Wistar rats were randomly divided into four groups.The pressure-loaded left ventricular hypertrophy model was established with abdominal aorta ligation method.Rats in A and B groups were intragastrically administered with physiological saline,while C and D groups were administered with Xinjikang and metoprolol,respectively.The changes in blood pressure.E/A ratio,myocardial pathological morphology,myocardial lipoperoxides and superoxide dismustase activity in four groups were observed and compared before and after treatment.Results:There were statistically significant differences in E/A ratio between C group after treatment and model group(P<0.05).while no difference was observed between A and D groups(P>0.05);after treatment the myocardial lipoperoxides and superoxide dismustase contents in C and D groups were improved significantly compared with model group(P<0.05).Conclusions:Xinjikang can improve myocardial injury,restore myocardial parenchyma and myocardial interstitial remodeling functions in hypertensive rats with the left ventricular hypertrophy.
基金supported by the National Natural Science Foundation of China(30901022)the Agricultural Science and Technology Innovation Program,China(ASTIPIAS05)the National Basic Research Program of China(2015CB943100)
文摘Myostatin, a member of the transforming growth factor beta(TGF-β) superfamily, is a dominant inhibitor that acts to limit skeletal muscle growth and development. In this study, we generated transgenic mice that express porcine myostatin containg mutations at its cleavage site(RSRR) to evaluate its effect on muscle mass. Results showed that the weight of four skeletal muscles including gastrocnemius, rectus femoris, tibialis anterior, and pectoralis increased by 17.83 and 28.39%, 21.76 and 28.70%, 34.31 and 41.62%, 53.21 and 27.54% in transgenic male and female mice, respectively, compared to their corresponding non-transgenic control mice. Measurement of muscle fiber size and number indicated that the mean myofiber size increased by 50.73 and 61.30% in transgenic male and female mice respectively compared to the non-transgenic controls. However, there was no difference in the number of myofiber between transgenic and non-transgenic male mice. These results clearly demonstrated that the increase in skeletal muscle mass in transgenic mice is caused by hypertrophy instead of hyperplasia.
文摘 Introduction
Left ventricular hypertrophy (LVH) is one of the vicious organ damages of essential hypertension.It contributes a lot to high mortality of essential hypertension due to sudden cardiac death,ventricular arrhythmia and heart failure.Many factors involve in the pathogenesis of hypertension-induced LVH including inherited variants as well as environmental factors.……
文摘Background: Increased relative wall thickness in hypertensive left ventricular hypertrophy (LVH) has been shown by echocardiography to allow preserved shortening at the endocardium despite depressed LV midwall circumferential shortening (MWCS). Depressed MWCS is an adverse prognostic indicator, but whether this finding reflects reduced global or regional LV myocardial function, as assessed by three-dimensional (3D) myocardial strain, is unknown. Methods and Results: Cardiac Magnetic Resonance (CMR) tissue tagging permits direct evaluation of regional 3D intramyocardial strain, independent of LV geometry. We evaluated 21 hypertensive patients with electrocardiographic LVH in the LIFE study and 8 normal controls using 3D MR tagging and echocardiography. Patients had higher MR LV mass than normals (116 ± 40 versus 63 ± 6 g/m2, P = 0.002). Neither echocardiographic fractional shortening (32 ± 6 versus 33% ± 3%), LVEF (63% versus 64%) or mean end-systolic stress (175 ± 27 versus 146 ± 28 g/cm2) were significantly different, yet global MWCS was decreased by both echocardiography (13.4 ± 2.8 versus 18.2% ± 1.5%, P P P = 0.002) in LVH and greater in lateral and anterior regions versus septal and posterior regions ( P P P 0.60, P = 0.001 for both). Conclusions: In patients with hypertensive LVH, despite normal LV function via echocardiography or CMR, CMR intramyocardial tagging show depressed global MWCS while 3D MR strain revealed marked underlying regional heterogeneity of LV dysfunction.
基金supported by grants from the National Nature Science Foundation of China(82000386,81970364f 82000299,81870171,82170436).
文摘Objective To explore the association between lipid profiles and left ventricular hypertrophy in a Chinese general population.Methods We conducted a retrospective observational study to investigate the relationship between lipid markers[including triglycerides,total cholesterol,low-density lipoprotein cholesterol,high-density lipoprotein(HDL)cholesterol,non-HDL-cholesterol,apolipoprotein A-I,apolipoprotein B,lipoprotein[a],and composite lipid profiles]and left ventricular hypertrophy.A total of 309,400 participants of two populations(one from Beijing and another from nationwide)who underwent physical examinations at different health management centers between 2009 and 2018 in China were included in the cross-sectional study.7,475 participants who had multiple physical examinations and initially did not have left ventricular hypertrophy constituted a longitudinal cohort to analyze the association between lipid markers and the new-onset of left ventricular hypertrophy.Left ventricular hypertrophy was measured by echocardiography and defined as an end-diastolic thickness of the mterventricular septum or left ventricle posterior wall>11 mm.The Logistic regression model was used in the cross-sectional study.Cox model and Cox model with restricted cubic splines were used in the longitudinal cohort.Results In the cross-sectional study for participants in the highest tertile of each lipid marker compared to the respective lowest,triglycerides[odds ratio(OR):1.2S0,95%CI:1.060 to 1.474],HDL-cholesterol(OR:0.780,95%CI:0.662 to 0.918),and lipoprotein(a)(OR:1.311,95%C7:1.115 to 1.541)had an association with left ventricular hypertrophy.In the longitudinal cohort,for participants in the highest tertile of each lipid marker at the baseline compared to the respective lowest,triglycerides[hazard ratio(HR):3.277,95%C/:1.720 to 6.244],HDL-cholesterol(HR:0.516,95%C7:0.283 to 0.940),non-HDL-cholesterol(HR:2.309,95%C/:1.296 to 4.112),apolipoprotein B(HR:2.244,95%CI:1.251 to 4.032)showed an association with new-onset left ventricular hypertrophy.In the Cox model with forward stepwise selection,triglycerides were the only lipid markers entered into the final model.Conclusion Lipids levels,especially triglycerides,are associated with left ventricular hypertrophy.Controlling triglycerides level potentiate to be a strategy in harnessing cardiac remodeling but deserve to be furdier investigated.
文摘Objective:Cardiac hypertrophy is an adaptive reaction of the heart against cardiac overloading,but continuous cardiac hypertrophy can lead to cardiac remodeling and heart failure.Cardiac hypertrophy is mostly considered reversible,and recent studies have indicated that decorin not only prevents cardiac fibrosis associated with hypertension,but also achieves therapeutic effects by blocking fibrosis-related signaling pathways.However,the mechanism of action of decorin remains unknown and unconfirmed.Methods:We determined the degree of myocardial hypertrophy by measuring the ratios of the heart weight/body weight and left ventricular weight/body weight,histological analysis and immunohistochemistry.Western blotting was performed to detect the expression levels of CaMKⅡ,p-CaMKⅡ and MEF-2 in the heart.Results:Our results confirmed that decorin can regulate the CaMKⅡ/MEF-2 signaling pathway,with inhibition thereof being similar to that of decorin in reducing cardiac hypertrophy.Conclusion:Taken together,the results of the present study showed that decorin induced cardiac hypertrophy by regulating the CaMKⅡ/MEF-2 signaling pathway in vivo,revealing a new therapeutic approach for the prevention of cardiac hypertrophy.
文摘Background : Hypertension and dyslipidemia are considered reversible risk factors for cardiovascular disease. The purpose of this study was to explore the impact of traditional and nontraditional blood lipid profiles on the risk of left ventricular hypertrophy(LVH) and to explore the superposition effect of dyslipidemia combined with hypertension.Methods : Data on 9134 participants(53.5 ±10.3 years old) from the Northeast China Rural Cardiovascular Health Study(NCRCHS) were statistically analyzed. The blood lipid profile was measured by total cholesterol(TC), low-density lipoprotein cholesterol(LDL-C), high-density lipoprotein cholesterol(HDL-C), total glyceride(TG), and calculated nontraditional blood lipid indices including non-HDL-C, atherosclerosis index(AI), TC/HDL-C, and residual cholesterol(RC).Results : After the adjustment of age and gender, the odds ratios(ORs) of LVH in patients with hypertension, high LDL-C, high non-HDL-C, high AI, and high TC/HDL-C were 3.97(3.31– 4.76), 1.27(1.02– 1.59), 1.21(1.04– 1.39), 1.33(1.15– 1.53), and 1.42(1.22– 1.65), respectively. After full adjustment of potential confounding factors, high AI and TC/HDL-C were associated with LVH rather than traditional blood lipid indices.The combination of hypertension and nontraditional dyslipidemia(defined by high AI and TC/HDL-C) was associated with the highest risk of LVH, especially in participants under 45 years of age. The risk was more significant in men, 5.09-fold and 6.24-fold,respectively, compared with 3.66-fold and 4.01-fold in women.Conclusions : People with dyslipidemia defined by nontraditional blood lipid indices(high AI and high TC/HDL-C) and hypertension were more likely to develop LVH.
基金supported by the National Natural Science Foundation of China(No.81760058,81560059,81660042,31800891)the Scientific Research Project of Health and Family Planning Commission of Hunan Province(No.C2017025)+1 种基金the Project of Medical and Health Science and Technology of Shaoxing City(No.2020A13063)the Startup Fund for Research of Shaoxing University(No.20205021)。
文摘Free fatty acids(FFAs)play important roles in cardiovascular disease.Studies have shown that it is an important way for FAs to exert biological effects through their own receptors besides directly participating biochemical reaction in body.Free fatty acid receptor 2(FFA2)can be activated by short-chain FAs and is involved in inflammatory reactions and lipid accumulation.Since the known pathological changes caused by FFA2 are also implicated in cardiac hypertrophy,we hypothesized that FFA2 might be pathogenic in cardiac hypertrophy.This paper showed that FFA2 expression significantly increased in cardiac hypertrophy in vivo and in vitro.FFA2 agonist 4-CMTB or TUG-1375 promoted the expression of the hypertrophy markers ANF and BNP and increased cell surface area in vitro,which was further strengthened by FFA2 overexpression,suggesting that FFA2 might contribute to cardiomyocyte hypertrophy.Furthermore,4-CMTB treatment or FFA2 overexpression combined with 4-CMTB treatment elevated the phosphorylation and transcriptional activity of GATA4 and STAT3,which were inhibited by an ERK1/2 inhibitor,and GATA4 and STAT3 knockdown inhibited the elevation of hypertrophy biomarkers in cardiomyocytes treated with 4-CMTB.Taken together,these data indicate that FFA2 can enhance cardiomyocyte hypertrophy by activating STAT3 and GATA4 via ERK1/2,providing a potential new target for therapy.
文摘Proline contents of parotid glands (PG) in pigs constantly increase after the inclusion of different amounts of ripe hulled acorns in the diet providing high polyphenols levels. The dose-response relationship was estimated on natural hydrolizable tannins (expressed as tannic acid equivalent TAE) amounts of 25.8 to 36.1 g TAE/kg DM in experimental diets. Macroscopic and histological morphometry of parotid glands greatly varied according to feed intake and dosages of TAE ingested. The PG response (hypertrophy grade) on acorns’ tannins content in the diet was positively correlated (R2 = 0.748): the response to the protein precipitating activity (PPA) of tannins consisted of a functional parotidomegaly (hypertrophy), 1.34 up to 3.55 folds than control PGs, following an oral dosage 0.596 up 1.72 TAE g·kg body weight·d-1 respectively, after one week exposure.
