A Clinical Study of Reversing Left Ventricular Hypertrophy in Hypertensive Patients by Adalat

Fourteen outpatients (10 men, 4 women, mean age 52.6 yrs) suffered from essential hypertension complicated with left ventricular hypertrophy (LVH) detected by echocardiography were treated with Adalat 30 mg daily orally. After 3 months administration, casual high blood pressue was satisfactorily controlled. Both thickness of inter ventricular septum and left ventricular posterior wall were decreased (1.47 cm vs 1.34 cm P<0.01, 1.43 cm vs 1.32 cm P<0.01). Left ventricular mass (LVM) and left ventricular mass index (LVMI) calculated according to Devereux corrective formula were significantly reversed (279.4 g vs 247.4 g P<0.01, 162.7 g/m 2 vs 146.5 g/m 2 P<0.01). Meanwhile, cardiac performance was assessed, and the results demonstrated that Adalat could maintain left ventricular systolic function and improve left ventricular diastolic function which was resulted from regression of LVH. No side effects of Adalat were present in the study patients.

Bicuspid aortic valve with associated aortopathy, significant left ventricular hypertrophy or concomitant hypertrophic cardiomyopathy: A diagnostic and therapeutic challenge

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.

Left ventricular hypertrophy amplifies the QT,and Tp-e intervals and the Tp-e/QT ratio of left chest ECG

Objective： To evaluate the changes in Tp-e interval （an interval from the peak to the end of the T wave）, QT interval and Tp-e/QT ratio of the body surface ECG in patients with left ventricular hypertrophy （LVH）. Methods： The Tp-e interval and QT interval were measured on body surface ECGs in 42 patients without either hypertension or LVH （control group）, 41 patients having hypertension but not LVH （non-LVH group）, and 38 patients with both hypertension and LVH （LVH group）. Results： The mean corrected QT （QTc） interval, and mean corrected Tp-e[T（p-e）c] interval were significantly longer in the LVH group （0.430±0.021s vs. 0.409±0.019s, p 〈 0.01; 0.098±0.013s vs. 0.088±0.011s, respectively） than those in the control group. The Tp-e/QT ratio was also amplified in LVH group （0.232± 0.028 vs.0.218± 0.027） （p 〈 0.05）. Conclusion： LVH increased the QT interval, Tp-e interval and Tp-e/QT ratio of the body surface ECG.

Effect of Salvia Miltiorrhiza Bge on Left Ventricular Hypertrophy and the Expression of Tumor Necrosis Factor-α in Spontaneously Hypertensive Rats

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.

Effect of amlodipine combined with telmisartan or compound amiloride on plasma ET-1 concentration and left ventricular diastolic function of essential hypertension patients with left ventricular hypertrophy

Objective： To observe the effect of different combination antihypertensive therapies on plasma endothelin-1 （ET-1） concentration and left ventricular diastolic function of essential hypertension patients with left ventricular hypertrophy （LVH） Methods： A total of 111 patients with essential hypertension were selected, including 60 cases （34 males, 26 females） aged （60.7±5.6） years with simple hypertension, and 51 cases （28 males, 23 females） aged （61.8±7.0） years with essential hypertension complicated with LVH. Essential hypertension patients with LVH were randomly divided into the group of amlodipine （2.5 mg/d） combined with telmisartan （40 mg/d, n=26） and the group of amlodipine （2.5 mg/d） combined with amiloride （half tablet/d, n=25）,and the treatment lasted for 1 year. Echocardiography was performed before and after the treatment. Left ventricular mass index （LVMI）, left ventricular isovolumic relaxation time （IVRT） and other indicators were detected, and plasma ET-1 concentrations were measured for comparative analysis. And 56 patients （31 males, 25 females） aged （59.3±6.7） years with normal blood pressure in the same period in our hospital were selected as the normal control group. Results： The general clinical characteristics were similar between hypertensive LVH group, simple hypertensive group and normal healthy control group. Plasma ET-1 concentrations, LVMI and IVRT of hypertensive LVH group were significantly higher than those of normal control group and simple hypertension group, and the difference was statistically significant. The patients＇ baseline blood pressure, ET-1, LVMI, interventricular septal thickness （IVST）, left ventricular posterior wall thickness （LVPWT）, left ventricular end-diastolic diameter （LVEDd） and other clinical parameters showed no significant difference （P〉0.05） between the group of amlodipine combined with telmisartan and the group of amlodipine combined with amiloride. It was found that compared with that before treatment, blood pressure could be effectively controlled （P〈0.05）, and LVMI, IVST, LVPWT and IVRT （P〈0.05） were all lowered, and ET-1 （P〈0.01） was significantly reduced after 1 year of antihypertensive therapy in both the group of amlodipine combined with telmisartan and the group of amlodipine combined with amiloride. The group of amlodipine combined with telmisartan was better in lowering blood pressure and reducing LVMI, IVST, LVPWT, IVRT and ET-1 than the group of amlodipine combined with amiloride （P〈0.05）. Conelus｜on： Amlodipine-based combination antthypertensive therapy could reverse LVH and improve left ventricular diastolic function partly by lowering blood pressure and ET-1, and the effect of amlodipine combined with telmisartan was superior to that ofamlodipine combined with amiloride

IN PATIENTS WITH HYPERTENSIVE LEFT VENTRICULAR HYPERTROPHY AND CORONARY HEART DISEASE,CORONARY FLOW RESERVE IS SIMILARLY IMPAIRED

Coronary blood flow reserve (CFR) was assessed by transesophageal Doppler echocardiography in normal subjects (group A. n=20),hypertensive non-left ventricular hypertrophy (non-LVH)Patients (group B,n=22). hypertensive patients with LVH(group C.n=32)and coronary heart disease patients (group D. n=33) with the volume sample placed at the bifurcation of the left main and left main and left descending coronary artery. Coronary blood flow velocity (CBFV)was evaluated at rest.2 minutes after dipyridamole (0. 56mg/kg. i. v.) . and 2 minutes after aminophylline i.v. The ratio of dipyridamole to rest maximal diastolic velocity (D/R PDV) was considered the index of coronary blood flow reserve.It was found that D/R PDV was significantly less in groups C and D compared with that in groups A and B (D PDC,1.84±0. 57. 1. 57±0. 41 versus 2.59±0.70 and 2.22+0.58,respectively),with no difference in D/R PDV between groups C and D.Twenty-four out of 32 patients in group C with D/R PDV were less than 2.0 compared to 29 out of 33 patients in group D (P>0.05).Significant negative correlation was found between D/R PDV. D/R PSV and interseptal thickness. left ventricular mass index in hypertensive patients.These data show that impaired CFR in hypertensive patients with LVH is comparable to that in patients with coronary heart disease.

Mitochondria and left ventricular hypertrophy

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.……

Association Between Lipid Profiles and Left Ventricular Hypertrophy:New Evidence from a Retrospective Study

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.

Function of the CaMKII-ryanodine receptor signaling pathway in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia

BACKGROUND:Calcium calmodulin-dependent kinase II(CaMKII) can be more active in patients with left ventricular hypertrophy(LVH),which in turn causes phosphorylation of ryanodine receptors,resulting in inactivation and the instability of intracellular calcium homeostasis.The present study aimed to determine the effect of CaMKII-ryanodine receptor pathway signaling in rabbits with left ventricular hypertrophy and triggered ventricular arrhythmia.METHODS:Forty New Zealand rabbits were randomized into four groups(10 per group):sham group,LVH group,KN-93 group(LVH+KN-93),and ryanodine group(LVH+ryanodine).Rabbits in the LVH,KN-93,and ryanodine groups were used to establish a left ventricular hypertrophy model by the coarctation of the abdominal aorta,while those in the sham group did not undergo the coarctation.After eight weeks,action potentials(APs) were recorded simultaneously in the endocardium and epicardium,and a transmural electrocardiogram(ECG) was also recorded in the rabbit left ventricular wedge model.Drugs were administered to the animals in the KN-93 and ryanodine groups,and the frequency of triggered APs and ventricular tachycardia was recorded after the rabbits were given isoprenaline(1 μmol/L) and high-frequency stimulation.RESULTS:The frequency(animals/group) of triggered APs was 0/10 in the sham group,10/10 in the LVH group,4/10 in the KN-93 group,and 1/10 in the ryanodine group.The frequencies of ventricular tachycardia were 0/10,9/10,3/10,and 1/10,respectively.The frequencies of polymorphic ventricular tachycardia or ventricular fibrillation were 0/10,7/10,2/10,and 1/10,respectively.The frequencies of triggered ventricular arrhythmias in the KN-93 and ryanodine groups were much lower than those in the LVH group(P<0.05).CONCLUSIONS:KN-93 and ryanodine can effectively reduce the occurrence of triggered ventricular arrhythmia in rabbits with LVH.The CaMKII-ryanodine signaling pathway can be used as a new means of treating ventricular arrhythmia.

Left ventricular hypertrophy in relation to systolic blood pressure and the angiotensin converting enzyme I/D polymorphism in Chinese

Objective There is little population-based data on the prevalence and the environmental or genetic determinants of left ventricular hypertrophy （LVH） in China. The purpose of this paper is to study LVH in relation to systolic blood pressure and the angiotensin converting enzyme （ACE） insertion/deletion（I/D） polymorphism in Chinese. Methods We recorded 12- lead ECG （CardioSoft, v4.2） in 1365 residents in the Jingning County, Zhejiang Province, China. LVH was defined according to the gender-specific Sokolow-Lyon and Cornell product ECG criteria. Results Regardless of whether the Sokolow-Lyon or Cornell product ECG criteria was used, the prevalence of LVH （20.7% and 4.8%, respectively） significantly （P〈0.0001） increased with male gender （odds ratio [OR] 2.33 and 7.15） and systolic blood pressure （per 10 mm Hg increase, OR 1.46 and 1.33）. If the Sokolow-Lyon criteria was used, the prevalence of LVH was also influenced by alcohol intake （OR 1.44, P=-0.03） and body mass index （OR 0.83, P=0.0005）. The association between the Sokolow-Lyon voltage amplitude and the ACE I/D polymorphism was dependent on antihypertensive therapy （P=0.01）. In 1262 untreated subjects, but not 103 patients on antihypertensive medication, the ACE DD compared with II subjects had significantly higher Sokolow-Lyon voltage amplitudes （29.8：-0.6 vs. 28.0-3：0.5 mV, P=-0.02） and higher risk of LVH （OR 1.74, 95% CI： 1.12-2.69, P=-0.01）. Conclusion LVH is prevalent in Chinese, and is associated with systolic blood pressure and the ACE D allele. The genetic association might be modulated by antihypertensive therapy（J Geriatr Cardio12009; 6：131-136）.

Anemia treatment and left ventricular hypertrophy in non-dialysis chronic kidney disease

To this day, the target hemoglobin level that minimizes cardiovascular risk in chronic kidney disease (CKD) patients remains unclear. When one examines the many randomized trials of epoetin therapy in aggregate, enhanced quality of life provides the most cogent argument for hemoglobin levels above 110 g/L. It remains unclear whether treatment of anemia improves longevity, or even a surrogate marker (such as left ventricular [LV] mass index), especially when applied at earlier phases of CKD.

The Effectand Mechanism of Forsinopril on Ventricular Hypertrophy of SHR and Left Ventricular Pressure overloading Rat

The effects and mechanism of long term angiotensin converting enzyme inhibitor (ACEI) Forsinopril on left ventricular hypertrophy of spontaneous hypertension rat (SHR) and left ventricular pressure overloading rat were studied. The left ventricular index (left ventricle weight/body weight) was used to evaluate left ventricular hypertrophy and the in situ hybridization to investigate the TGF β1 gene expression in left ventricle. The results showed that Forsinopril significantly decreased the left ventricular index of both SHR and left ventricle pressure overloading rat. Forsinopril reduced the integral photic density of TGF β1 gene statement from 2.836±0.314 to 1.91±0.217 ( P <0.01, n =8 ) of SHR rat and from 3.071±0.456 to 2.376±0.379 ( P <0.01, n =8) of left ventricular pressure overloading rat respectively. It was concluded that Forsinopril could prevent the occurrence of left ventricular hypertrophy and reduce the TGF-β1 gene expression in left ventricle of both SHR and left ventricular pressure overloading rat significantly.

Correlation between IL-33/sST2 signaling pathway and patients with essential hypertensive left ventricular hypertrophy

Objective:To detect the levels of interleukin-33(IL-33)and soluble ST2(sST2)in peripheral blood of patients with essential hypertensive left ventricular hypertrophy,and to discusstheir correlation with patients with essential hypertensive left ventricular hypertrophy was further discussed.Methods:A total of 220 patients with essential hypertension treated in the Department of Cardiovascular Medicine of the First Affiliated Hospital of Bengbu Medical College were enrolled as the experimental group.According to left ventricular mass index(LVMI),patients with essential hypertension were divided into the non-left ventricular hypertrophy group(NLVH,n=108 cases)and the left ventricular hypertrophy group(LVH,n=112 cases).We used ELISA to detect the serum levels of IL-33 and sST2,the expression levels of IL-33 in peripheral blood lymphocytes of the NLVH group and the LVH group(60 cases each)were detected by Western blot,and the relationship between IL-33 and LVMI,a marker of left ventricular hypertrophic condition,was analyzed by Pearson.The relationship between IL-33,sST2 and left ventricular hypertrophy in essential hypertension was studied.Results:Compared with the NLVH group,the expression levels of IL-33 and sST2 in the LVH group were significantly increased.The results of Western blot showed that the expression level of IL-33 in the LVH group(1.07±0.08)was higher than that in the NLVH group(0.63±0.05)(P<0.05).Pearson correlation analysis showed that IL-33 was positively correlated with LVMI,sST2 was positively correlated with LVMI.Conclusion:The levels of IL-33 and sST2 in serum and the expression levels of IL-33 protein in peripheral blood lymphocytes are significantly increased in patients with hypertensive left ventricular hypertrophy,and the occurrence and development of essential hypertensive left ventricular hypertrophy may be related to IL-33 and sST2.

Ultrasonic evaluation of the relationship between left ventricular hypertrophy or left ventricular geometry and endothelial function in patients with essential hypertension

Objective： To assess the relationship between left ventricular hypertrophy （LVH） or left ventricular geometry （LVG） and endothelial function in patients with essential hypertension （EH）. Methods： Seventy-six patients and 30 normal subjects were first examined by echocardiography. Brachial artery dilatation induced by reactive hyperemia （DIRH） or nitroglycerin （DING） was detected using high-resolution ultrasonography. Results： DIRH was lower in patients with hypertension than in the controls, and the decrease in DIRH was greater in the patients with LVH than that in patients without LVH （4.36±2.54% vs 8.56 ± 1.87 %; P 〈 0.0001）. There were no significant differences in age, serum concentrations of total cholesterol, triglycerides or sugar, blood pressure and the brachial artery dilatation induced by nitroglycerin between the two groups （P 〉 0.05）. While there was no significant difference in DIRH between the patients with normal left ventricular geometry or cardiac remodeling, the patients showing either eccentric or concentric left ventricular hypertrophy had lower DIRH than the patients with normal left ventricular geometry or cardiac remodeling. The DIRH was the lowest in patients with concentric hypertrophy. Although bivariate analysis showed that the left ventricular mass index （LVMI） correlated well with the brachial artery dilatation induced by reactive hyperemia, diastolic blood pressure and mean blood pressure （r=-0.61, P 〈 0.0001; r=0.27, P 〈 0.05; r=0.31, P 〈 0.05, respectively）, a multivariate stepwise regression demonstrated that LVMI correlated only with the brachial artery dilatation induced by reactive hyperemia. Conclusion： Left ventricular hypertrophy was related to endothelial dysfunction in essential hypertension. The endothelial dysfunction might be basic and important in the progression of left ventricular hypertrophy.

Effects and mechanism of different adrenergic receptor antagonists on left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats

Objective: To study the changes of a collagen-binding protein (Colligin) and myosin heavy chain isoform (α/β-MHC) gene and protein in left ventricular hypertrophy subsequent to coarctation of abdominal aorta in rats and the effects of three kinds of adrenergic receptor blockers: Carvedilol (CAR) , Metoprolol (MET) and Terazosin (TER) on these changes, and to elucidate the effects and new mechanism of CAR on left ventricular hypertrophy regression. Methods: A model of hypertrophy induced by coarctation of abdominal aorta(CAA)was used in this study. Thirty two male wistar rats were divided randomly into four groups 4 weeks after CAA operation: CAA, CAR, MET and TER. Hemodynamics, ventricular remodeling parameters, expressions of Colligin and α/β-MHC mRNA, protein expressions of Collagen Ⅰ / Ⅲ and Colligin were investigated in the four groups and sham operation group. Results: Left ventricle hypertrophy was observed clearly 16 weeks after operation. The ratio of α/β-MHC mRNA decreased, while expressions of Collagen Ⅰ /Ⅲ proteins and Colligin mRNA/protein increased( P < 0.05). CAR could ameliorate left ventricle hypertrophy prior to MET and TER. CAR could also change the expressions of α/β-MHC, Collagen Ⅰ /Ⅲ and Colligin in both gene and protein levels ( P < 0.05), while MET and TER have no effect on them ( P > 0.05). Conclusion: The effects of CAR on extracellular matrix proteins and MHC isoform shift regression of left ventricle may be due to antiproliferative or antioxidative mechanism, which was independent of beta-adrenergic receptor antagonist.

Genetic Association Study of KCNB1 Gene with the Susceptibility of Hypertension Related LVH （Left Ventricular Hypertrophy） Patients in Malaysia

LVH （Left ventricular hypertrophy） is an independent risk factor for the development of heart failure, cardiac arrhythmias and stroke. A recent genome-wide association study reported the involvement of a candidate gene namely KCNBI in mechanism for development of LVH in hypertension. This study aimed to replicate the finding by investigating the genetic association of KCNBI gene among the hypertensive LVH patients from Malaysia. We genotyped a SNP （single nucleotide polymorphism） located in KCNBI namely, rs6063397 among 200 subjects consisting of61 LVH and 139 non LVH patients using Sanger sequencing method. Statistical analysis revealed no significant association between the L VH susceptibility between the allele and genotype frequencies （P = 0.2719 and 0.4768, respectively）. This finding suggests that KCNBI may not playa role in LVH susceptibility in hypertensive patients in Southeast Asian populations.

Left ventricular regional and global diastolic function assessed using Quantitative Tissue velocity Imaging in patients with hypertrophic cardiomyopathy

Objectives The study was performed to assess the left ventricular (LV) regional and global diastolic function、left ventricular wall motion features in patients with Hypertrophic cardiomyopathy by Quantitative Tissue Velocity Imaging (QTVI). Methods 42 patients with hypertrophic cardiomyopathy and 36 age-matched normal subjects underwent QTVI study. Off-line LV regional muscular tissue velocity Imaging along LV apical long-axis view were obtained. Regional diastolic function was assessed in using peak tissue velocities of LV regional muscular tissue during early diastole (Ve)and LA contraction (Va), Ve/Va ratio, derived from Tissue Velocity Imaging. Global diastolic function was reflected by isovolumic relaxation time(IRT) and mitral valve peak flow velocity ( E/A ) calculated with pulsed wave doppler. The end-diastolic interventricular septal thickness (ⅣSt) was measured by conventional 2 - dimension echocardiography. Results ① Ve、 Va、 Ve/Va in the segments of hypertrophic interventricular septum (IVS) reduced wlhile E/A ratio significantly reduced and IRT markedly prolonged in HCM patients than in normal subjects。 ② Ve、 Ve/Va were significant reduced in the segments of hypertrophic interventricular septum compared with other LV segments in HCM patients . ③ There was a correlation between Ve/Va and E/A in HCM patients with abnormal E/A ratio (r = 0. 70). ④ There was a negative correlation between Ve/Va and ⅣSt in non -obstruction HCM patients (B group , r = -0.61 ) Conclusions QTVI offers a newer method in clinical practice which has a higher sensibility and accuracy in evaluating the LV regional and global diastolic function in HCM patients .

Losartan reduced connexin43 expression in left ventricular myocardium of spontaneously hypertensive rats

Objective:To assess the effect of angiotensin II type 1(AT1)receptor antagonist losartan on myocardium con- nexin43(Cx43)gap junction(GJ)expression in spontaneously hypertensive rats(SHRs)and investigate possible mechanisms. Methods:Sixteen 9-week-old male SHRs and 8 age-matched male Wistar-Kyoto(WKY)rats were included in this study.SHRs were randomly divided into two groups to receive losartan at 30 mg/(kg·d)by oral gavage once daily for 8 weeks(SHR-L)or vehicle(0.9%saline)to act as controls(SHR-V);WKY rats receiving vehicle for 8 weeks served as normotensive controls.At the end of the experiment,rats were sacrificed and the hearts were removed.Expressions of Cx43 and nuclear factor-kappaB p65 (NF-κB p65)proteins in all three groups were observed and further investigations on the effect of angiotensin II type 1 receptor antagonist losartan(30 mg/(kg·d),8 weeks)on Cx43 expression were conducted with Western blot and immunohistochemistry. NF-κB p65 protein in nuclear extracts was determined by Western blot.Results:Left ventricular(LV)hypertrophy was prominent in SHRs,Cx43 and NF-κB p65 protein expressions were obviously upregulated and Cx43 distribution was dispersed over the cell surface.Treatment with losarton reduced the over-expressions of Cx43 and NF-κB p65 in LV myocardium.The distribution of Cx43 gap junction also became much regular and confined to intercalated disk after losartan treatment.Conclu- sion:Cx43 level was upregulated in LV myocardium of SHR during early stage of hypertrophy.Angiotensin II type 1 receptor antagonist losartan prevented Cx43 gap junction remodeling in hypertrophied left ventricles,possibly through the NF-κB pathway.

Validity of electrocardiographic criteria for increased left ventricular mass in young patients in the general population

AIMTo investigate validity of electrocardiographic(ECG)criteria for left ventricular hypertrophy(LVH)in young adults.METHODS Retrospectively,echocardiograms showing LVH and concomitant electrocardiograms were collected in patients 18 to 39 years old.A control group of patients without LVH was collected.Using echocardiogram as the gold standard,electrocardiograms were analyzed using common voltage criteria.RESULTS Study included 100 subjects(52%male,mean age=28±6.8 years,96%Hispanic or African-American)with 50%LVH prevalence.Sensitivity and specificity for SokolowLyon criteria were 24%(95%CI:13.5%-38.4%)and 88%(95%CI:74.9%-95%).For Cornell criteria,sensitivity was 32%(95%CI:19.9%-46.8%)and specificity 98%(95%CI:87.9%-99.8%).For R in a VL criteria,sensitivity was 12%(95%CI:4.9%-25%)and specificity 100%(95%CI:91.1%-100%).CONCLUSION In young adults common ECG voltage criteria have low sensitivities and high specificities similar to other age groups.Low sensitivities preclude these ECG criteria from serving as effective screening tests.

Effect of early correction of anemia with erythropoietin on left ventricular mass in predialysis patients:a multi-center trial

Objective To assess the effects of early correction of anemia with recombinant human erythropoietin(rHuEPO)on the development and progression of left ventricular hypertrophy(LVH)in patients with mild-to-moderate chronic renal insufficiency(CRI)who are not on hemodialysis.Methods A total of 158 patients with serum creatinine from 147μmol/L to 400μmol/L were nrolled in this prospective,multicenter study.Eighty-six patients with hemoglobin(Hb)<110g/L received rHuEPO treatment with a target Hb of≥110g/L(Group A).Forty patients with comparable Hb concentration(<110g/L)but did not receive rHuEPO(Group B)and 32 patients with Hb≥110g/L and without rHuEPO treatment(Group C)were served as controls.Left ventricular mass index(LVMI)was evaluated by echocardiography at baseline and every 3 months for 2 years.Results There was no difference in age,gender,etiology of renal failure,blood pressure and cardiovascular risk factors among the 3 groups.At baseline,the prevalence of LVH was 72.1%in group A,72.5%in group B and 59.4%in group C.LVMI was inversely correlated with Hb levels(r=0.70,P<0.01).During the 2-year period,the mean LVMI decreased from 142.6±25.7g/m^(2)to 132.4±18.5 g/m^(2)in group A,while increased significantly in both group B and group C.The mean Hb concentration increased from 93.8±14.6g/L to 111.2±10.3g/L(P<0.05)in group A,but tended to decrease in group B and group C.There was no significant change of the mean blood pressure,number of anti-hypertensive drugs and serum creatinine concentrations in all 3 groups.However,patients'serum creatinine doubled more often in group B and group C than in group A.Conclusions LVH was common in predialysis CRI patients and was associated with the severity of anemia.Early intervention with rHuEPO may reverse LVH in these patients.