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.

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.

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.

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.

Characteristics of coronary microvascular lesions in autopsied elderly with hypertensive left ventricular hypertrophy

OBJECTIVE: To observe the characteristics of coronary microvascular lesions (CML) in the autopsied elderly cases with hypertensive left ventricular hypertrophy (LVH) and the difference of CML among the groups of essential hypertension (EHT), coronary heart disease (CHD) and diabetes (NIDDM) also with LVH. METHODS: A retrospective study was performed in 206 cases > or = 60 years old of EHT, CHD and NIDDM with LVH and 30 normal cases as control, out of 3195 consecutive autopsied cases from 1954 to 1996 in our hospital. Arterioles with diameters of 10 - 60 microm and capillaries in the muscular layer were shown by the methods of HE, Elastic fiber + VG staining and immunohistochemistry of CD31. Quantitative measurements on the arteriole density (AD), the ratio of arteriolar wall and cavity (RWC), capillary density (CD) and the area of endothelial cell (AEC) were performed with light microscope observation and image analysis by computer. According to the thickness of the left ventricle free wall, the severity of LVH was divided into four degrees from 0 to III. LVH of degree 0-III was observed in EHT group, while only LVH of degree I was found in CHD, EHT + CHD, and NIDDM groups. SAS system was used for statistical analysis. RESULTS: AD and RWC increased while CD and AEC decreased significantly with the progression of LVH in EHT groups (P

Effects of Combined Therapy of Xuezhikang Capsule(血脂康胶囊)and Valsartan on Hypertensive Left Ventricular Hypertrophy and Heart Rate Turbulence

Objective：To observe the effect of combined therapy with Xuezhikang Capsule（血脂康胶囊,XZK） and Valsartan on left ventricular hypertrophy（LVH） and heart rate turbulence（HRT） in hypertensive patients. Methods：Ninety primary hypertensive patients with LVH were randomly assigned to three groups.Basic treatment,including aspirin,β-blockers,calcium antagonists,etc.were administered to all patients.Additionally, Valsartan（VS,80 mg once a day） was given to the 30 patients in the VS group.Valsartan（in the same dosage） and XZK（600 mg,twice a day） were given to the 32 patients in the Chinese medicine（CM） group,while none was given to the 28 patients in the control group.The therapeutic course lasted for 24 months.Changes in left ventricular mass index（LVMI） measured by cardiac ultrasonic indices,HRT parameters,including the original heart rate（TO） and slope coefficient（TS）,systolic and diastolic blood pressures（SBP and DBP）,as well as blood cholesterol level（TC） were measured before and after treatment.Results：After treatment,TO and LVMI were lowered,while TS increased in both the VS group and the CM group（P〈0.01）,but changed insignificantly in the control group.Significant differences between the CM group and the control group were shown in terms of TO,LVMI,SBP,DBP and TS（P〈0.01）;and between the CM group and the VS group in terms of TO,LVMI and TS（P〈0.01）.Moreover,HRT parameters showed an evident correlation with LVMI（r=0.519-0.635,P〈0.01）. Conclusion：Combined therapy with XZK and Valsartan can improve hypertensive LVH and HRT parameters, and lessen the damage on the autonomous nervous system.

Prevalence and risk factors for left ventricular hypertrophy and left ventricular geometric abnormality in the patients with hypertension among Han Chinese

Background Left ventricular hypertrophy （LVH） and geometric abnormality are associated with morbidity and mortality of cardiovascular disease and stroke. Hypertension is the major cause of LVH. Yet the prevalence and other risk factors of LVH and geometric abnormality in Chinese hypertensive population are unknown. The objective of this study was to investigate the prevalence and risk factors of LVH and geometric abnormality in community-based Chinese hypertensive population. Methods The study was a community-based cross-sectional study, and comprised 4270 hypertension patients with integrated clinical and echocardiographic data. Left ventricular mass was measured by transthoracic echocardiography. LVH was diagnosed by using the criteria of over 49.2 g/m^2.7 for men and 46.7 g/m^2.7 for women. LV geometric patterns （normal, concentric remodeling, concentric or eccentric hypertrophy） were calculated according to LVH and relative wall thickness. Logistic regression model was used to determine the odds ratio （OR） and 95% confidence intervals （CI） of the risk factors of LVH. Results The prevalence of LVH was 42.7% in 4270 hypertensive patients, with 37.4% in males and 45.4% in females, respectively. The prevalence of concentric remodeling, concentric or eccentric hypertrophy was 24.7%, 20.2%, and 22.6%, respectively. In Logistic regression model, female （OR 1.3, 95%C/ 1.1-1.5, P 〈0.01）, age （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01）, body mass index （OR 1.2, 95%C/1.15-1.20, P 〈0.01）, systolic blood pressure （OR 1.02, 95%C/ 1.01-1.03, P 〈0.01 ）, and serum triglyceride （OR 1.10, 95% CI 1.00-1.20, P 〈0.01 ） were risk factors of LVH. Female, age, body mass index, systolic blood pressure and serum triglyceride were also risk factors of left ventricular geometric abnormality. Conclusions The echocardiographic LVH is the major complication of patients with hypertension in rural area of China, especially for women. To effectively treat hypertension, weight loss and control of serum triglyceride may help to prevent LVH in hypertensive population.

Variants of tumor necrosis factor-induced protein 3 gene are associated with left ventricular hypertrophy in hypertensive patients

Background Tumor necrosis factor-induced protein 3 （TNFAIP3） gene has been shown important in cardiac remodeling. The aim of the present study was to investigate whether the variants of TNFAIP3 gene are associated with left ventricular hypertrophy （LVH） in hypertensive patients.Methods Four representatives of all the other single nucleotide polymorphisms （SNPs） in TNFAIP3 gene were tested for association with hypertrophy in two independent hypertensive populations （n=2120 and n=324）.Results We found that only the tag SNP （rs5029939） was consistently lower in the hypertensives with cardiac hypertrophy than in those without cardiac hypertrophy in the two study populations, indicating a protective effect on LVH （odds ratio （OR） （95% confidence interval （CI））0.58 （0.358-0.863）, P=0.035; OR （95% CI）=0.477 （0.225-0.815）, P〈0.05,respectively）. Multiple regression analyses confirmed that the patients with G allele of rs5029939 had less thickness in inter-ventricular septum, left ventricular posterior wall, relative wall thickness and left ventricular mass index than did those with CC allele in the hypertensive patients in both study populations （all P〈0.01）.Conclusion These findings indicate that the SNP （rs5029939） in the TNFAIP3 gene may serve as a novel protective genetic marker for the development of LVH in patients with hypertension

Molecular mechanisms and therapeutic perspectives of left ventricular hypertrophy in systemic hypertension

Background Left ventricular hypertrophy （LVH） induced by systemic hypertension represents a maladaptive response to the increased overload. However antihypertensive treatments are not always useful to regress or prevent LVH. Thoroughly understanding the mechanisms will help to find new therapeutic targets that prevent or reverse left ventricular hypertrophy. A number of regulators and molecular signaling pathways have been shown to be involved in the hypertrophic process, such as angiotensin II, heat shock proteins 90, microRNAs, TRPC, mTOR, HDAC and PI3K/Akt signaling pathways. Therefore, other treatments, such as G1 cyclin antagonists, HSP90 inhibitor, Rho-kinase inhibitor, calcineurin blockers, CS866, statins, scutellarin, and aldosterone antagonist could prevent left ventricular hypertrophy.

Renal sympathetic denervation reduces left ventricular hypertrophy and improves cardiac function in patients with resistant hypertension

This study investigated the effect of catheter-based renal sympathetic denervation （RD） on left ventricular hypertrophy （LVH） and systolic and diastolic function in patients with resistant hypertension. LVH and diastolic dysfunction are associated with elevated sympathetic activity and increased morbidity and mortality. The effect of RD on LVH and LV function is unclear