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.

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.

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.

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 .

Left Ventricle Geometry Remolding after Heart Transplantation:A Two-dimensional Ultrasound Study

The function of the transplanted heart will be affected by acute allograft rejection, chronic rejection, high blood pressure and so on, which may induce the reconstruction of the left ventricle and the increase of left ventricular mass （LVM）, and eventually lead to left ventricular hypertrophy that will significantly affect the prognosis of heart transplantation （HT）. The purpose of this study was to dy- namically monitor the changes of left ventricular geometric patterns after HT using two-dimensional echocardiography and to understand the remodeling process and its possible influencing factors. The left ventricular internal diameter, interventricular septal wall thickness, posterior wall thickness at end dias- tole were measured and the relative wall thickness （RWT）, left ventricular mass, left ventricular mass index were calculated respectively in 34 HT patients and 34 healthy volunteers by two-dimensional echocardiography. The type of left ventricular geometry was identified based on the echocardiographic determination of LVM index （LVMI） and RWT. The HT patients were divided into three groups ac- cording to the time length after surgery： A （3 months postoperatively）, B （6 months postoperatively） and C （12 months postoperatively）. We compared the parameters of left ventricle between HT group and normal control group, and explored the risk factors causing the increase of LVM. The results showed that 4 patients （16%） in group A had concentric remodeling. Nine patients （34.62%） in group B had re- construction, including 5 cases of concentric remodeling, 2 cases of concentric hypertrophy and 2 cases of eccentric hypertrophy. The hypertrophy incidence rate was 15.4% in group B. 15 patients （62.5%） had reconstruction in group C, including 9 cases of concentric remodeling, 5 cases of concentric hyper- trophy, and 1 case of eccentric hypertrophy. The prevalence of hypertrophy was 25%. Multivariate analysis showed that hypertension and acute rejection history were the risk factors that resulted in left ventricular hypertrophy. It is concluded that the left ventricular remodeling occurs following cardiac transplantation at an early stage and the incidence of left ventricular hypertrophy increases with survival time. In this study, the one-year prevalence of left ventricular hypertrophy was 25% after surgery. Hy- pertension and acute rejection history are risk factors that can predict the left ventricular hypertrophy.

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

Enzyme replacement therapy in two patients with classic Fabry disease from the same family tree:Two case reports

BACKGROUND The pathophysiology of Fabry disease(FD)-induced progressive vital organ damage is irreversible.Disease progression can be delayed using enzyme replacement therapy(ERT).In patients with classic FD,sporadic accumulation of globotriaosylceramide(GL-3)in the heart and kidney begins in utero;however,until childhood,GL-3 accumulation is mild and reversible and can be restored by ERT.The current consensus is that ERT initiation during early childhood is paramount.Nonetheless,complete recovery of organs in patients with advanced FD is challenging.CASE SUMMARY Two related male patients,an uncle(patient 1)and nephew(patient 2),presented with classic FD.Both patients were treated by us.Patient 1 was in his 50s,and ERT was initiated following end-organ damage;this was subsequently ineffective.He developed cerebral infarction and died of sudden cardiac arrest.Patient 2 was in his mid-30s,and ERT was initiated when the patient was diagnosed with FD,during which the damage to vital organs was not overtly apparent.Although he had left ventricular hypertrophy at the beginning of this treatment,the degree of hypertrophy progression was limited to a minimal range after>18 years of ERT.CONCLUSION We obtained discouraging ERT outcomes for older patients but encouraging outcomes for younger adults with classic FD.

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.

EFFECT OF PERINDOPRIL AND METOPROLOL ON LEFT VENTRICULAR HYPERTROPHY AND PERFORMANCE IN ESSENTIAL HYPERTENSION

The effects of perindopril and metoprolol on left ventricular hypertrophy (LVH) and function were studied in 47 essential hypertensive patients with LVH. Previous antihypertensive drugs were discontinued for at least 2 weeks, after which patients were randomly divided into 2 groups. 25 subjects were treated with perindopril 4 to 8 mg once daily in the morning (Group A) and 22 subjects with metoprolol 25 to 62.5 mg twice daily (Group B). The subjects were evaluated before and after 4 and 8 weeks of treatment by use of echocardiography. Before treatment LV mass indexes (LVMI) of two groups were respectively 143.2 ± 21.3 g / m2 and 140.6 ± 23.7 g / m2 (P>0.05). In Group A, reduction of LVMI occurred after 4 weeks of treatment, and more pronounced after 8 weeks (from 143.2 ± 21.3 g / m2 to 126.6 ± 15.3 g / m2, P< 0.001), whereas reduction of LVMI occurred only after 8 weeks in Group B (from 140.6 ± 23.7 g / m2 to 133.4 ± 13.2 g / m2, P< 0.001). In addition, there was a significant (P<0.05) difference in LVMI between the two groups after 8 weeks. LV systolic function remained unchanged, whereas E / A increased significantly (P< 0.001) in two groups after 8 weeks. In conclusion, antihypertensive treatment with perindopril and metoprolol induced a significant regression of LVH associated with improvement in LV diastolic performance. Perindopril, compared with metoprolol, was more effective in reversing LVH.