scholarly journals HuoXue QianYang QuTan Recipe attenuates left ventricular hypertrophy in obese hypertensive rats by improving mitochondrial function through SIRT1/PGC-1α deacetylation pathway

2019 ◽  
Vol 39 (12) ◽  
Author(s):  
Jing Wang ◽  
Zhen-Hua Dong ◽  
Ming-Tai Gui ◽  
Lei Yao ◽  
Jian-Hua Li ◽  
...  
Keyword(s):  
Body Weight ◽  
Left Ventricular Hypertrophy ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Ventricular Hypertrophy ◽  
Vital Role ◽  
Left Ventricular ◽  
Therapeutic Effects ◽  
Glycolipid Metabolism ◽  
Obesity Hypertension

Abstract Mitochondrial dysfunction plays a vital role in the progression of left ventricular hypertrophy (LVH). Previous studies have confirmed that the disorder of SIRT1/PGC-1α deacetylation pathway aggravated mitochondrial dysfunction. HuoXue QianYang QuTan Recipe (HQQR) is a commonly used prescription that has shown therapeutic effects on obesity hypertension and its complications. However, the potential mechanisms are still unclear. In the present study, obesity hypertension (OBH) was established in rats and we investigated the efficacy and mechanisms of HQQR on LVH. Rats were divided into the five groups: (1) WKY-ND group, (2) SHR-ND group, (3) OBH-HF group, (4) OBH-HF/V group and (5) OBH-HF/H group. We evaluated body weight, Lee index and blood pressure (BP) before and every 2 weeks after treatment. After 10 weeks of treatment, we mainly detected glycolipid metabolic index, the severity of LVH, mitochondrial function along with SIRT1/PGC-1α deacetylation pathway. Our results showed that HQQR significantly lowered body weight, Lee index, BP and improved the disorder of glycolipid metabolism in OBH rats. Importantly, we uncovered HQQR could alleviate mitochondrial dysfunction in OBH rats by regulating SIRT1/PGC-1α deacetylation pathway. These changes could be associated with the inhibition of LVH.

scholarly journals A randomized controlled trial of metformin on left ventricular hypertrophy in patients with coronary artery disease without diabetes: the MET-REMODEL trial

2019 ◽  
Vol 40 (41) ◽  
pp. 3409-3417 ◽  
Author(s):  
Mohapradeep Mohan ◽  
Shaween Al-Talabany ◽  
Angela McKinnie ◽  
Ify R Mordi ◽  
Jagdeep S S Singh ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Coronary Artery Disease ◽  
Body Weight ◽  
Coronary Artery ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Haemoglobin A1c ◽  
Metformin Treatment ◽  
Artery Disease

Abstract Aim We tested the hypothesis that metformin may regress left ventricular hypertrophy (LVH) in patients who have coronary artery disease (CAD), with insulin resistance (IR) and/or pre-diabetes. Methods and results We randomly assigned 68 patients (mean age 65 ± 8 years) without diabetes who have CAD with IR and/or pre-diabetes to receive either metformin XL (2000 mg daily dose) or placebo for 12 months. Primary endpoint was change in left ventricular mass indexed to height1.7 (LVMI), assessed by magnetic resonance imaging. In the modified intention-to-treat analysis (n = 63), metformin treatment significantly reduced LVMI compared with placebo group (absolute mean difference −1.37 (95% confidence interval: −2.63 to −0.12, P = 0.033). Metformin also significantly reduced other secondary study endpoints such as: LVM (P = 0.032), body weight (P = 0.001), subcutaneous adipose tissue (P = 0.024), office systolic blood pressure (BP, P = 0.022) and concentration of thiobarbituric acid reactive substances, a biomarker for oxidative stress (P = 0.04). The glycated haemoglobin A1C concentration and fasting IR index did not differ between study groups at the end of the study. Conclusion Metformin treatment significantly reduced LVMI, LVM, office systolic BP, body weight, and oxidative stress. Although LVH is a good surrogate marker of cardiovascular (CV) outcome, conclusive evidence for the cardio-protective role of metformin is required from large CV outcomes trials.

A novel therapeutic approach for reversal of left ventricular hypertrophy and blood pressure control in hypertensive patients treated with alpha-methyldopa or propranolol

1985 ◽  
Vol 63 (4) ◽  
pp. 304-308
Author(s):  
P. G. Fernandez ◽  
W. Snedden ◽  
B. K. Kim ◽  
C. C. Lee
Keyword(s):  
Blood Pressure ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Antihypertensive Drugs ◽  
Left Ventricular ◽  
Stepwise Discriminant Analysis ◽  
Therapeutic Effects ◽  
Long Term Effects ◽  
Hypertensive Patients ◽  
Blood Pressures

A recently added goal in the control of primary hypertension is the reversal of left ventricular hypertrophy which may occur early in the disease and which can have serious consequences. We have attempted to define the hemodynamic parameters which distinguish most sensitively between the long-term effects of two antihypertensive drugs, alpha-methyldopa and propranolol, with a view to determining the optimal conditions under which each of the drugs may be used therapeutically. Twenty matched hypertensive patients, all with established left ventricular hypertrophy, were divided at random into two groups who received either alpha-methyldopa or propranolol as monotherapy. Dosage was titrated until blood pressures were normalized (diastolic blood pressure (DBP) ≤ 95 mmHg) (1 mmHg = 133.322 Pa); then therapy was maintained for 48–52 weeks. Supine and erect blood pressures, heart rates, and eight echocardiographic indices were recorded before commencement of therapy and at the 48- to 52-week period. Stepwise discriminant analysis identified erect DBP, erect heart rate, and posterior wall thickness of the left ventricle as being the parameters which distinguished most clearly the therapeutic effects of the chosen drugs. Using these three parameters, all 20 patients were correctly classified into their respective drug groups. We propose that these results may form the basis of a more rational choice of antihypertensive therapy with alpha-methyldopa or propranolol for hypertensive patients based on the initial determination of these three parameters.

scholarly journals Pathogenetic features of hypertension treatment in patients with concomitant abdominal obesity and underweight

2014 ◽  
Vol 18 (2 (70)) ◽  
Author(s):  
V. K. Tashchuk ◽  
V. I. Denysiuk ◽  
H. I. Hrebtii
Keyword(s):  
Body Weight ◽  
Left Ventricular Hypertrophy ◽  
Endothelial Function ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Lipid Lowering ◽  
Vascular Endothelial ◽  
Hypertension Treatment ◽  
Vascular Endothelial Function ◽  
Atorvastatin Therapy

The study analyzed the performance of the structural remodeling of the myocardium and vascular endothelial function in patients with hypertension and varying body weight during the 3- and 6-month antihypertensive (lisinopril, amlodipine) and lipid-lowering (atorvastatin) therapy. Results of the study show that the smallest speaker regression of left ventricular hypertrophy and improvement of endothelial function of the vessels is determined in patients with deficiency of body weight.

Abstract P345: Left Ventricular Hypertrophy Screening via Machine Learning for Young Adults

Circulation ◽  
2020 ◽  
Vol 141 (Suppl_1) ◽  
Author(s):  
Gen-min Lin
Keyword(s):  
Machine Learning ◽  
Young Adults ◽  
Body Weight ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Body Height ◽  
Left Ventricular ◽  
Test Set ◽  
Ecg Criteria ◽  
Ecg Data

Background: A use of conventional 12-lead electrocardiographic (ECG) criteria and machine learning for the ECG parameters to identify the presence of left ventricular hypertrophy (LVH) is estimated 20%-30% in the general population. We developed an ECG system with simple anthropometric data using machine learning to increase the sensitivity in screening for LVH. Methods: In a large sample of 2,196 males, aged 17-45 years, the support vector machine (SVM) classifier with linear kernel is used as the machine learning method for 31 characteristics including age, body height, and body weight in addition to 28 ECG parameters such as axes, intervals and voltages to link the output of LVH. The diagnosis of LVH is based on the echocardiographic criteria for young adult males as 116 g/m 2 (left ventricular mass (LVM)/body surface area) or 49 g/m 2.7 (LVM/body height 2.7 ). The samples are divided into a training/validation set and a test set. By applying the synthetic minority over-sampling technique (SMOTE) in pre-processing of training data, the imbalance in sample size between the Non-LVH and LVH cases can be solved. Results: For the test set with 440 cases, average accuracy, specificity, sensitivity, precision and F 1 score are 76.1%, 75.1%, 92.6%, 19.5% and 32.3%, respectively. The AUCs of ROC and PR curves are 0.871 and 0.272, respectively. To compare with the Cornell and Sokolow-Lyon voltage criteria as shown in Fig.1, all data of the 2,196 young males are also tested in the model. With the specificity of 73.3%, our SVM technique provides much better sensitivity 86.7% compared to 3.3% and 52.7% for the Cornell and Sokolow-Lyon voltage criteria, respectively. The body height and body weight are the most important factors among the 31 features in our SVM model. Conclusions: We provide a novel screening tool using simple anthropometrics and several ECG data to identify LVH in young adults and improves much in sensitivity as compared with the conventional ECG criteria or using machine learning for ECG data alone to identify LVH.

scholarly journals A randomized controlled trial of dapagliflozin on left ventricular hypertrophy in people with type two diabetes: the DAPA-LVH trial

2020 ◽  
Vol 41 (36) ◽  
pp. 3421-3432 ◽  
Author(s):  
Alexander J M Brown ◽  
Stephen Gandy ◽  
Rory McCrimmon ◽  
John Graeme Houston ◽  
Allan D Struthers ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Body Weight ◽  
Adipose Tissue ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Controlled Trial ◽  
High Sensitivity ◽  
Left Ventricular ◽  
Model Assessment ◽  
Protective Effects

Abstract Aim We tested the hypothesis that dapagliflozin may regress left ventricular hypertrophy (LVH) in people with type 2 diabetes (T2D). Methods and results We randomly assigned 66 people (mean age 67 ± 7 years, 38 males) with T2D, LVH, and controlled blood pressure (BP) to receive dapagliflozin 10 mg once daily or placebo for 12 months. Primary endpoint was change in absolute left ventricular mass (LVM), assessed by cardiac magnetic resonance imaging. In the intention-to-treat analysis, dapagliflozin significantly reduced LVM compared with placebo with an absolute mean change of −2.82g [95% confidence interval (CI): −5.13 to −0.51, P = 0.018]. Additional sensitivity analysis adjusting for baseline LVM, baseline BP, weight, and systolic BP change showed the LVM change to remain statistically significant (mean change −2.92g; 95% CI: −5.45 to −0.38, P = 0.025). Dapagliflozin significantly reduced pre-specified secondary endpoints including ambulatory 24-h systolic BP (P = 0.012), nocturnal systolic BP (P = 0.017), body weight (P < 0.001), visceral adipose tissue (VAT) (P < 0.001), subcutaneous adipose tissue (SCAT) (P = 0.001), insulin resistance, Homeostatic Model Assessment of Insulin Resistance (P = 0.017), and high-sensitivity C-reactive protein (hsCRP) (P = 0.049). Conclusion Dapagliflozin treatment significantly reduced LVM in people with T2D and LVH. This reduction in LVM was accompanied by reductions in systolic BP, body weight, visceral and SCAT, insulin resistance, and hsCRP. The regression of LVM suggests dapagliflozin can initiate reverse remodelling and changes in left ventricular structure that may partly contribute to the cardio-protective effects of dapagliflozin. ClinicalTrials.gov Identifier NCT02956811

Abstract 79: Autophagy Is Necessary in Reversal of Left Ventricular Hypertrophy

2012 ◽  
Vol 111 (suppl_1) ◽  
Author(s):  
Jota Oyabu ◽  
Osamu Yamaguchi ◽  
Kinya Otsu
Keyword(s):  
Body Weight ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Cross Sectional Area ◽  
Cardiomyocyte Hypertrophy ◽  
Sectional Area ◽  
Cross Sectional ◽  
Lv Mass ◽  
Continuous Injection

Myocardial hypertrophy occurs in response to a variety of stresses as a compensatory mechanism to maintain cardiac output and normalize wall stress. Left ventricular hypertrophy (LVH) in the long term is an independent risk factor for a range of adverse consequences, such as cardiac dysfunction and cardiac mortality. Therefore, prevention or regression of LVH can be a major therapeutic target. Although reversal of LVH occurs after control of etiological factors, the molecular mechanisms remain to be clarified. We have previously reported that inhibition of autophagy, an evolutionarily conserved process for the bulk degradation of cytoplasmic components, induces cardiomyocyte hypertrophy. In the present study, we investigated the role of autophagy in the course of reversal of LVH. Wild-type mice showed left ventricular hypertrophy by continuous injection of angiotensin II (A-II) for 14 days using osmotic mini-pump, and LVH was reversed 7 days after removal of pump. Autophagy was induced after removal of pump, as evidenced by an increase in LC3-II protein levels. Next, we crossed floxed Atg5 mice with transgenic mice expressing Cre recombinase in cardiac specific manner to generate cardiac-specific autophagy-deficient mice (CKO). We subjected CKO and control mice (CTL) to continuous injection of A-II for 14 days. CKO and CTL showed LVH similarly (LV weight/body weight, CKO 4.60±0.16 versus CTL 4.44±0.08, p=n.s., LV mass index, CKO 69.0±5.5 versus CTL 72.1±2.2, p=n.s.) without showing contractile dysfunction 14 days after injection of A-II. Cross-sectional area of cardiomyocytes was similar in CKO and CTL (CKO 281.0±1.0 μm 2 versus CTL 274.0±1.5 μm 2 , p=n.s.). 7days after removal of pump, CKO showed significantly less reversal of LVH compared with CTL (LV weight/body weight, CKO 4.30±0.13 versus CTL 3.65±0.09, p<0.05, LV mass index, CKO 67.8±3.8 versus CTL 56.2±2.6, p<0.05). Cross-sectional area of cardiomyocytes also showed less reversal of LVH in CKO (CKO 270.6.0±7.0 μm 2 versus CTL 220.9±11.4 μm 2 , p<0.05), indicating that reversal of LVH didn’t occur sufficiently in autophagy-deficient heart. Autophagy was suppressed during reversal of LVH in CKO. These results suggest that autophagy is necessary in reversal of LVH.

Sign in / Sign up

Export Citation Format

Share Document