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

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.

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

Bioscience Reports ◽

10.1042/bsr20192909 ◽

2019 ◽

Vol 39 (12) ◽

Cited By ~ 2

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.

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

European Heart Journal ◽

10.1093/eurheartj/ehz203 ◽

2019 ◽

Vol 40 (41) ◽

pp. 3409-3417 ◽

Cited By ~ 27

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.

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