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 14866: Hyperglycemia is an Independent Predictor of Left Ventricular Hypertrophy

Circulation ◽  
2014 ◽  
Vol 130 (suppl_2) ◽  
Author(s):  
Mohan Thanikachalam ◽  
Vijaykumar Harivanzan ◽  
Jahnavi Sunderarajan ◽  
Ragavendra Baliga ◽  
Sadagopan Thanikachalam
Keyword(s):  
Insulin Resistance ◽  
Left Ventricular Hypertrophy ◽  
Odds Ratio ◽  
Aortic Stiffness ◽  
Ventricular Hypertrophy ◽  
Blood Lipids ◽  
Independent Predictor ◽  
Left Ventricular ◽  
Model Assessment ◽  
Lv Mass

Background: Diabetes mellitus (DM) is a risk factor for cardiovascular morbidity and mortality. In the current study we examine the association of hyperglycemic with left ventricular hypertrophy (LVH) independent of major correlates of LVH, such as, age, body size, blood pressure (BP) and aortic stiffness. Methods: We conducted a population-based, cross-sectional survey in 8,080 South Indians over the age of 20 years. The study included anthropometric, socioeconomic, psychosocial, BP, blood lipids, insulin, HbA1C, glucose tolerance test and carotid-femoral pulse wave velocity (PWV) assessments. Insulin resistance (IR) was defined as the 25% of the population with the highest values for homeostasis model assessment of insulin resistance (HOMA-IR). LV mass and relative wall thickness (RWT) were determined using echocardiography. LVH was defined as LV mass index (LVMI) >109 g/m 2 for men and >89 g/m 2 for women. Results: After the exclusion of people with hypertension, 5,841 subjects (mean age 41 years, 59% women) constituted the study sample. The mean LVMI in subjects with normoglycemia (n=3585), pre-DM (impaired fasting and/or post prandial blood sugar; n=1315) and DM (n=888) was 78.5 ± 17.5, 80.7 ± 19.4 and 87.2 ± 20.3, while mean RWT was 0.46 ± 0.09, 0.48 ± 0.09 and 0.51 ± 0.1, respectively (p<0.01). After adjustments for age, sex, BMI, BP, PWV, blood lipids, history of coronary artery disease, socioeconomic and smoking status, and physical activity, when compared to persons with normoglycemia, the odds ratio (95% CI) for LVH in pre-DM and DM men was 1.12 (0.89, 1.42) and 1.37 (1.04, 1.8), respectively; the odds ratio in pre-DM and DM women was 1.07 (0.89, 1.28) and 1.4 (1.08, 1.82), respectively. Among the persons with normoglycemia those with IR the odds ratio for LVH was 1.23 (0.85, 1.78) in men and 1.01 (0.79, 1.30) in women. In the multi-linear regression models HbA1c was independently correlated with LVMI. The correlation coefficients were higher in men (β= 0.07, p <0.001) compared to women (β= 0.037, p = 0.032). Conclusion: Hyperglycemia is an independent predictor of LVH in South Asian population. These findings indicate potential adverse myocardial effects of DM independent of associated risk factors, such as obesity, BP and aortic stiffness.

Candesartan, an angiotensin II receptor blocker, improves left ventricular hypertrophy and insulin resistance

Metabolism ◽  
2004 ◽  
Vol 53 (6) ◽  
pp. 777-781 ◽  
Author(s):  
Futoshi Anan ◽  
Naohiko Takahashi ◽  
Tatsuhiko Ooie ◽  
Masahide Hara ◽  
Hironobu Yoshimatsu ◽  
...  
Keyword(s):  
Insulin Resistance ◽  
Angiotensin Ii ◽  
Left Ventricular Hypertrophy ◽  
Ventricular Hypertrophy ◽  
Left Ventricular ◽  
Receptor Blocker ◽  
Angiotensin Ii Receptor Blocker ◽  
Angiotensin Ii Receptor

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.

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