Metformin and heart failure–related outcomes in patients with or without diabetes: a systematic review of randomized controlled trials

Dludla, Phiwayinkosi V.; Nyambuya, Tawanda M.; Johnson, Rabia; Silvestri, Sonia; Orlando, Patrick; Mazibuko-Mbeje, Sithandiwe E.; Gabuza, Kwazi B.; Mxinwa, Vuyolwethu; Mokgalaboni, Kabelo; Tiano, Luca; Muller, Christo J. F.; Louw, Johan; Nkambule, Bongani B.

doi:10.1007/s10741-020-09942-y

Cited by 27 publications

(21 citation statements)

References 46 publications

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Section: Insulin Sensitizersmentioning

confidence: 99%

“…Abrogation of cardiac insulin resistance is shown to mitigate inflammatory cardiac dysfunction by decreased production of pro-inflammatory adhesion molecules, C-reactive protein (CRP), and IL-6 ( Dandona et al, 2009 ; Al-Huseini et al, 2019 ). Metformin, the first-line anti-diabetic drug in clinics, promotes glucose homeostasis and improves impaired heart function in patients with diabetes by blocking pro-inflammatory markers such as CCL11 ( Dludla et al, 2020 ). Notably, metformin also exhibits its anti-inflammatory effects by inhibiting NF-κB ( Hattori et al, 2006 ), reducing CRP production from vessel walls ( Li et al, 2009 ), and blocking monocyte differentiation into macrophages ( Vasamsetti et al, 2015 ), irrespective of diabetic status.…”

Section: Therapeutic Strategies For Prevention Of Dcm By Targeting Inflammationmentioning

confidence: 99%

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Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

et al. 2021

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The incidence of heart failure (HF) continues to increase rapidly in patients with diabetes. It is marked by myocardial remodeling, including fibrosis, hypertrophy, and cell death, leading to diastolic dysfunction with or without systolic dysfunction. Diabetic cardiomyopathy (DCM) is a distinct myocardial disease in the absence of coronary artery disease. DCM is partially induced by chronic systemic inflammation, underpinned by a hostile environment due to hyperglycemia, hyperlipidemia, hyperinsulinemia, and insulin resistance. The detrimental role of leukocytes, cytokines, and chemokines is evident in the diabetic heart, yet the precise role of inflammation as a cause or consequence of DCM remains incompletely understood. Here, we provide a concise review of the inflammatory signaling mechanisms contributing to the clinical complications of diabetes-associated HF. Overall, the impact of inflammation on the onset and development of DCM suggests the potential benefits of targeting inflammatory cascades to prevent DCM. This review is tailored to outline the known effects of the current anti-diabetic drugs, anti-inflammatory therapies, and natural compounds on inflammation, which mitigate HF progression in diabetic populations.

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Section: Insulin Sensitizersmentioning

confidence: 99%

Section: Therapeutic Strategies For Prevention Of Dcm By Targeting Inflammationmentioning

confidence: 99%

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

et al. 2021

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“…Although currently used therapeutic drugs such as metformin and statins can effectively reduce blood glucose or lipid levels to prolong the lives of patients with metabolic syndrome, the long-term use of these drugs has been associated with several limitations including toxicity, ultimately leading to increased CVD risk [ 86 , 87 , 88 ]. Certainly, from evidence presented in the current review ( Table 2 and Table 3 ), we hypothesize that increased EFT occurs concurrently with raised circulating levels of TBARS, hs-CRP, and IL-6, indicating oxidative stress and chronic low-grade inflammation.…”

Section: Discussionmentioning

confidence: 99%

Physical Exercise Potentially Targets Epicardial Adipose Tissue to Reduce Cardiovascular Disease Risk in Patients with Metabolic Diseases: Oxidative Stress and Inflammation Emerge as Major Therapeutic Targets

et al. 2021

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Excess epicardial adiposity, within a state of obesity and metabolic syndrome, is emerging as an important risk factor for the development of cardiovascular diseases (CVDs). Accordingly, increased epicardial fat thickness (EFT) implicates the exacerbation of pathological mechanisms involving oxidative stress and inflammation within the heart, which may accelerate the development of CVDs. This explains increased interest in targeting EFT reduction to attenuate the detrimental effects of oxidative stress and inflammation within the setting of metabolic syndrome. Here, we critically discuss clinical and preclinical evidence on the impact of physical exercise on EFT in correlation with reduced CVD risk within a setting of metabolic disease. This review also brings a unique perspective on the implications of oxidative stress and inflammation as major pathological consequences that link increased EFT to accelerated CVD risk in conditions of metabolic disease.

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“…2 Effective modulation of some heart failure-related outcomes with metformin treatment was related to its beneficial effects in ameliorating insulin resistance and blocking pro-inflammatory markers such as the agingassociated cytokine CCL11 (C-C motif chemokine ligand 11). 3 Insulin resistance is a well-established composite index of systemic inflammatory and metabolic disorders. Mounting evidence reveals that insulin resistance predicts and, to some extent, mediates the development of atherosclerosis, myocardial infarction and in-stent restenosis.…”

Section: Introductionmentioning

confidence: 99%

Correlation between Insulin Resistance and LVEF in non Diabetic Chronic Heart Failure Patients admitted in a Tertiary Care Hospital

et al. 2021

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Background: Insulin resistance is a well-established composite index of systemic inflammatory and metabolic disorders. A wide variety of methods like, HOMA-IR (Homeostatic model assessment insulin resistance), FGIR (Fasting glucose insulin ratio), ISI-Composite (an index of whole body insulin sensitivity), QUICKI (quantitative insulin sensitivity check index) etc are available for assessing IR. Objective: To find out the correlation between insulin resistance and LVEF in non diabetic chronic heart failure patients. Methodology: This cross sectional study was carried out in the Department of Cardiology in Bangabandhu Sheikh Mujib Medical University, Shahbagh, Dhaka from February, 2019 to June, 2020. Patients admitted with chronic heart failure with reduced ejection fraction were included in this study. Patients with diabetic, prediabetic and patient who did not give written informed consent were excluded in this study. Results: LVEF 25-29% was 16 patients out of which 10(66.7%) had significant insulin resistance. LVEF 30- 34% was found in 28 patients, among them 16(41.0%) had no insulin resistance. LVEF 35-39% was found in 19 patients out of which 18(46.2%) had no insulin resistance. The difference was statistically significant (p<0.05). A negative correlation (r=-0.340; p=0.006) was found between insulin resistance and LVEF. Conclusion: Majority non diabetic chronic heart failure patients had no insulin resistance. Significant negative correlation was found between insulin resistance and LVEF. University Heart Journal Vol. 17, No. 2, Jul 2021; 99-102

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Metformin and heart failure–related outcomes in patients with or without diabetes: a systematic review of randomized controlled trials

Cited by 27 publications

References 46 publications

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

Mechanisms and Therapeutic Prospects of Diabetic Cardiomyopathy Through the Inflammatory Response

Physical Exercise Potentially Targets Epicardial Adipose Tissue to Reduce Cardiovascular Disease Risk in Patients with Metabolic Diseases: Oxidative Stress and Inflammation Emerge as Major Therapeutic Targets

Correlation between Insulin Resistance and LVEF in non Diabetic Chronic Heart Failure Patients admitted in a Tertiary Care Hospital

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