Effects of oral antidiabetic drugs and glucagon-like peptide-1 receptor agonists on left ventricular diastolic function in patients with type 2 diabetes mellitus: a systematic review and network meta-analysis

Ida, Satoshi; Kaneko, Ryutaro; Imataka, Kanako; Ôkubo, Kaoru; Shirakura, Yoshitaka; Azuma, Kentaro; Fujiwara, Ryoko; Takahashi, Hiroka; Murata, Kazuya

doi:10.1007/s10741-020-09936-w

Cited by 17 publications

(10 citation statements)

References 40 publications

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“…Both parameters are relevant for diabetic cardiomyopathy and HFpEF (100). In addition, a systematic review comparing the effect of GLP-1 agonists to different antidiabetics on LV diastolic function has concluded that liraglutide monotherapy offers a considerably beneficial outcome (101). Interestingly, the EAT was found to express GLP-1 receptors in contrast to subcutaneous fat in the same patient (102).…”

Section: Glucagon-like Peptide-1 Receptor Agonistsmentioning

confidence: 99%

Epicardial Fat Expansion in Diabetic and Obese Patients With Heart Failure and Preserved Ejection Fraction—A Specific HFpEF Phenotype

Elsanhoury

Nelki

Kelle

et al. 2021

Front. Cardiovasc. Med.

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Graphical AbstractEpicardial adipose tissue (EAT)-related heart failure with preserved ejection fraction (HFpEF). Obesity and type 2 diabetes mellitus (T2DM) are common triggers of HFpEF, frequently associated with EAT expansion. EAT plays metabolic and mechanical roles in HFpEF development via para/vasocrine factors and pericardial restrain, respectively. Life-style modifications including healthy diet and regular exercise can quash the EAT expansion. Statins, proprotein convertase subtilisin/kexin type 9 (PCSK9) inhibitors and fat-modulating antidiabetics including metformin, sodium-glucose cotransporter 2 (SGLT2) inhibitors and glucagon-like peptide-1 (GLP-1) agonists can target EAT. FFA, free fatty acids; AGEs, advanced glycation end-products; NO, nitric oxide; ROS, reactive oxygen species; Ang-II, angiotensin II; TGF-β, Transforming growth factor beta; MCP-1, monocyte chemoattractant protein 1; IL-6, interleukin 6; TNF-α, tumor necrosis factor alpha. Figure created via Servier Medical Art and BioRender tools.

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Section: Glucagon-like Peptide-1 Receptor Agonistsmentioning

confidence: 99%

Epicardial Fat Expansion in Diabetic and Obese Patients With Heart Failure and Preserved Ejection Fraction—A Specific HFpEF Phenotype

Elsanhoury

Nelki

Kelle

et al. 2021

Front. Cardiovasc. Med.

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“…Among these, a study with liraglutide demonstrated a reduction in LV filling pressure and an improvement in diastolic function, both parameters relevant for progression of diabetic cardiomyopathy and symptomatic HFpEF [171]. This result was confirmed by a systematic review [172]. Other experimental studies support an effect of fat mass reduction of GLP-1 RAs by increasing insulin sensitivity, lipolysis, and energy expenditure.…”

Section: Incretin-based Therapymentioning

confidence: 69%

Dysregulated Epicardial Adipose Tissue as a Risk Factor and Potential Therapeutic Target of Heart Failure with Preserved Ejection Fraction in Diabetes

et al. 2022

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Cardiovascular (CV) disease and heart failure (HF) are the leading cause of mortality in type 2 diabetes (T2DM), a metabolic disease which represents a fast-growing health challenge worldwide. Specifically, T2DM induces a cluster of systemic metabolic and non-metabolic signaling which may promote myocardium derangements such as inflammation, fibrosis, and myocyte stiffness, which represent the hallmarks of heart failure with preserved ejection fraction (HFpEF). On the other hand, several observational studies have reported that patients with T2DM have an abnormally enlarged and biologically transformed epicardial adipose tissue (EAT) compared with non-diabetic controls. This expanded EAT not only causes a mechanical constriction of the diastolic filling but is also a source of pro-inflammatory mediators capable of causing inflammation, microcirculatory dysfunction and fibrosis of the underlying myocardium, thus impairing the relaxability of the left ventricle and increasing its filling pressure. In addition to representing a potential CV risk factor, emerging evidence shows that EAT may guide the therapeutic decision in diabetic patients as drugs such as metformin, glucagon-like peptide‑1 (GLP-1) receptor agonists and sodium-glucose cotransporter 2 inhibitors (SGLT2-Is), have been associated with attenuation of EAT enlargement.

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“…The absence of RCTs that met pooling criteria precluded planned meta-analyses. Previously published indirect net-work metaanalyses focused on intermediate outcomes of diastolic dysfunction regardless of baseline HFpEF and did not find consistent superiority of SGLT2 inhibitors when compared with placebo or other anti-diabetic medications [74,75] . Previously published direct meta-analysis concluded that SGLT2 inhibitors reduced the risk of cardiovascular death or heart-failure hospitalization regardless of baseline heart failure diagnosis [15] .…”

Section: Discussionmentioning

confidence: 95%

“…We found no studies that reported adverse effects from SGLT2 inhibitors specifically in adults with HFpEF [73] . Limited evidence of some improvement in intermediate outcomes of diastolic dysfunction lack clinical significance with valid prediction of better patient-centered outcomes and healthcare utilization required in future studies [74,75] . The absence of RCTs that met pooling criteria precluded planned meta-analyses.…”

Section: Discussionmentioning

confidence: 99%

Insufficient evidence regarding benefits from sodium-glucose cotransporter-2 inhibitors in heart failure with preserved ejection fraction

Shamliyan¹,

Avanesova²,

Aronow³

2020

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Aim: Sodium-glucose cotransporter-2 (SGLT2)-inhibitors improve survival in adults with reduced ejection fraction. Clinical outcomes in adults with heart failure (HF) with preserved ejection fraction (HFpEF) have not been systematically reviewed. Methods: We conducted a systematic rapid literature review and appraised the quality of evidence using the Grading of Recommendations Assessment, Development and Evaluation methodology. Results: We identified post-hoc subgroup analyses of four randomized controlled clinical trials (RCTs) and unpublished results from 2 RCTs. In 2 RCTs vs. placebo, Canagliflozin reduced the risk of fatal or hospitalized HF in adults with HF and documented or assumed left ventricular ejection fraction (LVEF) ≥ 50% (hazard rate ratio, HR = 0.71, 95%CI: 0.52-0.97) but had no effect in a subpopulation with documented LVEF ≥ 50% (HR = 0.83, 95%CI: 0.55-1.25). Dapagliflozin or ertugliflozin did not improve all-cause or cardiovascular death or hospitalization for HF in adults with HF and LVEF > 45% in two pivotal RCTs vs. placebo. Empagliflozin did not improve exercise ability, patient-reported outcomes or congestion, diuretic use and all-cause healthcare resource utilization in unpublished RCT vs. placebo. Various definitions of HFpEF, post-hoc interaction analyses suggesting outcome improvement

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Effects of oral antidiabetic drugs and glucagon-like peptide-1 receptor agonists on left ventricular diastolic function in patients with type 2 diabetes mellitus: a systematic review and network meta-analysis

Cited by 17 publications

References 40 publications

Epicardial Fat Expansion in Diabetic and Obese Patients With Heart Failure and Preserved Ejection Fraction—A Specific HFpEF Phenotype

Epicardial Fat Expansion in Diabetic and Obese Patients With Heart Failure and Preserved Ejection Fraction—A Specific HFpEF Phenotype

Dysregulated Epicardial Adipose Tissue as a Risk Factor and Potential Therapeutic Target of Heart Failure with Preserved Ejection Fraction in Diabetes

Insufficient evidence regarding benefits from sodium-glucose cotransporter-2 inhibitors in heart failure with preserved ejection fraction

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