Diabetic cardiomyopathy - A comprehensive updated review

Murtaza, Ghulam; Virk, Hafeez Ul Hassan; Khalid, Muhammad; Lavie, Carl J.; Ventura, Héctor O.; Mukherjee, Debabrata; Ramu, Vijay; Bhogal, Sukhdeep; Kumar, Gautam; Shanmugasundaram, Madhan; Paul, Timir K.

doi:10.1016/j.pcad.2019.03.003

Cited by 230 publications

(204 citation statements)

References 110 publications

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“…Atrial fibrillation (AF) is the most common sustained cardiac arrhythmia worldwide, and it is associated with higher risks of ischemic stroke, heart failure hospitalization and mortality [ 1 – 3 ]. Diabetes mellitus (DM) is associated with higher risks of ischemic cardiovascular events, heart failure event irrespective to ischemic event, and mortality, and also a 40% higher risk of AF in the general population [ 4 – 7 ]. In patients with DM and established cardiovascular disease, those with AF at baseline had a higher risk of worse heart failure outcomes than those without AF [ 8 , 9 ].…”

Section: Introductionmentioning

confidence: 99%

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Ling

Chan

Chen

et al. 2020

Cardiovasc Diabetol

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Background Sodium glucose cotransporter 2 inhibitor (SGLT2i) reduces the risk of hard cardiovascular endpoints in type 2 diabetes mellitus (T2DM) patients with/without established cardiovascular diseases. Whether SGLT2i is associated with a lower risk of new-onset atrial fibrillation (AF) in T2DM patients is unclear. We aimed to evaluate the risk of new-onset AF associated with the use of SGLT2i compared to dipeptidyl peptidase-4 inhibitor (DPP4i) among a longitudinal cohort of diabetic patients. Methods We used medical data from a multi-center healthcare provider in Taiwan, which included a total of 15,606 and 12,383 patients treated with SGLT2i and DPP4i, respectively, from June 1, 2016 to December 31, 2018. We used propensity-score weighting to balance covariates across study groups. Patients were followed up from the drug index date until the occurrence of new-onset AF, discontinuation of the index drug, or the end of the study period, whichever occurred first. Results Overall, 55%, 45%, and 0% of the patients were treated with empagliflozin, dapagliflozin, and canagliflozin, respectively. Most patients in the DPP4i group were prescribed with linagliptin (51%), followed by sitagliptin (24%), saxagliptin (13%), vildagliptin (8%) and alogliptin (5%). The use of SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i after propensity-score weighting [hazard ratio: 0.61; 95% confidential interval: 0.50–0.73; P < 0.001]. Subgroup analysis revealed that the use of SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i across several subgroups including old age, female in gender, the presence of cardiovascular disease, hemoglobin A1c $$\ge$$ ≥ 8%, and chronic kidney disease. The advantage of SGLT2i over DPP4i persisted with different SGLT2i (dapagliflozin or empagliflozin) and either low- or standard-dose SGLT2i. Conclusions SGLT2i was associated with a lower risk of new-onset AF compared with DPP4i among T2DM patients in real-world practice.

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Section: Introductionmentioning

confidence: 99%

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Ling

Chan

Chen

et al. 2020

Cardiovasc Diabetol

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“…Alteration in the BNP level suggests myocardial structural and functional dysfunction. Elevated BNP levels showed a positive correlation with LV dysfunction in DCM [15]. Cardiomyocyte hypertrophy is a common structural hallmark in patients with DCM [16,17].…”

Section: Discussionmentioning

confidence: 89%

Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT-Foxo1 signaling pathway

Wang

Bai

Duan³

et al. 2020

Preprint

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Background: Diabetic cardiomyopathy (DCM) severely impairs the health of diabetic patients. Previous studies have shown that the expression of inwardly rectifying potassium channel 6.1 (Kir6.1) in heart mitochondria is significantly reduced in type 1 diabetes. However, whether its expression and function are changed and what role it plays in type 2 DCM have not been reported. This study investigated the role and mechanism of Kir6.1 in DCM.Methods: The cardiac function in mice was analyzed by echocardiography, ELISA, hematoxylin and eosin staining, TUNEL and transmission electron microscopy. The mitochondrial function in cardiomyocytes was measured by the oxygen consumption rate and the mitochondrial membrane potential (ΔΨm). Kir6.1 expression at the mRNA and protein levels was analyzed by quantitative real-time PCR and western blotting (WB), respectively. The protein expression of t-AKT, p-AKT, t-Foxo1, and p-Foxo1 was analyzed by WB.Results: We found that the cardiac function and the Kir6.1 expression in DCM mice were decreased. Kir6.1 overexpression improved cardiac dysfunction and upregulated the phosphorylation of AKT and Foxo1 in the DCM mouse model. Furthermore, Kir6.1 overexpression also improved cardiomyocyte dysfunction and upregulated the phosphorylation of AKT and Foxo1 in cardiomyocytes with insulin resistance. In contrast, cardiac-specific Kir6.1 knockout aggravated the cardiac dysfunction and downregulated the phosphorylation of AKT and Foxo1 in DCM mice. Furthermore, Foxo1 activation downregulated the expression of Kir6.1 and decreased the ΔΨm in cardiomyocytes. In contrast, Foxo1 inactivation upregulated the expression of Kir6.1 and increased the ΔΨm in cardiomyocytes. Chromatin immunoprecipitation assay demonstrated that the Kir6.1 promoter region contains a functional Foxo1-binding site .Conclusions: Kir6.1 improves cardiac dysfunction in DCM, probably through the AKT-Foxo1 signaling pathway. Moreover, the crosstalk between Kir6.1 and the AKT-Foxo1 signaling pathway may provide new strategies for reversing the defective signaling in DCM.

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“…V kardiomyocytoch dochádza k akumulácii toxických produktov mastných kyselín v cytoplazme, pretože je prekročená oxidačná kapacita mitochondrií. Lipotoxicita tiež zhoršuje kontraktilitu myokardu a má aj pro-apoptotické a pro--zápalové účinky, čím ďalej prehlbuje dysfunkciu myokardu (10). Inzulín pôsobí ako rastový faktor a hyperinzulinémia pri DM II prispieva k hypertrofii myokardu, ktorá vzniká nezávisle od hypertenzie.…”

Section: Patofyziológia Srdcového Zlyhávania Pri Diabeteunclassified

Srdcové zlyhávanie a diabetes mellitus. Nebezpečné spojenie / Heart failure and diabetes mellitus. Dangerous association

Gonçalvesová¹

2020

Cardiol

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Increased risk of cardiovascular disease in type 2 diabetes mellitus (DM II) is generally understood in association with the higher incidence of atherosclerotic vascular occlusive events such as myocardial infarction, stroke and atherosclerotic peripheral artery disease. However, one of the most common and serious cardiovascular disorders in patients with diabetes is heart failure (HF). Patients-men with DM II are at more than three times higher risk of developing HF; in women with diabetes the risk is up to five times higher. After the clinical manifestation of HF in a diabetic patient, prognosis is much worse than without HF. Some surveys show that in diabetic patients over 65 years of age, the one-year mortality after HF manifestation is almost nine times higher than in comparable subjects without HF. Arterial hypertension, coronary disease and metabolic disorders resulting from diabetes itself play a role in the development of HF. Thus, we can in general speak of damage to the heart due to diabetes and associated disorders. The pharmacological treatment of heart failure in patients with DM II is not different in comparison with non-diabetics. Thorough control of blood glucose and other risk factors of cardiovascular disease reduces the risk of developing HF in diabetic patients. In patients with DM II who have already developed HF, the strategy of strict control of DM II no longer reduces the risk of death or other cardiovascular events. In patients with DM II who are at risk of developing HF (patients with hypertension and / or myocardial infarction treatment), treatment with SGLT2 inhibitors reduces the risk of cardiovascular death, incidence and hospitalization for HF. Other antidiabetic drugs have a negative or neutral effect on HF. These unique properties of SGLT2 inhibitors have also been reflected in the 2019 Guidelines of European Society of Cardiology which recognize them as first-line drugs in patients with DM II and atherosclerotic cardiovascular disease, or at very high or high risk of atherosclerotic cardiovascular disease. Fig. 2, Tab.1, Ref. 31, on-line full text (Free, PDF) www.cardiologyletters.sk

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Diabetic cardiomyopathy - A comprehensive updated review

Cited by 230 publications

References 110 publications

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

The risk of new-onset atrial fibrillation in patients with type 2 diabetes mellitus treated with sodium glucose cotransporter 2 inhibitors versus dipeptidyl peptidase-4 inhibitors

Kir6.1 improves cardiac dysfunction in diabetic cardiomyopathy via the AKT-Foxo1 signaling pathway

Srdcové zlyhávanie a diabetes mellitus. Nebezpečné spojenie / Heart failure and diabetes mellitus. Dangerous association

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