Peer-reviewed veterinary case report
Metformin helps protect dog hearts from atrial fibrillation changes
By Li, Jiayi et al.·Published in Life sciences·2020·Department of Cardiology, China·View original on PubMed →
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Original publication title: Metformin therapy confers cardioprotection against the remodeling of gap junction in tachycardia-induced atrial fibrillation dog model.
- Species:
- dog
Plain-English summary
A group of Beagle dogs with induced atrial fibrillation (AF) were treated with metformin, a medication commonly used for diabetes, to see if it could help their heart condition. The dogs showed a significant reduction in how easily they could develop AF and how long it lasted after being treated with metformin. This treatment also helped maintain important heart cell connections that were weakened due to the condition. While metformin was effective in chronic cases, its benefits were limited in acute situations. Overall, metformin appears to offer some heart protection for dogs with AF.
People also search for: dog atrial fibrillation treatment · Beagle heart problems · metformin for dogs heart health
Abstract
OBJECTIVE: Metformin, introduced in 1957, is widely used as an anti-diabetic drug and has considerable benefits in cardiovascular disease reportedly, dependent or independent on its glucose-lowering effects. Aim of this study was to investigate the effect of metformin on gap junction and the inducibility of AF. METHODS: Beagle dogs were subjected to acute or chronic pacing at right atrial appendage by a pacemaker to develop an AF model and electrophysiological parameters were measured. In vitro study, a cell fast pacing model was developed by CardioExcyte 96. We performed Western blot, histology immunohistochemical staining and electron microscopy to detect the effect of metformin. RESULTS: In chronic AF model, the inducibility and duration of AF increased obviously after pacing for 6 weeks compared with sham-operated group (Inducibility, 3.33 ± 5.77 vs. 85.33 ± 7.89%, P<0.0001; Duration, 0.8 ± 0.84 vs. 11 ± 2.67 ms, P<0.0001). Effective refractory periods (ERP) decreased at left and right left atrium and atrial appendages compared with sham-operated group (123.95 ± 6.57 vs. 89.96 ± 7.39 ms P<0.0001). Metformin attenuated the pacing-induced increase in EPR (89.96 ± 7.39 vs. 105.83 ± 7.45 ms, P<0.05), AF inducibility and AF duration (Inducibility, 85.33 ± 7.89 vs. 64.17 ± 7.36%, Duration, 11 ± 2.67 vs. 8.62 ± 1.15 ms, P<0.05). The expression of Cx43 shows a significant downregulation(about 38%, P<0.001) after chronic pacing and treating with metformin could alleviate this decrease(P<0.01). However, the effect of metformin in acute pacing model is limited. The immunohistochemical staining of cardiac tissue also shown that there is more lateralized Cx43 under pacing condition (87.67 ± 2.52 vs. 60.8 ± 9.13%, P<0.005). These pacing-induced lateralize Cx43 could be alleviated by the metformin (48.4 ± 8.62 vs. 60.8 ± 9.13%, P<0.05). Additionally, metformin could affect the interactions of ZO-1 with p-Src/Cx43 via decrease the abnormal cAMP level after pacing (84.04 ± 4.58 vs. 69.34 ± 4.5 nmol/L, P<0.001). CONCLUSIONS: Metformin could alleviate the vulnerability of AF and attenuate the downregulation of gap junction under pacing condition via AMPK pathway and decreasing the P-Src level.
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Search related cases →Original publication on PubMed: https://pubmed.ncbi.nlm.nih.gov/32389830/