Brief-preischemic vagal stimulation outcomes on acute myocardial infarction and long term left ventricular remodeling

FRANCO RIVEROS V; MÉNDEZ DIODATI N; MORALES C; BERNATENÉ E; GIMÉNEZ S; DONATO M; BUCHHOLZ B; GELPI RJ

Congreso; V International Congress in Translational Medicine. International Master Program in Biomedical Sciences; 2021

Background and aimsAs we previously described, vagal stimulation (VS) mimicks myocardial preconditioning by reducing acutemyocardial infarct size (IS) without an improvement in left ventricularfunction (LVF). Nevertheless, it is unknown whether VS effects can ameliorate theevolution of chronic infarction, by improving LVF and remodeling. Our aim was to analyze the effects of brief VS applied beforeischemia on acute myocardial infarction and its long-term benefitson an experimental ischemia-reperfusion and non-reperfusion model.MethodsWe performed a regional myocardial ischemia on theleft descendant coronary artery on male FVB mice during45 min, followed by either 2 hours, 28 days of reperfusion or no reperfusion atall, with or without 10 min of pre-ischemic VS. LVF was assessed by catheterization of the leftventricle through the left carotid artery and by echocardiography.Participation of muscarinic receptors was determined byadministration of atropine during VS. Morphometric parameters were also analyzed comparing the weight of bothventricles (VW) and the lungs? weight (LW) with the tail?s (TL) and tibia?s(TiL) length. Lastly, IS on the 2h reperfused hearts was measuredwith TTC, and heart sampleswere cross-sectioned from base to apex for assessment of changes in cardiacstructure.Results IS measured after 2 hours ofreperfusion decreased significantly with VS, from 65.3±1.7% to 43±2.1% and administration of atropine reversed this protection(IS: 60.4±1.6% vs VS+IR-2h; p<0.001). In chronic groups with VS and 28 daysof reperfusion, we observed an improvement in LVF evidenced by a lower LVPDF(Sham-28d: 3.8±0.2 mmHg; IR-28d: 6.8±0.5 mmHg; VS+IR-28d: 3.7±1 mmHg;p<0.01), higher EF% (Sham-28d: 77.3±11.7%; IR-28d: 59.7±2.8%; VS+IR-28d:69.6±2.4%; p<0.05), and lower TRIV (Sham-28d: 19.4±1.4; IR-28d: 30.3±1.2;VS+IR-28d: 25±0.9; p<0.05). Likewise, VS significantly improved LVF ingroups without reperfusion (LVDP: I28d: 8.4±1 mmHg; VS+I28d: 3.1±0.8;p<0.05; EF%: I28d: 50.6±4; VS+I28d: 69.5±1; p<0.05). Normalizedbiventricular weight was increased in all chronic groups, including those withVS. Finally, we observed an increment in the cross-sectional area of ​​myocytesin the groups with ischemia. ConclusionsBrief VS applied before ischemia reduces acuteinfarct size and improves long-termLVF in ischemic hearts with or without reperfusion independently of muscarinicreceptors? action or infarct size.