Transient atrial inflammation in a murine model of Coxsackievirus B3‐induced myocarditis

Abstract

Atrial dysfunction is a relatively common complication of acute myocarditis, although its pathophysiology is unclear. There is limited information on myocarditis-associated histological changes in the atria and how they develop in time. The aim of this study therefore was to investigate inflammation, fibrosis and viral genome in the atria in time after mild CVB3-induced viral myocarditis (VM) in mice. C3H mice (n = 68) were infected with 10 5 PFU of Coxsackievirus B3 (CVB3) and were compared with uninfected mice (n = 10). Atrial tissue was obtained at days 4, 7, 10, 21, 35 or 49 post-infection. Cellular infiltration of CD45+ lymphocytes, MAC3+ macrophages, Ly6G+ neutrophils and mast cells was quantified by (immuno)histochemical staining. The CVB3 RNA was determined by in situ hybridization, and fibrosis was evaluated by elastic van Gieson (EvG) staining. In the atria of VM mice, the numbers of lymphocytes on days 4 and 7 (p < .05) and days 10 (p < .01); macrophages on days 7 (p < .01) and 10 (p < .05); neutrophils on days 4 (p < .05); and mast cells on days 4 and 7 (p < .05) increased significantly compared with control mice and decreased thereafter to basal levels. No cardiomyocyte death was observed, and the CVB3 genome was detected in only one infected mouse on Day 4 post-infection. No significant changes in the amount of atrial fibrosis were found between VM and control mice. A temporary increase in inflammation is induced in the atria in the acute phase of CVB3induced mild VM, which may facilitate the development of atrial arrhythmia and contractile dysfunction.

Prognostic Significance of Cardiac Magnetic Resonance in Left Atrial and Biventricular Strain Analysis during the Follow-Up of Suspected Myocarditis

“…In our study, LAEF was identified as the only functional parameter showing statistically significant recovery, whereas the improvement in LV function was not statistically significant. This finding may be the result of the involvement of LA in the inflammatory process of myocarditis, as demonstrated recently in a murine model with viral myocarditis [ 26 ]. However, it may also be due to a change in LV filling pressures, which was believed to be a determinant of the LA reservoir and pump strain that were measured by speckle tracking echocardiography [ 27 ].…”

Atrial and Ventricular Strain Imaging Using CMR in the Prediction of Ventricular Arrhythmia in Patients with Myocarditis

“…The LA actively modulates left ventricular filling through its distinct phases [17,40,53]. Another hypothesis is that the direct involvement of the atria during myocarditis contributes to proarrhythmogenic remodeling of the atria [54]. Our results demonstrate that utilizing atrial and ventricular strain serves as helpful and supportive non-contrast CMR parameters for risk stratifying patients with myocarditis at risk of arrhythmic complications.…”

Changes in glutamic oxaloacetic transaminase 2 during rat physiological and pathological cardiomyocyte hypertrophy

“…Subsequently, the homogenized solution was frozen three times at − 80 °C and centrifuged at 4 °C, and the supernatant was isolated for conducting tests. Following the instructions of the aspartate aminotransferase assay kit (Nanjing Jiancheng Bioengineering Institute, China) [ 29 ], we divided the samples into test and control wells, and simultaneously prepared standard concentration wells. After 30 min of reaction with the substrate solution, 20 min with the 2,4-dinitrophenylhydrazine solution, and 15 min with NaOH, the absorbance values were measured using a microplate reader at a wavelength of 510 nm.…”