Right Ventricle Remodelling in Left-Sided Heart Failure in Rats: The Role of Calcium Signalling

Abstract

Right ventricular dysfunction (RVD) can follow primary pulmonary diseases, but the most common cause of its development is left-sided heart failure (HF). RVD is associated with HF progression, increased risk of death and hospitalisation. The mechanism of right ventricle (RV) remodelling leading to RVD due to left-sided HF is not fully elucidated. Rats underwent LAD ligation to induce extensive left ventricle (LV) myocardial infarction (MI) and subsequent left-sided HF. Sham-operated animals served as controls. After 8 weeks of follow-up, the animals underwent LV and RV catheterisation, and systolic function and intracellular Ca2+ signalling were assessed in cardiomyocytes isolated from both ventricles. We demonstrated that rats with LV failure induced by extensive LV myocardial infarction also develop RV failure, leading to symptomatic biventricular HF, despite only mildly increased RV afterload. The contractility of RV cardiomyocytes was significantly increased, which could be related to increased amplitude of Ca2+ transient, preserved SERCA2a activity and reduced Ca2+ efflux via NCX1 and PMCA. Our study indicates that RV failure associated with post-MI LV failure in a rat model cannot be explained by a decline in cardiomyocyte function. This indicates that other factors may play a role here, pointing to the need for further research to better understand the biology of RV failure in order to ultimately develop therapies targeting the RV.

WITHDRAWN: The evaluation of right ventricular function in patients with triple-vessel coronary artery disease without myocardial infraction in two-dimensional speckle tracking echocardiography

“…In addition to this, the left and right ventricles are in the same limited pericardial cavity and there is a connected blood circulation. When the left ventricle fails, the left ventricle cannot maintain preload and the right ventricle function will be altered accordingly [30] . In this study, the LVEF of patients in group C decreased compared with groups A and B (P<0.05), suggesting that the systolic diminish of the left ventricle of patients, when the ventricular beat volume of patients is reduced, making the systemic performance of hypotension and hypoperfusion state, further weakening the lling state of the right ventricle, reducing the right coronary artery blood supply, and aggravating the injury of the right ventricle [31] .…”