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

Area of Science:

• Cardiology
• Physiology
• Pathophysiology

Background:

• Left-sided heart failure (HF) is a common cause of right ventricular dysfunction (RVD).
• The mechanisms underlying right ventricle (RV) remodeling in the context of left-sided HF remain unclear.
• RVD is linked to HF progression and increased mortality.

Purpose of the Study:

• To investigate the mechanisms of RV remodeling and dysfunction in a rat model of left-sided HF.
• To assess RV cardiomyocyte function and intracellular calcium signaling in response to left ventricular myocardial infarction (MI).

Main Methods:

• Induction of extensive left ventricular (LV) myocardial infarction (MI) in rats via LAD ligation.
• LV and RV catheterization to assess cardiac function.
• Assessment of intracellular Ca2+ signaling in isolated RV and LV cardiomyocytes.

Main Results:

• Rats with LV failure developed symptomatic biventricular HF, with mildly increased RV afterload.
• RV cardiomyocyte contractility was significantly increased.
• Increased Ca2+ transient amplitude, preserved SERCA2a activity, and reduced Ca2+ efflux via NCX1 and PMCA were observed in RV cardiomyocytes.

Conclusions:

• RV failure in this post-MI LV failure model is not explained by a decline in RV cardiomyocyte function.
• Other factors likely contribute to RV failure, necessitating further research into RV biology.
• Understanding these factors is crucial for developing targeted RV therapies.