Right ventricular failure: a comorbidity or a clinical emergency?

Area of Science:

• Cardiology
• Physiology
• Pathophysiology

Background:

• Left ventricle (LV) hypertrophy progression to failure is well-understood.
• Right ventricle (RV) failure (RVF) mechanisms, especially due to overload, are less understood.
• RVF is a critical risk in conditions like pulmonary hypertension and carcinoid syndrome.

Purpose of the Study:

• To review the pathophysiology of RVF.
• To highlight differences in molecular responses to stress between RV and LV.
• To emphasize the need for RV-specific heart failure (HF) therapies.

Main Methods:

• Review of existing literature on RV and LV pathophysiology.
• Analysis of advanced imaging techniques in RV studies.
• Comparison of ventricular remodeling and cellular responses to stress.

Main Results:

• RV remodeling under stress differs from LV, with increased oxidative stress and apoptosis in RV.
• Diminished angiogenesis contributes to RV failure progression.
• Standard heart failure therapies are often ineffective for RVF.

Conclusions:

• RVF pathophysiology is distinct from LV failure, necessitating tailored treatment strategies.
• Understanding RV's unique anatomical and physiological characteristics is key for therapeutic development.
• Further research into RV-specific molecular responses to stress is required for optimized RV-specific HF management.