Right ventricular failure: a comorbidity or a clinical emergency?

There has been ample data providing a convincing perception about the underlying mechanism pertaining to left ventricle (LV) hypertrophy progressing towards LV failure. In comparison, data available on the feedback of right ventricle (RV) due to volume or pressure overload is minimal. Advanced imaging techniques have aided the study of physiology, anatomy, and diseased state of RV. However, the treatment scenario of right ventricular failure (RVF) demands more attention. It is a critical clinical risk in patients with carcinoid syndrome, pulmonary hypertension, atrial septal defect, and several other concomitant diseases. Although the remodeling responses of both ventricles on an increase of end-diastolic pressure are mostly identical, the stressed RV becomes more prone to oxidative stress activating the apoptotic mechanism with diminished angiogenesis. This instigates the advancement of RV towards failure in contrast to LV. Empirical heart failure (HF) therapies have been ineffective in improving the mortality rate and cardiac function in patients, which prompted a difference between the underlying pathophysiology of RVF and LV failure. Treatment strategies should be devised, taking into consideration the anatomical and physiological characteristics of RV. This review would emphasize on the pathophysiology of the RVF and the differences between two ventricles in molecular response to stress. A proper insight into the underlying pathophysiology is required to develop optimized therapeutic management in RV-specific HF.