Epigenetics, inflammation and metabolism in right heart failure associated with pulmonary hypertension. (June 2017)

• Record Type: Journal Article
• Authors: Samson, Nolwenn; Paulin, Roxane
• Is Part Of: Pulmonary circulation. Volume 7:Number 3(2017)
• Page Start: 572
• Page End: 587
• Publication Date: 2017-06
• Subjects: right ventricle hypertrophy -- cytokines -- mitochondrial switch; Pulmonary circulation -- Periodicals; Pulmonary circulation; Electronic journals -- Sciences; Periodicals; 616.24005
• DOI: 10.1177/2045893217714463
• Languages: English
• ISSNs: 2045-8932

Abstract

Right ventricular failure (RVF) is the most important prognostic factor for both morbidity and mortality in pulmonary arterial hypertension (PAH), but also occurs in numerous other common diseases and conditions, including left ventricle dysfunction. RVF remains understudied compared with left ventricular failure (LVF). However, right and left ventricles have many differences at the morphological level or the embryologic origin, and respond differently to pressure overload. Therefore, knowledge from the left ventricle cannot be extrapolated to the right ventricle. Few studies have focused on the right ventricle and have permitted to increase our knowledge on the right ventricular-specific mechanisms driving decompensation. Here we review basic principles such as mechanisms accounting for right ventricle hypertrophy, dysfunction, and transition toward failure, with a focus on epigenetics, inflammatory, and metabolic processes.