Namazi Mehrshad, Eftekhar Seyed Parsa, Mosaed Reza, Shiralizadeh Dini Saeed, Hazrati Ebrahim
Trauma and Surgery Research Center, AJA University of Medical Sciences, Tehran, Iran.
Clinical Biomechanics and Ergonomics Research Center, AJA University of Medical Sciences, Tehran, Iran.
Clin Med Insights Cardiol. 2024 Sep 9;18:11795468241274744. doi: 10.1177/11795468241274744. eCollection 2024.
Pulmonary hypertension (PH) is a pulmonary vascular disease characterized by elevated pulmonary vascular pressure. Long-term PH, irrespective of its etiology, leads to increased right ventricular (RV) pressure, RV hypertrophy, and ultimately, RV failure.
Research indicates that RV failure secondary to hypertrophy remains the primary cause of mortality in pulmonary arterial hypertension (PAH). However, the impact of PH on RV structure and function under increased overload remains incompletely understood. Several mechanisms have been proposed, including extracellular remodeling, RV hypertrophy, metabolic disturbances, inflammation, apoptosis, autophagy, endothelial-to-mesenchymal transition, neurohormonal dysregulation, capillary rarefaction, and ischemia.
Studies have demonstrated the significant role of oxidative stress in the development of RV failure. Understanding the interplay among these mechanisms is crucial for the prevention and management of RV failure in patients with PH.
肺动脉高压（PH）是一种以肺血管压力升高为特征的肺血管疾病。长期的肺动脉高压，无论其病因如何，都会导致右心室（RV）压力升高、右心室肥厚，最终导致右心衰竭。
研究表明，肥厚继发的右心衰竭仍然是肺动脉高压（PAH）患者死亡的主要原因。然而，在负荷增加的情况下，肺动脉高压对右心室结构和功能的影响仍未完全明确。已经提出了几种机制，包括细胞外重塑、右心室肥厚、代谢紊乱、炎症、凋亡、自噬、内皮-间充质转化、神经激素失调、毛细血管稀疏和缺血。
研究已经证明氧化应激在右心衰竭发展过程中具有重要作用。了解这些机制之间的相互作用对于肺动脉高压患者右心衰竭的预防和管理至关重要。
