Pulmonary Hypertension and Right Ventricle: A Pathophysiological Insight.

IF 2.3 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS Clinical Medicine Insights. Cardiology Pub Date : 2024-09-09 eCollection Date: 2024-01-01 DOI:10.1177/11795468241274744

Mehrshad Namazi, Seyed Parsa Eftekhar, Reza Mosaed, Saeed Shiralizadeh Dini, Ebrahim Hazrati

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Abstract

Background: 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.

Main body: 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.

Conclusions: 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.

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肺动脉高压与右心室：病理生理学透视。

背景：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。无论病因如何，长期的肺动脉高压都会导致右心室（RV）压力升高、RV 肥厚，并最终导致 RV 衰竭：研究表明，继发于肥厚的 RV 衰竭仍然是肺动脉高压（PAH）患者死亡的主要原因。然而，在超负荷增加的情况下，PH 对 RV 结构和功能的影响仍不完全清楚。目前已提出多种机制，包括细胞外重塑、RV 肥厚、代谢紊乱、炎症、细胞凋亡、自噬、内皮细胞向间质转化、神经激素失调、毛细血管稀疏和缺血：研究表明，氧化应激在 RV 衰竭的发生中起着重要作用。了解这些机制之间的相互作用对于预防和治疗 PH 患者的 RV 衰竭至关重要。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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