Katz S D
Columbia Presbyterian Medical Center, Division of Circulatory Physiology, New York, NY 10032, USA.
Curr Opin Cardiol. 1997 May;12(3):259-64. doi: 10.1097/00001573-199705000-00007.
The pathogenesis of heart failure is determined by the ventricular and vascular responses to myocellular injury. Experimental and clinical studies suggest that the vascular endothelium may play an important role in modulating progression of ventricular and vascular remodeling in heart failure. Endothelial cell dysfunction has been described in the coronary and skeletal muscle circulations of patients with heart failure and appears to be characterized by decreased endothelial synthesis of nitric oxide and increased production of endothelin-1. The pathogenesis of endothelial dysfunction in heart failure is unknown, but may be related to increased oxidative stress, abnormal regional flow conditions, and cytokine and neurohormonal activation. The specific role of endothelial dysfunction in the pathogenesis of heart failure remains to be determined. If endothelial dysfunction does contribute to progression of disease in early heart failure, specific therapies to enhance endothelial dysfunction may improve long-term morbidity and mortality.
心力衰竭的发病机制取决于心室和血管对心肌细胞损伤的反应。实验和临床研究表明，血管内皮可能在调节心力衰竭时心室和血管重塑的进展中发挥重要作用。心力衰竭患者的冠状动脉和骨骼肌循环中已发现内皮细胞功能障碍，其特征似乎是一氧化氮的内皮合成减少和内皮素-1的产生增加。心力衰竭中内皮功能障碍的发病机制尚不清楚，但可能与氧化应激增加、局部血流状况异常以及细胞因子和神经激素激活有关。内皮功能障碍在心力衰竭发病机制中的具体作用仍有待确定。如果内皮功能障碍确实在早期心力衰竭疾病进展中起作用，增强内皮功能的特定疗法可能会改善长期发病率和死亡率。
