射血分数保留型心力衰竭发病机制的研究进展

Research Progress in Pathophysiological Mechanisms of Heart Failure with Preserved Ejection Fraction

射血分数保留型心力衰竭(HFpEF)因其复杂的发病机制和缺乏有效的治疗方案而成为目前急诊医学领域的研究难点,其发病率及死亡率均高于射血分数降低型心力衰竭。以往关于HFpEF病理生理机制的研究以探索舒张功能障碍为主,近年来学者们发现左心房收缩功能受损及心房活动不同步、左心室肥厚及收缩功能不全也参与了HFpEF的病理生理发展,且学者们逐渐认识到肥胖及代谢异常对舒张功能障碍影响的重要性,其中一些新的靶点(如胰岛素样生长因子结合蛋白7、转化生长因子-β及成纤维细胞生长因子21)也被发现与舒张功能障碍有关。

Heart failure with preserved ejection fraction(HFpEF)has become a difficulty in the field of emergency medicine due to its complicated pathogenesis and lack of effective treatment,and its morbidity and mortality rates are higher than that of heart failure with reduced ejection fraction.Previous studies on the pathophysiological mechanisms of HFpEF mainly explored diastolic dysfunction.In recent years,scholars have found that impaired left atrial systolic function,unsynchronized atrial activity,left ventricular hypertrophy and systolic dysfunction are also involved in the pathophysiological development of HFpEF,and the importance of obesity and metabolic abnormalities effect on the diastolic dysfunction are gradually recognized by the researchers.New targets such as insulin-like growth factor-binding protein 7,transforming growth factor-βand fibroblast growth factor 21 have also been linked to the diastolic dysfunction.