Weil Brian R, Techiryan George, Suzuki Gen, Konecny Filip, Canty John M
Department of Physiology and Biophysics, University at Buffalo, Buffalo, New York.
The Clinical and Translational Research Center, University at Buffalo, Buffalo, New York.
JACC Basic Transl Sci. 2019 Aug 26;4(4):527-541. doi: 10.1016/j.jacbts.2019.04.002. eCollection 2019 Aug.
Swine subjected to 2 weeks of repetitive pressure overload (RPO) exhibited significant myocyte loss, but left ventricular (LV) systolic function was preserved, and chamber dilatation did not occur. Instead, myocardial remodeling characterized by myocyte hypertrophy and interstitial fibrosis led to a marked reduction in LV diastolic compliance, which protected the heart from stretch-induced myocyte injury and preserved LV ejection fraction without anatomic LV hypertrophy. These results support a novel paradigm that links cardiac adaptations to RPO with the pathogenesis of reduced LV diastolic compliance and may explain how LV stiffening can occur in the absence of sustained hypertension or anatomic hypertrophy.
经历2周重复性压力超负荷(RPO)的猪表现出明显的心肌细胞丢失,但左心室(LV)收缩功能得以保留,且未发生心室扩张。相反,以心肌细胞肥大和间质纤维化为特征的心肌重塑导致LV舒张顺应性显著降低,这保护心脏免受拉伸诱导的心肌细胞损伤,并在无解剖学LV肥大的情况下保留LV射血分数。这些结果支持了一种新的范式,即将心脏对RPO的适应性与LV舒张顺应性降低的发病机制联系起来,并且可能解释了在没有持续性高血压或解剖学肥大的情况下LV僵硬度是如何发生的。