Division of Cardiovascular Disease, Department of Medicine, The University of Alabama at Birmingham, Alabama.
Am J Physiol Heart Circ Physiol. 2018 Feb 1;314(2):H255-H267. doi: 10.1152/ajpheart.00528.2017. Epub 2017 Nov 3.
Heart failure (HF) secondary to myocardial infarction (MI) is linked to kidney complications that comprise cellular, structural, functional, and survival indicators. However, HF research is focused on left ventricular (LV) pathology. Here, we determined comprehensive functional analysis of the LV using echocardiography in transition from acute heart failure (AHF) to progressive chronic heart failure (CHF) pathology and developed a histological compendium of the cardiosplenic and cardiorenal networks in pathological remodeling. In surgically induced MI using permanent coronary ligation, the LV dysfunction is pronounced, with myocardium necrosis, wall thinning, and 20-30% LV rupture events that indicated AHF and CHF pathological remodeling in C57BL/6 male mice (2-4 mo old, n = 50). Temporal LV function analysis indicated that fractional shortening and strain are reduced from day 1 to day 5 in AHF and sustained to advance to CHF from day 28 to day 56 compared with naïve control mice ( n = 6). During the transition of AHF ( day 1 to day 5) to advanced CHF ( day 28 to day 56), histological and cellular changes in the spleen were definite, with bimodal inflammatory responses in kidney inflammatory biomarkers. Likewise, there was a unidirectional, progressive, and irreversible deposition of compact collagen in the LV along with dynamic changes in the cardiosplenic and cardiorenal networks post-MI. The renal histology and injury markers suggested that cardiac injury triggers irreversible dysregulation that actively alters the cardiosplenic and cardiorenal networks. In summary, the novel strategies or pathways that modulate comprehensive cardiosplenic and cardiorenal networks in AHF and CHF would be effective approaches to study either cardiac repair or cardiac pathology. NEW & NOTEWORTHY The present compendium shows irreversible ventricular dysfunction as assessed by temporal echocardiography while histological and structural measurements of the spleen and kidney added a novel direction to study cardiosplenic and cardiorenal networks in heart failure pathology. Therefore, the consideration of systems biology and integrative approach is essential to develop novel treatments.
心肌梗死(MI)继发的心力衰竭(HF)与肾脏并发症相关,这些并发症包括细胞、结构、功能和存活指标。然而,HF 研究主要集中在左心室(LV)病理学上。在这里,我们使用超声心动图确定了从急性心力衰竭(AHF)到进行性慢性心力衰竭(CHF)病理的 LV 全面功能分析,并开发了心脏脾和心脏肾网络在病理性重构中的组织学纲要。在使用永久性冠状动脉结扎术诱导的手术性 MI 中,LV 功能障碍明显,心肌坏死、壁变薄以及 20-30%的 LV 破裂事件表明 C57BL/6 雄性小鼠(2-4 月龄,n=50)出现 AHF 和 CHF 病理性重构。LV 功能的时间分析表明,与天真对照小鼠(n=6)相比,AHF 时的分数缩短和应变从第 1 天减少到第 5 天,并且从第 28 天持续到第 56 天进展为 CHF。在 AHF(第 1 天至第 5 天)向晚期 CHF(第 28 天至第 56 天)的过渡期间,脾脏的组织学和细胞变化是明确的,并且在肾脏炎症生物标志物中存在双模态炎症反应。同样,在 MI 后,LV 中存在单向、进行性和不可逆转的致密胶原沉积,并且心脏脾和心脏肾网络发生动态变化。肾脏组织学和损伤标志物表明,心脏损伤触发不可逆的失调,积极改变心脏脾和心脏肾网络。总之,调节 AHF 和 CHF 中全面心脏脾和心脏肾网络的新策略或途径将是研究心脏修复或心脏病理学的有效方法。
本纲要显示了通过时间超声心动图评估的不可逆心室功能障碍,而脾脏和肾脏的组织学和结构测量为研究心力衰竭病理学中的心脏脾和心脏肾网络提供了新方向。因此,考虑系统生物学和综合方法对于开发新的治疗方法至关重要。