Department of Medicine, University of Pittsburgh Medical Center, Pittsburgh, Pennsylvania.
Division of Cardiology, Department of Medicine, Northwestern University Feinberg School of Medicine, Chicago, Illinois, USA.
Curr Opin Support Palliat Care. 2019 Mar;13(1):24-30. doi: 10.1097/SPC.0000000000000414.
Right-sided heart failure, which is often present in the setting of advanced heart failure, is associated with cardiac cachexia, the cardiorenal syndrome, and adverse outcomes. Improved understanding of venous congestion of the splanchnic circulation, which may play a key role in the pathogenesis of right-sided heart failure, could lead to novel therapeutics to ameliorate heart failure. Here we provide an overview of right-sided heart failure, splanchnic hemodynamics, fluid homeostasis, and the intestinal microenvironment. We review recent literature to describe pathophysiologic mechanisms and possible therapeutics.
Several possible mechanisms centered around upregulation of sodium-hydrogen exchanger-3 (NHE3) may form a causal link between right ventricular dysfunction, splanchnic congestion, and worsening heart failure. These include an anaerobic environment in enterocytes, resulting in reduced intracellular pH; increased sodium absorption by the gut via NHE3; decreased pH at the intestinal brush border thus altering the gut microbiome profile; increased bacterial synthesis of trimethylamine N-oxide; and decreased bacterial synthesis of short-chain fatty acids causing abnormal intestinal barrier function.
Splanchnic congestion in the setting of right-sided heart failure may serve an important role in the pathogenesis of advanced heart failure, and further exploration of these mechanisms may lead to new therapeutic advances.
右心衰竭常发生于晚期心力衰竭患者，与心脏恶病质、心肾综合征和不良预后相关。对内脏循环静脉淤血（可能在右心衰竭发病机制中起关键作用）的理解的提高，可能会带来改善心力衰竭的新疗法。本文概述了右心衰竭、内脏血流动力学、液体平衡和肠道微环境，并复习了相关文献，以描述病理生理机制和可能的治疗方法。
几种可能的机制集中在钠氢交换体 3（NHE3）的上调上，可能在右心室功能障碍、内脏淤血和心力衰竭恶化之间形成因果关系。这些机制包括肠细胞中的厌氧环境导致细胞内 pH 值降低；肠道通过 NHE3 吸收更多的钠；肠道刷状缘的 pH 值降低，从而改变肠道微生物组谱；细菌合成三甲胺 N-氧化物增加；以及短链脂肪酸合成减少导致肠道屏障功能异常。
右心衰竭时的内脏淤血可能在晚期心力衰竭的发病机制中起重要作用，对这些机制的进一步探索可能会带来新的治疗进展。
