Department of Cardiology, Ziekenhuis Oost-Limburg, Genk, Belgium.
J Am Coll Cardiol. 2013 Aug 6;62(6):485-95. doi: 10.1016/j.jacc.2013.04.070. Epub 2013 Jun 7.
Current pathophysiological models of congestive heart failure unsatisfactorily explain the detrimental link between congestion and cardiorenal function. Abdominal congestion (i.e., splanchnic venous and interstitial congestion) manifests in a substantial number of patients with advanced congestive heart failure, yet is poorly defined. Compromised capacitance function of the splanchnic vasculature and deficient abdominal lymph flow resulting in interstitial edema might both be implied in the occurrence of increased cardiac filling pressures and renal dysfunction. Indeed, increased intra-abdominal pressure, as an extreme marker of abdominal congestion, is correlated with renal dysfunction in advanced congestive heart failure. Intriguing findings provide preliminary evidence that alterations in the liver and spleen contribute to systemic congestion in heart failure. Finally, gut-derived hormones might influence sodium homeostasis, whereas entrance of bowel toxins into the circulatory system, as a result of impaired intestinal barrier function secondary to congestion, might further depress cardiac as well as renal function. Those toxins are mainly produced by micro-organisms in the gut lumen, with presumably important alterations in advanced heart failure, especially when renal function is depressed. Therefore, in this state-of-the-art review, we explore the crosstalk between the abdomen, heart, and kidneys in congestive heart failure. This might offer new diagnostic opportunities as well as treatment strategies to achieve decongestion in heart failure, especially when abdominal congestion is present. Among those currently under investigation are paracentesis, ultrafiltration, peritoneal dialysis, oral sodium binders, vasodilator therapy, renal sympathetic denervation and agents targeting the gut microbiota.
当前充血性心力衰竭的病理生理模型不能令人满意地解释充血与心肾功能之间的有害联系。腹部充血(即内脏静脉和间质充血)在大量晚期充血性心力衰竭患者中表现出来,但定义不明确。内脏血管顺应性降低和腹部淋巴流量不足导致间质水肿,这两者都可能导致心内充盈压升高和肾功能障碍。事实上,作为腹部充血的极端标志物的腹内压升高与晚期充血性心力衰竭中的肾功能障碍相关。有趣的发现提供了初步证据,表明肝脏和脾脏的改变可能导致心力衰竭中的全身充血。最后,肠道来源的激素可能影响钠稳态,而由于充血导致肠道屏障功能受损,肠毒素进入循环系统可能进一步抑制心脏和肾脏功能。这些毒素主要由肠道腔中的微生物产生,在晚期心力衰竭中可能发生重要改变,尤其是在肾功能下降时。因此,在这篇综述中,我们探讨了充血性心力衰竭中心、腹和肾之间的相互作用。这可能提供新的诊断机会和治疗策略,以实现心力衰竭中的去充血,尤其是当存在腹部充血时。目前正在研究的方法包括腹腔穿刺、超滤、腹膜透析、口服钠结合剂、血管扩张剂治疗、肾交感神经去神经和靶向肠道微生物组的药物。