Colombo Paolo C, Doran Amanda C, Onat Duygu, Wong Ka Yuk, Ahmad Myra, Sabbah Hani N, Demmer Ryan T
Division of Cardiology, College of Physicians & Surgeons, Department of Medicine, Columbia University, 622 West 168th Street, PH 12-134, New York, NY, 10032, USA,
Curr Heart Fail Rep. 2015 Jun;12(3):215-22. doi: 10.1007/s11897-015-0254-8.
Venous congestion and endothelial and neurohormonal activation are known to occur in acute decompensated heart failure (ADHF), yet the temporal role of these processes in the pathophysiology of decompensation is not fully understood. Conventional wisdom presumes congestion to be a consequence of worsening cardiovascular function; however, the biomechanically driven effects of venous congestion are biologically plausible contributors to ADHF that remain largely unexplored in vivo. Recent experimental evidence from human models suggests that fluid accumulation and venous congestion are not simply consequences of poor cardiovascular function, but rather are fundamental pro-oxidant, pro-inflammatory, and hemodynamic stimuli that contribute to acute decompensation. The latest advances in the monitoring of volume status using implantable devices allow for the detection of venous congestion before symptoms arise. This may ultimately lead to improved treatment strategies including not only diuretics, but also specific, adjuvant interventions to counteract endothelial and neurohormonal activation during early preclinical decompensation.
已知静脉充血以及内皮和神经激素激活会在急性失代偿性心力衰竭（ADHF）中发生，然而这些过程在失代偿病理生理学中的时间作用尚未完全明确。传统观点认为充血是心血管功能恶化的结果；然而，静脉充血由生物力学驱动产生的效应在生物学上可能是ADHF的促成因素，而这在体内很大程度上仍未得到探索。来自人体模型的最新实验证据表明，液体潴留和静脉充血并非仅仅是心血管功能不佳的后果，而是促成急性失代偿的基本促氧化剂、促炎和血流动力学刺激因素。使用可植入设备监测容量状态的最新进展使得在症状出现之前就能检测到静脉充血。这最终可能会带来改进的治疗策略，不仅包括利尿剂，还包括在临床前早期失代偿期间对抗内皮和神经激素激活的特定辅助干预措施。
