Hamad Eman, Mather Paul J, Srinivasan Siva, Rubin Sharon, Whellan David J, Feldman Arthur M
Jefferson Medical College of Thomas Jefferson University, Philadelphia, Pennsylvania, USA.
Am J Cardiovasc Drugs. 2007;7(4):235-48. doi: 10.2165/00129784-200707040-00002.
Over the past 2 decades, investigators have learned more about the pathophysiologic changes that occur in systolic and diastolic dysfunction. Ironically, in some cases, the biologic pathways that have protected the heart during acute dysfunction are the same pathways that cause progressive deleterious effects with chronic activation. In particular, it is the activation of the neurohormonal system that has a significant impact on disease progression. As a result, the neurohormonal system has provided a key target for pharmacologic therapy in patients with heart failure secondary to systolic dysfunction. These targets include the renin-angiotensin-aldosterone system as well as the sympathetic nervous system. Neurohormonal manipulation, however, is often ineffective in the pharmacologic therapy of patients with endstage heart failure, therefore other treatment strategies - including the use of inotropic agents to improve pump function and diuretics to control fluid balance are needed.
在过去20年里,研究人员对收缩功能障碍和舒张功能障碍中发生的病理生理变化有了更多了解。具有讽刺意味的是,在某些情况下,在急性功能障碍期间保护心脏的生物学途径与慢性激活时导致渐进性有害影响的途径相同。特别是,神经激素系统的激活对疾病进展有重大影响。因此,神经激素系统已成为收缩功能障碍所致心力衰竭患者药物治疗的关键靶点。这些靶点包括肾素-血管紧张素-醛固酮系统以及交感神经系统。然而,神经激素调节在终末期心力衰竭患者的药物治疗中往往无效,因此需要其他治疗策略,包括使用正性肌力药物改善泵功能和利尿剂控制液体平衡。