Lechat P
Pharmacology Department, Pitié-Salpétrière Hospital, Paris, France.
Eur Heart J. 1998 Feb;19 Suppl B:B12-8.
Heart failure results from damage and stress to the myocardium whatever the aetiology. An increase in stress by cardiac overload is initially overcome by compensatory mechanisms that maintain blood pressure through a combination of the sympathetic nervous system and the renin-angiotensin-aldosterone system. These mechanisms may also alter myocyte function and induce progressive cell death and replacement by fibrous tissue. Disease therapy must reduce cardiac loading and avoid blood pressure control by mechanisms that have deleterious effects. Therapy includes diuretics, vasodilators and alpha- and beta-adrenergic blockade. Complete blockade of all receptors involved in the adverse effects of neurohormonal stimulation might represent an ultimate therapy objective, and improve subsequent prognosis. Large clinical trials are in progress to determine the therapy of choice in the prevention of progression of heart failure.
无论病因如何，心力衰竭都是由心肌损伤和应激引起的。心脏负荷增加所导致的应激增加最初会被代偿机制所克服，这些机制通过交感神经系统和肾素-血管紧张素-醛固酮系统的共同作用来维持血压。这些机制也可能改变心肌细胞功能，并诱导渐进性细胞死亡以及被纤维组织替代。疾病治疗必须减轻心脏负荷，并避免通过具有有害作用的机制来控制血压。治疗方法包括利尿剂、血管扩张剂以及α和β肾上腺素能阻滞剂。完全阻断参与神经激素刺激不良反应的所有受体可能是最终的治疗目标，并改善后续预后。目前正在进行大型临床试验，以确定预防心力衰竭进展的首选治疗方法。
