Young J B
Department of Cardiology, Cleveland Clinic Foundation, OH 44195, USA.
Pharmacotherapy. 1996 Mar-Apr;16(2 Pt 2):78S-84S.
Heart failure is a common disorder caused by many different diseases. At the root of the problem is diminished myocyte contractility, which ultimately results in failure of the pump to generate adequate peripheral flow. An interplay of hemodynamic, neurohumoral, and inflammatory perturbations initially improves cardiac flow and cellular respiration, but ultimately worsens the syndrome. Inotropic drug therapy was an attractive option in patients with heart failure even before the pump failure aspect of the disease was recognized. Increased contractility should lead to increased cardiac output, which would likely ameliorate hemodynamic and metabolic derangements. Although inotropes increase cardiac contractility at least transiently, this effect does not generally translate into improved survival in clinical trials. Indeed, in patients with advanced heart failure, these drugs frequently increase death rates. It is important to put the issue of inotropic therapeutics into perspective when considering treatment options for these patients. It may well be that certain inotropes in yet to be defined dosages will substantially improve morbidity and mortality when combined with drugs designed to interdict metabolic and neurohumoral components of the syndrome.
心力衰竭是一种由多种不同疾病引起的常见病症。问题的根源在于心肌细胞收缩力减弱，最终导致心脏泵血功能衰竭，无法产生足够的外周血流。血流动力学、神经体液和炎症紊乱之间的相互作用最初会改善心脏血流和细胞呼吸，但最终会使该综合征恶化。甚至在认识到心力衰竭的泵血功能衰竭这一疾病特征之前，强心药物治疗对心力衰竭患者来说就是一个有吸引力的选择。心肌收缩力增强应会导致心输出量增加，这可能会改善血流动力学和代谢紊乱。尽管强心剂至少能暂时增加心肌收缩力，但在临床试验中，这种效果一般不会转化为生存率的提高。事实上，在晚期心力衰竭患者中，这些药物常常会增加死亡率。在考虑这些患者的治疗方案时，正确看待强心治疗问题很重要。很可能某些尚未确定剂量的强心剂与旨在阻断该综合征代谢和神经体液成分的药物联合使用时，将能显著改善发病率和死亡率。
