Katz A M
Department of Medicine, University of Connecticut, Health Center, Farmington 06030.
Cardiologia. 1993 Dec;38(12 Suppl 1):39-43.
In most patients with heart failure, an imbalance between energy production and energy utilization leads to a state of chronic energy starvation. This imbalance is due both to increased energy demands caused by overloading of myocardial cells in the failing heart, and to a decreased energy supply caused by reduced perfusion, altered cell architecture, and molecular changes in the hypertrophied heart. Energy starvation has important therapeutic implications in the failing heart. Because the systems that relax the heart are especially sensitive to energetic state, inotropic agents could exacerbate relaxation abnormalities and promote arrhythmias. More important is the likelihood that inotropic agents, which increase cardiac energy expenditure, accelerate cell damage and so worsen prognosis in this condition. Vasodilators and negative inotropic agents, on the other hand, by decreasing energy utilization should improve the balance between energy delivery and energy expenditure in the failing heart.
在大多数心力衰竭患者中，能量产生与能量利用之间的失衡会导致慢性能量饥饿状态。这种失衡既归因于衰竭心脏中心肌细胞负荷过重导致的能量需求增加，也归因于灌注减少、细胞结构改变以及肥厚心脏中的分子变化所引起的能量供应减少。能量饥饿在衰竭心脏中具有重要的治疗意义。由于使心脏舒张的系统对能量状态特别敏感，正性肌力药物可能会加剧舒张异常并促发心律失常。更重要的是，增加心脏能量消耗的正性肌力药物很可能会加速细胞损伤，从而恶化这种情况下的预后。另一方面，血管扩张剂和负性肌力药物通过减少能量利用，应该可以改善衰竭心脏中能量供应与能量消耗之间的平衡。
