Katz A M
Cardiology Division, University of Connecticut School of Medicine, Farmington 06030-1305, USA.
Eur Heart J. 1995 Dec;16 Suppl O:110-4. doi: 10.1093/eurheartj/16.suppl_o.110.
The poor prognosis in heart failure, which can be reproduced by overloading the normal heart, may reflect molecular abnormalities associated with cardiac hypertrophy. Because terminally differentiated adult cardiac myocytes have little or no capacity to divide, overload-induced hypertrophy represents an unnatural growth response. The mechanism by which this unnatural growth response shortens survival remains speculative, but may involve apoptosis caused when overload reactivates growth factors to which the adult heart cannot respond with normal cell division. The ability of converting enzyme inhibitors and nitrates, which have growth inhibitory as well as vasodilator effects, to improve prognosis in heart failure may reflect the ability of these drugs to modify this unnatural growth response.
心力衰竭预后不佳，正常心脏负荷过重也会出现这种情况，这可能反映了与心肌肥大相关的分子异常。由于终末分化的成年心肌细胞几乎没有或完全没有分裂能力，负荷诱导的肥大代表了一种不自然的生长反应。这种不自然的生长反应缩短生存期的机制仍属推测，但可能涉及负荷使成年心脏无法通过正常细胞分裂做出反应的生长因子重新激活时所引发的细胞凋亡。具有生长抑制和血管舒张作用的转换酶抑制剂和硝酸盐能够改善心力衰竭的预后，这可能反映了这些药物改变这种不自然生长反应的能力。
