Arai S, Nakamura T, Suwa N
Tohoku J Exp Med. 1976 Apr;118(4):299-309. doi: 10.1620/tjem.118.299.
In almost all of the cases of cardiac hypertrophy due to sustained hypertension, left ventricular capacity is increased in proportion to increased left ventricular weight, even in the absence of manifest cardiac insufficiency. The condition is regarded as the general expression of cardiac response to pressure load, and the concept of "isomorphic hypertrophy" is proposed. Concentric hypertrophy of the current concept is observed only on rare special occasions, and its role in cardiac adaptation to pressure load is obscure. The increase in myocardial mass is sufficient to maintain the work done by a unit myocardial volume at a normal level. However, the calculation on pertinent models demonstrates that hypertrophied hearts of any type expel the normal stroke volume with smaller shortening of muscle fibers under larger stress, which is further elevated with the progress of cardiac contraction. Because the maximum force generated by muscle fibers declines with advancing cardiac contraction, hypertrophied hearts harbor a latent risk of mechanical insufficiency. Even under pressure load, ventricular dilation seems to precede the re-inforcement of ventricular wall in the development of cardiac hypertrophy. A common mechanism may be therefore assumed underlying the development and performance of all types of hypertrophied hearts, regardless of the difference in the character of physical loads.
在几乎所有因持续性高血压导致的心脏肥大病例中，即使在没有明显心脏功能不全的情况下，左心室容量也会随着左心室重量的增加而成比例增加。这种情况被视为心脏对压力负荷反应的一般表现，并提出了“同构肥大”的概念。当前概念中的向心性肥大仅在极少数特殊情况下观察到，其在心脏对压力负荷适应中的作用尚不清楚。心肌质量的增加足以使单位心肌体积所做的功维持在正常水平。然而，相关模型计算表明，任何类型的肥大心脏在更大的应力下以较小的肌纤维缩短排出正常的每搏量，且随着心脏收缩的进行，这种情况会进一步加剧。由于肌纤维产生的最大力量随着心脏收缩的推进而下降，肥大心脏存在机械功能不全的潜在风险。即使在压力负荷下，在心脏肥大的发展过程中，心室扩张似乎也先于心室壁的再强化。因此，可以假定所有类型肥大心脏的发展和功能存在一个共同机制，而不论物理负荷特征的差异。
