Cardiac growth and remodeling in the form of chamber dilation and wall thinning are typical hallmarks of infarct-induced heart failure. Over time, the infarct region stiffens, the remaining muscle takes over function, and the chamber weakens and dilates. Current therapies seek to attenuate these effects by removing the infarct region or by providing structural support to the ventricular wall. However, the underlying mechanisms of these therapies are unclear, and the results remain suboptimal. Here we show that myocardial infarction induces pronounced regional and transmural variations in cardiac form. We introduce a mechanistic growth model capable of predicting structural alterations in response to mechanical overload. Under a uniform loading, this model predicts non-uniform growth. Using this model, we simulate growth in a patient-specific left ventricle. We compare two cases, growth in an infarcted heart, pre-operative, and growth in the same heart, after the infarct was surgically excluded, post-operative. Our results suggest that removing the infarct and creating a left ventricle with homogeneous mechanical properties does not necessarily reduce the driving forces for growth and remodeling. These preliminary findings agree conceptually with clinical observations.

中文翻译：

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左心室的生长和重塑：心肌梗死和手术心室修复的案例研究

心腔扩张和壁变薄形式的心脏生长和重塑是梗塞性心力衰竭的典型标志。随着时间的推移，梗塞区域变硬，剩余的肌肉接管功能，腔室减弱和扩张。目前的疗法试图通过去除梗塞区域或通过为心室壁提供结构支撑来减弱这些影响。然而，这些疗法的潜在机制尚不清楚，结果仍然不理想。在这里，我们表明心肌梗塞会引起心脏形式的明显区域和透壁变化。我们引入了一种机械增长模型，能够预测响应机械过载的结构变化。在均匀载荷下，该模型预测非均匀生长。使用这个模型，我们模拟特定患者左心室的生长。我们比较了两个病例，梗塞心脏的生长，术前，和同一心脏的生长，梗塞被手术排除后，术后。我们的结果表明，去除梗塞并创建具有均匀机械特性的左心室并不一定会降低生长和重塑的驱动力。这些初步发现在概念上与临床观察一致。