Martonová Denisa, Holz David, Brackenhammer Dorothea, Weyand Michael, Leyendecker Sigrid, Alkassar Muhannad
Institute of Applied Dynamics, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Department of Cardiac Surgery, Friedrich-Alexander-Universität Erlangen-Nürnberg, Erlangen, Germany.
Front Cardiovasc Med. 2022 Jul 6;9:850274. doi: 10.3389/fcvm.2022.850274. eCollection 2022.
The present computational study investigates the effects of an epicardial support pressure mimicking a heart support system without direct blood contact. We chose restrictive cardiomyopathy as a model for a diseased heart. By changing one parameter representing the amount of fibrosis, this model allows us to investigate the impairment in a diseased left ventricle, both during diastole and systole. The aim of the study is to determine the temporal course and value of the support pressure that leads to a normalization of the cardiac parameters in diseased hearts. These are quantified the end-diastolic pressure, end-diastolic volume, end-systolic volume, and ejection fraction. First, the amount of fibrosis is increased to model diseased hearts at different stages. Second, we determine the difference in the left ventricular pressure between a healthy and diseased heart during a cardiac cycle and apply for the epicardial support as the respective pressure difference. Third, an epicardial support pressure is applied in form of a piecewise constant step function. The support is provided only during diastole, only during systole, or during both phases. Finally, the support pressure is adjusted to reach the corresponding parameters in a healthy rat. Parameter normalization is not possible to achieve with solely diastolic or solely systolic support; for the modeled case with 50% fibrosis, the ejection fraction can be increased by 5% with purely diastolic support and 14% with purely systolic support. However, the ejection fraction reaches the value of the modeled healthy left ventricle (65.6%) using a combination of diastolic and systolic support. The end-diastolic pressure of 13.5 mmHg cannot be decreased with purely systolic support. However, the end-diastolic pressure reaches the value of the modeled healthy left ventricle (7.5 mmHg) with diastolic support as well as with the combination of the diastolic and systolic support. The resulting negative diastolic support pressure is -4.5 mmHg, and the positive systolic support pressure is 90 mmHg. We, thereby, conclude that ventricular support during both diastole and systole is beneficial for normalizing the left ventricular ejection fraction and the end-diastolic pressure, and thus it is a potentially interesting therapy for cardiac insufficiency.
本计算研究探讨了模拟无直接血液接触的心脏支持系统的心外膜支持压力的影响。我们选择限制型心肌病作为患病心脏的模型。通过改变一个代表纤维化程度的参数,该模型使我们能够研究患病左心室在舒张期和收缩期的功能损害。本研究的目的是确定能使患病心脏的心脏参数恢复正常的支持压力的时间进程和数值。这些参数通过舒张末期压力、舒张末期容积、收缩末期容积和射血分数来量化。首先,增加纤维化程度以模拟不同阶段的患病心脏。其次,我们确定心动周期中健康心脏和患病心脏之间左心室压力的差异,并将相应的压力差作为心外膜支持压力施加。第三,以分段常数阶跃函数的形式施加心外膜支持压力。支持仅在舒张期、仅在收缩期或在两个阶段提供。最后,调整支持压力以使其达到健康大鼠的相应参数。仅通过舒张期或仅通过收缩期支持无法实现参数正常化;对于模拟的50%纤维化病例,单纯舒张期支持可使射血分数提高5%,单纯收缩期支持可使射血分数提高14%。然而,使用舒张期和收缩期支持相结合的方式,射血分数可达到模拟健康左心室的值(65.6%)。单纯收缩期支持无法降低13.5 mmHg的舒张末期压力。然而,通过舒张期支持以及舒张期和收缩期支持相结合的方式,舒张末期压力可达到模拟健康左心室的值(7.5 mmHg)。由此产生的舒张期支持负压为-4.5 mmHg,收缩期支持正压为90 mmHg。因此,我们得出结论,舒张期和收缩期的心室支持对于使左心室射血分数和舒张末期压力恢复正常是有益的,因此它是一种潜在的有趣的心力衰竭治疗方法。