Modeling left ventricular diastolic dysfunction: classification and key in dicators
Modeling left ventricular diastolic dysfunction: classification and key in dicators
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DOI：
10.1186/1742-4682-8-14
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发表时间：
2011-05-09
影响因子：
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通讯作者：
Clark, John W., Jr.
中科院分区：
文献类型：
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作者：
Luo, Chuan;Ramachandran, Deepa;Clark, John W., Jr.
背景：在左室射血分数（HFNEF）正常的情况下，数学建模可以克服分离临床心力衰竭机制的实际困难。在人类心血管呼吸系统（H-CRS）模型中，我们介绍了三例左室舒张功能障碍（LVDD）：(1)左室主动舒张功能受损（ir型）；(2)增加被动刚度（限制性或r型）；(3)伪正常型或pn型混合产生HFNEF。还考虑了增加收缩性的影响。模型结果显示随后的心力衰竭和机制的报道。方法：我们采用先前描述的改良肺顺应性的H-CRS模型来更好地模拟正常的肺部血液分布。ir型通过改变左心室（LV）的激活功能来建模，r型通过增加左室壁和隔膜的舒张刚度来建模。采用5阶Cash-Karp龙格-库塔数值积分法求解模型微分方程。结果：ir型和r型均可降低左室搏量、心输出量、射血分数（EF）和平均全身动脉压。心率、肺压、肺容量、肺脏和全身动静脉O-2和CO2差异增大。ir型降低，r型增加二尖瓣E/A比。pn型产生描述良好的伪正常二尖瓣流入模式。三种类型的LVDD均降低右心室（RV）和左室EF，但后者保持正常或接近正常。模拟结果显示，EF的减少部分会因收缩僵硬度的增加而恢复，这是一种代偿机制，如果临床医生只考虑LVEF和左室功能的其他指标，可能会导致他们忽略HF的存在。使用H-CRS模型的模拟表明，RV功能的变化很可能是诊断性的。本研究也强调了室间隔力学在LVDD中的重要性。结论：该模型表明，单是左室舒张功能异常就能导致左室和右室收缩功能下降，而这是以前没有意识到的，并有助于心衰的临床综合征。此外，右室舒张性能的改变是存在的，可能是左室舒张参数改变的标志，可用于更好地临床识别左室舒张性心脏病。
Background: Mathematical modeling can be employed to overcome the practical difficulty of isolating the mechanisms responsible for clinical heart failure in the setting of normal left ventricular ejection fraction (HFNEF). In a human cardiovascular respiratory system (H-CRS) model we introduce three cases of left ventricular diastolic dysfunction (LVDD): (1) impaired left ventricular active relaxation (IR-type); (2) increased passive stiffness (restrictive or R-type); and (3) the combination of both (pseudo-normal or PN-type), to produce HFNEF. The effects of increasing systolic contractility are also considered. Model results showing ensuing heart failure and mechanisms involved are reported.Methods: We employ our previously described H-CRS model with modified pulmonary compliances to better mimic normal pulmonary blood distribution. IR-type is modeled by changing the activation function of the left ventricle (LV), and R-type by increasing diastolic stiffness of the LV wall and septum. A 5(th)-order Cash-Karp Runge-Kutta numerical integration method solves the model differential equations.Results: IR-type and R-type decrease LV stroke volume, cardiac output, ejection fraction (EF), and mean systemic arterial pressure. Heart rate, pulmonary pressures, pulmonary volumes, and pulmonary and systemic arterial-venous O-2 and CO2 differences increase. IR-type decreases, but R-type increases the mitral E/A ratio. PN-type produces the well-described, pseudo-normal mitral inflow pattern. All three types of LVDD reduce right ventricular (RV) and LV EF, but the latter remains normal or near normal. Simulations show reduced EF is partly restored by an accompanying increase in systolic stiffness, a compensatory mechanism that may lead clinicians to miss the presence of HF if they only consider LVEF and other indices of LV function. Simulations using the H-CRS model indicate that changes in RV function might well be diagnostic. This study also highlights the importance of septal mechanics in LVDD.Conclusion: The model demonstrates that abnormal LV diastolic performance alone can result in decreased LV and RV systolic performance, not previously appreciated, and contribute to the clinical syndrome of HF. Furthermore, alterations of RV diastolic performance are present and may be a hallmark of LV diastolic parameter changes that can be used for better clinical recognition of LV diastolic heart disease.