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通过运动学建模解决“舒张期逆问题”可确定心室特性,并为舒张性心力衰竭提供机制性见解。

Solution of the 'inverse problem of diastole' via kinematic modeling allows determination of ventricular properties and provides mechanistic insights into diastolic heart failure.

作者信息

Kovács Sándor J

机构信息

Department of Internal Medicine, Washington University, St. Louis, MO 63110, USA.

出版信息

Annu Int Conf IEEE Eng Med Biol Soc. 2009;2009:2354-7. doi: 10.1109/IEMBS.2009.5335021.

DOI:10.1109/IEMBS.2009.5335021
PMID:19965185
Abstract

Because 50% of heart failure hospital admissions have diastolic heart failure (DHF) quantifying diastolic function (DF) has reached new prominence. Conventionally DF indices have been computed from shape-based features (height, duration, area) of Doppler waveforms such as the E-wave, (transmitral flow velocity), or E'-wave (mitral annular velocity) without regard to causal mechanisms. Solution of the 'inverse problem' has been achieved via the parametrized diastolic filling (PDF) formalism, a linear, kinematic model which treats the elastic, recoil-driven suction-pump attribute of the left ventricle as a damped simple harmonic oscillator (SHO). PDF uses the E-wave as input and generates stiffness (k), relaxation/ damping (c) and load (x(o)) as output. Scientific successes include the prediction that filling must be driven by a linear, bi-directional spring, later validated as a property of the giant cardiac protein titin, which generates a recoiling force at the cellular level in early diastole. Selected recent kinematic modeling achievements include: explanation why E-wave deceleration time must be determined jointly by stiffness (k) and relaxation (c), rather than by stiffness alone; LV equilibrium volume is the volume at diastasis; solution of the load-independent index of diastolic function (LIIDF) problem; solution of the isovolumic pressure decay (IVPD) problem. Clinical application reveals that contrary to dogma, chamber relaxation/viscoelasticity (PDF parameter c) rather than chamber stiffness (PDF parameter k) most often differentiates between controls vs. diastolic dysfunction subjects, thereby providing mechanistic insights into DHF.

摘要

由于50%的心力衰竭住院病例为舒张性心力衰竭(DHF),对舒张功能(DF)进行量化已变得格外重要。传统上,DF指标是根据多普勒波形(如E波,即跨二尖瓣血流速度,或E'波,即二尖瓣环速度)基于形状的特征(高度、持续时间、面积)计算得出的,而未考虑其因果机制。“逆问题”已通过参数化舒张期充盈(PDF)形式得以解决,这是一种线性运动学模型,将左心室的弹性、反冲驱动的抽吸泵属性视为一个阻尼简谐振荡器(SHO)。PDF以E波作为输入,并生成刚度(k)、松弛/阻尼(c)和负荷(xₒ)作为输出。该理论在科学上的成功之处包括预测充盈必须由线性双向弹簧驱动,后来这一特性在巨大的心脏蛋白肌联蛋白中得到验证,肌联蛋白在舒张早期在细胞水平产生反冲力。近期在运动学建模方面取得的成就包括:解释了为何E波减速时间必须由刚度(k)和松弛(c)共同决定,而非仅由刚度决定;左心室平衡容积是舒张末期容积;解决了舒张功能负荷无关指数(LIIDF)问题;解决了等容压力衰减(IVPD)问题。临床应用表明,与传统观念相反,心室舒张/粘弹性(PDF参数c)而非心室刚度(PDF参数k)最常区分对照组与舒张功能障碍患者,从而为DHF提供了机制上的见解。

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