The Living Heart Project: A robust and integrative simulator for human heart function

Abstract

The heart is not only our most vital, but also our most complex organ: Precisely controlled by the interplay of electrical and mechanical fields, it consists of four chambers and four valves, which act in concert to regulate its filling, ejection, and overall pump function. While numerous computational models exist to study either the electrical or the mechanical response of its individual chambers, the integrative electro-mechanical response of the whole heart remains poorly understood. Here we present a proof-of-concept simulator for a four-chamber human heart model created from computer topography and magnetic resonance images. We illustrate the governing equations of excitation-contraction coupling and discretize them using a single, unified finite element environment. To illustrate the basic features of our model, we visualize the electrical potential and the mechanical deformation across the human heart throughout its cardiac cycle. To compare our simulation against common metrics of cardiac function, we extract the pressure-volume relationship and show that it agrees well with clinical observations. Our prototype model allows us to explore and understand the key features, physics, and technologies to create an integrative, predictive model of the living human heart. Ultimately, our simulator will open opportunities to probe landscapes of clinical parameters, and guide device design and treatment planning in cardiac diseases such as stenosis, regurgitation, or prolapse of the aortic, pulmonary, tricuspid, or mitral valve.

Keywords: Abaqus; Cardiac mechanics; Electro-mechanics; Excitation-contraction; Finite element analysis.

Figure 1

Anatomic model of the human heart created from computer tomography and magnetic resonance images. The model displays the characteristic anatomic features: The aortic arch, the pulmonary artery, and the superior vena cava; the two upper chambers, the left and right atria; and the two lower chambers, the left and right ventricles; adopted with permission from [50].

Figure 2

Circulatory model of the human heart created from computer tomography and magnetic resonance images. The model displays the characteristic circulatory features: The tricuspid and mitral valves, which connect the right and left atria to the right and left ventricles; and the pulmonary and aortic valves, which connect the right and left ventricles to the pulmonary and systemic circulation; adopted with permission from [50].

Figure 3

Solid model of the human heart with anatomic details including the aortic arch, pulmonary artery and superior vena cava, left and right atria, and left and right ventricles.

Figure 4

Finite element model of the human heart discretized with 208,561 linear tetrahedral elements, 47,323 nodes, and 189,292 degrees of freedom, of which 47,323 are electrical and 141,969 are mechanical.

Figure 5

Muscle fiber model of the human heart with 208,561 discrete fiber and sheet directions interpolated and assigned to each integration point.

Figure 6

Blood flow model of the human heart with surface-based fluid cavity representation of the right atrium, right ventricle, left atrium, and left ventricle connected through viscous resistance models of Windkessel type for the tricuspid valve, pulmonary circulation, mitral valve, aortic valve, and systemic circulation.

Figure 7

Spatio-temporal evolution of electrical potential, mechanical deformation, and muscle fiber strain across the human heart. During systole, the heart depolarizes rapidly from −80mV to +20mV, the muscle fibers contract and shorten up to 20% to induce ventricular ejection. During diastole, the heart repolarizes gradually from +20mV to −80mV, the muscle fibers relax and relengthen to their initial length to induce ventricular filling.

Figure 8

Temporal evolution of electrical potential. During excitation, cardiac cells rapidly depolarize and the electrical potential increases from −80mV to +20mV within the order of milliseconds. During relaxation, cardiac cells gradually repolarize and return to the stable baseline state at −80mV.

Figure 9

Temporal evolution of long-axis shortening. During ventricular ejection, the distance between apex and base decreases rapidly as the ventricles shorten by approximately 7mm. During ventricular filling, the long axis gradually returns to its initial length as the heart muscle relaxes.

Figure 10

Pressure-volume loop of the human heart with characteristic phases of ventricular filling, isovolumetric contraction, ventricular ejection, and isovolumetric relaxation. The enclosed area characterizes the work performed throughout the cardiac cycle.