A Novel Rule-Based Algorithm for Assigning Myocardial Fiber Orientation to Computational Heart Models

Abstract

Electrical waves traveling throughout the myocardium elicit muscle contractions responsible for pumping blood throughout the body. The shape and direction of these waves depend on the spatial arrangement of ventricular myocytes, termed fiber orientation. In computational studies simulating electrical wave propagation or mechanical contraction in the heart, accurately representing fiber orientation is critical so that model predictions corroborate with experimental data. Typically, fiber orientation is assigned to heart models based on Diffusion Tensor Imaging (DTI) data, yet few alternative methodologies exist if DTI data is noisy or absent. Here we present a novel Laplace–Dirichlet Rule-Based (LDRB) algorithm to perform this task with speed, precision, and high usability. We demonstrate the application of the LDRB algorithm in an image-based computational model of the canine ventricles. Simulations of electrical activation in this model are compared to those in the same geometrical model but with DTI-derived fiber orientation. The results demonstrate that activation patterns from simulations with LDRB and DTI-derived fiber orientations are nearly indistinguishable, with relative differences ≤6%, absolute mean differences in activation times ≤3.15 ms, and positive correlations ≥0.99. These results convincingly show that the LDRB algorithm is a robust alternative to DTI for assigning fiber orientation to computational heart models.

Distinct Aspects of Left Ventricular Mechanical Function Are Differentially Associated With Cardiovascular Outcomes and All‐Cause Mortality in the Community

“…similarly observed in a study of HF patients that decrements in circumferential, rather than longitudinal, strain predicted recurrent HF events or death 12. Of all quantifiable LV strain measures, circumferential strain is felt to best represent function of the mesomyocardial fibers that are oriented circumferentially and located between the subendo‐ and epicardial layers of the ventricle 37. Impairments in myofiber contraction in all orientations are likely precursors of global pump dysfunction.…”

“…This finding is consistent with previous work demonstrating that alterations in longitudinal strain are associated with traditional risk factors for CHD (eg, hypertension) in the absence of overt disease31, 32, 33, 34; in turn, longitudinal strain is also considered among the most sensitive markers of active myocardial ischemia 35, 36. On echocardiography, longitudinal strain is measured along the endocardial surface of the LV cavity, in approximate alignment with the longitudinal orientation of myocardial fibers located along the subendocardial layers of the LV 37. Thus, echocardiographic longitudinal strain is considered the most sensitive measure of endocardial as well as subendocardial function, which is the myocardial layer of the ventricle considered most susceptible to stressors such as ischemia, mechanical stretch, and afterload resistance.…”

Optogenetic defibrillation terminates ventricular arrhythmia in mouse hearts and human simulations

“…The ventricular mesh had 2,110,030 points and 2,687,615 volumetric elements. Finally, myocardial fiber orientations were assigned throughout this mesh using a previously validated rules-based approach (42 , D = 0.292 mm, δ = 4.66 mm) (60). Relevant measurements of the mammalian pericardium were not found in the literature; thus, for the pericardium in our model, we used optical parameters reported for the human peritoneum (μ a = 0.0270 mm -1 , μ′ s = 1.83 mm -1 , D = 0.180 mm, δ = 2.56 mm) (61,62).…”

Influence of atrial contraction dynamics on cardiac function

“…The change in fibre angle across the wall leads to a twisting motion during ejection. Due to the highly structured nature of these fibres, and increasing numbers of measurements from histology and diffusion tensor MRI imaging (DTMRI), fully automated rule-based algorithms exist for accurately reproducing these fibre fields in the ventricles [26,15,3].…”