An isogeometric analysis framework for ventricular cardiac mechanics

The finite element method (FEM) is commonly used in computational cardiac simulations. For this method, a mesh is constructed to represent the geometry and, subsequently, to approximate the solution. To accurately capture curved geometrical features many elements may be required, possibly leading to unnecessarily large computation costs. Without loss of accuracy, a reduction in computation cost can be achieved by integrating geometry representation and solution approximation into a single framework using the Isogeometric Analysis (IGA) paradigm. In this study, we propose an IGA framework suitable for echocardiogram data of cardiac mechanics, where we show the advantageous properties of smooth splines through the development of a multi-patch anatomical model. A nonlinear cardiac model is discretized following the IGA paradigm, meaning that the spline geometry parametrization is directly used for the discretization of the physical fields. The IGA model is benchmarked with a state-of-the-art biomechanics model based on traditional FEM. For this benchmark, the hemodynamic response predicted by the high-fidelity FEM model is accurately captured by an IGA model with only 320 elements and 4,700 degrees of freedom. The study is concluded by a brief anatomy-variation analysis, which illustrates the geometric flexibility of the framework. The IGA framework can be used as a first step toward an efficient workflow for an improved understanding of, and clinical decision support for, the treatment of cardiac diseases like heart rhythm disorders

Numerical simulation of blood flow and pressure drop in the pulmonary arterial and venous circulation

A novel multiscale mathematical and computational model of the pulmonary circulation is presented and used to analyse both arterial and venous pressure and flow. This work is a major advance over previous studies by Olufsen et al. (Ann Biomed Eng 28:1281–1299, 2012) which only considered the arterial circulation. For the first three generations of vessels within the pulmonary circulation, geometry is specified from patient-specific measurements obtained using magnetic resonance imaging (MRI). Blood flow and pressure in the larger arteries and veins are predicted using a nonlinear, cross-sectional-area-averaged system of equations for a Newtonian fluid in an elastic tube. Inflow into the main pulmonary artery is obtained from MRI measurements, while pressure entering the left atrium from the main pulmonary vein is kept constant at the normal mean value of 2 mmHg. Each terminal vessel in the network of ‘large’ arteries is connected to its corresponding terminal vein via a network of vessels representing the vascular bed of smaller arteries and veins. We develop and implement an algorithm to calculate the admittance of each vascular bed, using bifurcating structured trees and recursion. The structured-tree models take into account the geometry and material properties of the ‘smaller’ arteries and veins of radii ≥ 50 μ m. We study the effects on flow and pressure associated with three classes of pulmonary hypertension expressed via stiffening of larger and smaller vessels, and vascular rarefaction. The results of simulating these pathological conditions are in agreement with clinical observations, showing that the model has potential for assisting with diagnosis and treatment for circulatory diseases within the lung

Dependence of Intramyocardial Pressure and Coronary Flow on Ventricular Loading and Contractility: A Model Study

The phasic coronary arterial inflow during the normal cardiac cycle has been explained with simple (waterfall, intramyocardial pump) models, emphasizing the role of ventricular pressure. To explain changes in isovolumic and low afterload beats, these models were extended with the effect of three-dimensional wall stress, nonlinear characteristics of the coronary bed, and extravascular fluid exchange. With the associated increase in the number of model parameters, a detailed parameter sensitivity analysis has become difficult. Therefore we investigated the primary relations between ventricular pressure and volume, wall stress, intramyocardial pressure and coronary blood flow, with a mathematical model with a limited number of parameters. The model replicates several experimental observations: the phasic character of coronary inflow is virtually independent of maximum ventricular pressure, the amplitude of the coronary flow signal varies about proportionally with cardiac contractility, and intramyocardial pressure in the ventricular wall may exceed ventricular pressure. A parameter sensitivity analysis shows that the normalized amplitude of coronary inflow is mainly determined by contractility, reflected in ventricular pressure and, at low ventricular volumes, radial wall stress. Normalized flow amplitude is less sensitive to myocardial coronary compliance and resistance, and to the relation between active fiber stress, time, and sarcomere shortening velocity

Using progress feedback to enhance treatment outcomes: a narrative review

We face increasing demand for greater access to effective routine mental health services, including telehealth. However, treatment outcomes in routine clinical practice are only about half the size of those reported in controlled trials. Progress feedback, defined as the ongoing monitoring of patients’ treatment response with standardized measures, is an evidence-based practice that continues to be under-utilized in routine care. The aim of the current review is to provide a summary of the current evidence base for the use of progress feedback, its mechanisms of action and considerations for successful implementation. We reviewed ten available meta-analyses, which report small to medium overall effect sizes. The results suggest that adding feedback to a wide range of psychological and psychiatric interventions (ranging from primary care to hospitalization and crisis care) tends to enhance the effectiveness of these interventions. The strongest evidence is for patients with common mental health problems compared to those with very severe disorders. Effect sizes for not-on-track cases, a subgroup of cases that are not progressing well, are found to be somewhat stronger, especially when clinical support tools are added to the feedback. Systematic reviews and recent studies suggest potential mechanisms of action for progress feedback include focusing the clinician’s attention, altering clinician expectations, providing new information, and enhancing patient-centered communication. Promising approaches to strengthen progress feedback interventions include advanced systems with signaling technology, clinical problem-solving tools, and a broader spectrum of outcome and progress measures. An overview of methodological and implementation challenges is provided, as well as suggestions for addressing these issues in future studies. We conclude that while feedback has modest effects, it is a small and affordable intervention that can potentially improve outcomes in psychological interventions. Further research into mechanisms of action and effective implementation strategies is needed

Adaptive Volumetric Growth of the Heart

Introduction In response to changed mechanical loading conditions cardiac muscle is able to adapt its structure and geometry. One of the main adapative mechanisms is volumetric growth or atrophy of the cardiac heart wall. Better understanding of adaptive growth is needed to improve clinical treatment, e.g. in concentric hypertrophy or with cardiac pacing. Figure 1 : Echocardiographic short-axis images of left ventricle (LV). Left: Normal heart. Right: After 6 months of LV free wall pacing. The adaptive process leads to wall thinning at the pacing site (1) and wall thickening at the opposite site (2). Objective The objective of this study is to increase understanding of the volumetric growth process by numerical modeling and animal experiments. Numerical model Hypothesis: # Both the stimulus and the adaptive reponse act on the local level [1]. # The stimulus for growth is a strain related quantity [2].

Effect of ventricular contraction, pressure, and wall stretch on vessels at different locations in the wall

A cylindrical model of the heart was used to calculate the influence of ventricular filling and (isovolumic and isobaric) contraction on the cross-sectional area and resistance of a subendocardial and subepicardial maximally dilated arteriole and venule. Contraction is defined as the difference between static diastole and static systole. Furthermore, a small piece of rectangular myocardium containing the vessel was modeled to distinguish between the individual contributions of contractility (i.e., myocardial elastic properties), ventricular pressure, and local circumferential stretch to the changes in vascular area and resistance during contraction. Calculations were performed assuming the muscle fibers ran in either an apex-to-base or a circumferential direction. The results were similar for the two directions. Assuming constant, physiological arteriolar and venular pressures of 45 and 10 mmHg, respectively, coronary blood vessels were predicted not to collapse during ventricular contraction. Moreover, vascular area reduction was found to be larger for the arteriole (approximately 50%) than for the venule (approximately 30%) during both isovolumic and isobaric contractions. Consequently, arteriolar resistance was found to increase more than venular resistance (approximately 340 and 120%, respectively). Subendocardial area reductions were found to be somewhat smaller than subepicardial area reductions for the venule (by approximately 10%) but not for the arteriole. Contractility was found to be the main contributor to the changes in vascular area and resistance in the subepicardium but to contribute by <50% to the changes in the subendocardium. Because pressure does, but stretch does not, contribute to the area change during isovolumic contraction and the reverse is true during isobaric contraction, it was concluded that although changes in vascular area and resistance may be similar for different contractions, the causes for these changes are very different

Modeling the relation between cardiac pump fuction and myofiber mechanics

Abstract Complexity of the geometry and structure of the heart hampers easy modeling of cardiac mechanics. The modeling can however be simplified considerably when using the hypothesis that in the normal heart myofiber structure and geometry adapt, until load is evenly distributed. A simple and realistic relationship is found between the hemodynamic variables cavity pressure and volume, and myofiber load parameters stress and strain. The most important geometric parameter in the latter relation is the ratio of cavity volume to wall volume, while actual geometry appears practically irrelevant. Applying the found relationship, a realistic maximum is set to left ventricular pressure after chronic pressure load. Pressures exceeding this level are likely to cause decompensation and heart failure. Furthermore, model is presented to simulate left and right ventricular pump function with left-right interaction.