Fecobionics in proctology: review and perspectives.

Fecobionics is a novel integrated technology for assessment of anorectal function. It is a defecatory test with simultaneous measurements of pressures, orientation, and device angle (a proxy of the anorectal angle). Furthermore, the latest Fecobionics prototypes measure diameters (shape) using impedance planimetry during evacuation of the device. The simultaneous measurement of multiple variables in the integrated test allows new metrics to be developed including more advanced novel defecation indices, enabling mechanistic insight in the defecation process at an unprecedented level in patients with anorectal disorders including patients suffering from obstructed defecation, fecal incontinence, and low anterior resection syndrome. The device has the consistency and shape of a normal stool (type 3-4 on the Bristol Stool Form Scale). Fecobionics has been validated on the bench and in animal studies and used in clinical trials to study defecation phenotypes in normal human subjects and patients with obstructed defecation, fecal incontinence, and low anterior resection syndrome after rectal cancer surgery. Subtypes have been defined, especially of patients with obstructed defecation. Furthermore, Fecobionics has been used to monitor biofeedback therapy in patients with fecal incontinence to predict the outcome of the therapy (responder versus non-responder). Most Fecobionics studies showed a closer correlation to symptoms as compared to current technologies for anorectal assessment. The present article outlines previous and ongoing work, and perspectives for future studies in proctology, including in physiological assessment of function, diagnostics, monitoring of therapy, and as a tool for biofeedback therapy.

New developments in defecatory studies based on biomechatronics.

Introduction: Defecation is a complex process that is difficult to study and analyze directly. In anorectal disease conditions, the defecation process may be disturbed, resulting in symptoms including fecal incontinence and constipation. Current state-of-the-art technology measures various aspects of anorectal function but detailed analysis is impossible because they are stand-alone tests rather than an integrated multi-dimensional test. Objectives: The need for physiologically-relevant and easy-to-use diagnostic tests for identifying underlying mechanisms is substantial. We aimed to advance the field with integrated technology for anorectal function assessment. Methods: We developed a simulated stool named Fecobionics that integrates several tests to assess defecation pressures, dimensions, shape, orientation and bending during evacuation. A novelty is that pressures are measured in axial direction, i.e. in the direction of the trajectory. Using this novel tool, we present new analytical methods to calculate physiologically relevant parameters during expulsion in normal human subjects. Results: Data are reported from 28 human subjects with progressively more advanced versions of Fecobionics. A new concept utilizes the rear-front pressure (preload-afterload) diagram for computation of novel defecation indices. Fecobionics obtained physiological data that cannot be obtained with current state-of-the-art technologies. Conclusion: Fecobionics measures well known parameters such as expulsion time and pressures as well as new metrics including defecation indices. The study suggests that Fecobionics is effective in evaluation of key defecatory parameters and well positioned as an integrated technology for assessment of anorectal function and dysfunction.

Novel bionics developments in gastroenterology: fecobionics assessment of lower GI tract function.

Biomechatronics (bionics) is an applied science that is interdisciplinary between biology and engineering (mechanical, electrical and electronics engineering). Biomechatronics covers a wide area and is probably best known in development of prosthetic limbs, vision aids, robotics and neuroscience. Although the gastrointestinal tract is difficult to study, it is particularly suited for a bionics approach as demonstrated by recent developments. Ingestible capsules that travel the tract and record physiological variables have been used in the clinic. Other examples include sacral nerve stimulators that seek to restore normal anorectal function. Recently, we developed a simulated stool termed fecobionics. It has the shape of normal stool and records a variety of parameters including pressures, bending (anorectal angle) and shape changes during colonic transit and defecation, i.e. it integrates several current tests. Fecobionics has been used to study defecation patterns in large animals as well as in humans (normal subjects and patient groups including patients with symptoms of obstructed defecation and fecal incontinence). Recently, it was applied in a canine colon model where it revealed patterns consistent with shallow waves originating from slow waves generated by the interstitial cells of Cajal. Furthermore, novel analysis such as the rear-front pressure (preload-afterload) diagram and quantification of defecation indices have been developed that enable mechanistic insight. This paper reviews the fecobionics technology and outlines perspectives for future applications.

Mechanical stimuli for left ventricular growth during pressure overload.

BACKGROUND: The mechanical stimulus (i.e. stress or stretch) for growth occurring in the pressure-overloaded left ventricle (LV) is not exactly known. OBJECTIVE: To address this issue, we investigate the correlation between local ventricular growth (indexed by local wall thickness) and the local acute changes in mechanical stimuli after aortic banding. METHODS: LV geometric data were extracted from 3D echo measurements at baseline and 2 weeks in the aortic banding swine model (n = 4). We developed and calibrated animal-specific finite element (FE) model of LV mechanics against pressure and volume waveforms measured at baseline. After the simulation of the acute effects of pressure-overload, the local changes of maximum, mean and minimum myocardial stretches and stresses in three orthogonal material directions (i.e., fiber, sheet and sheet-normal) over a cardiac cycle were quantified. Correlation between mechanical quantities and the corresponding measured local changes in wall thickness was quantified using the Pearson correlation number (PCN) and Spearman rank correlation number (SCN). RESULTS: At 2 weeks after banding, the average septum thickness decreased from 10.6 ± 2.92mm to 9.49 ± 2.02mm, whereas the LV free-wall thickness increased from 8.69 ± 1.64mm to 9.4 ± 1.22mm. The FE results show strong correlation of growth with the changes in maximum fiber stress (PCN = 0.5471, SCN = 0.5111) and changes in the mean sheet-normal stress (PCN= 0.5266, SCN = 0.5256). Myocardial stretches, however, do not have good correlation with growth. CONCLUSION: These results suggest that fiber stress is the mechanical stimuli for LV growth in pressure-overload.

Using machine learning to characterize heart failure across the scales.

Heart failure is a progressive chronic condition in which the heart undergoes detrimental changes in structure and function across multiple scales in time and space. Multiscale models of cardiac growth can provide a patient-specific window into the progression of heart failure and guide personalized treatment planning. Yet, the predictive potential of cardiac growth models remains poorly understood. Here, we quantify predictive power of a stretch-driven growth model using a chronic porcine heart failure model, subject-specific multiscale simulation, and machine learning techniques. We combine hierarchical modeling, Bayesian inference, and Gaussian process regression to quantify the uncertainty of our experimental measurements during an 8-week long study of volume overload in six pigs. We then propagate the experimental uncertainties from the organ scale through our computational growth model and quantify the agreement between experimentally measured and computationally predicted alterations on the cellular scale. Our study suggests that stretch is the major stimulus for myocyte lengthening and demonstrates that a stretch-driven growth model alone can explain [Formula: see text] of the observed changes in myocyte morphology. We anticipate that our approach will allow us to design, calibrate, and validate a new generation of multiscale cardiac growth models to explore the interplay of various subcellular-, cellular-, and organ-level contributors to heart failure. Using machine learning in heart failure research has the potential to combine information from different sources, subjects, and scales to provide a more holistic picture of the failing heart and point toward new treatment strategies.

Multiscale characterization of heart failure.

Dilated cardiomyopathy is a progressive irreversible disease associated with contractile dysfunction and heart failure. During dilated cardiomyopathy, elevated diastolic wall strains trigger mechanotransduction pathways that initiate the addition of sarcomeres in series and an overall increase in myocyte length. At the whole organ level, this results in a chronic dilation of the ventricles, an increase in end diastolic and end systolic volumes, and a decrease in ejection fraction. However, how exactly changes in sarcomere number translate into changes in myocyte morphology, and how these cellular changes translate into ventricular dilation remains incompletely understood. Here we combined a chronic animal study, continuum growth modeling, and machine learning to quantify correlations between sarcomere dynamics, myocyte morphology, and ventricular dilation. In an eight-week long volume overload study of six pigs, we found that the average sarcomere number increased by +3.8%/week, from 47 to 62, resulting in a myocyte lengthening of +3.3%/week, from 85 to 108 µm, while the sarcomere length and myocyte width remained unchanged. At the same time, the average end diastolic volume increased by +6.0%/week. Using continuum growth modeling and Bayesian inference, we correlated alterations on the subcellular, cellular, and organ scales and found that the serial sarcomere number explained 88% of myocyte lengthening, which, in turn, explained 54% of cardiac dilation. Our results demonstrate that sarcomere number and myocyte length are closely correlated and constitute the major determinants of dilated heart failure. We anticipate our study to be a starting point for more sophisticated multiscale models of heart failure. Our study suggests that altering sarcomere turnover-and with it myocyte morphology and ventricular dimensions-could be a potential therapeutic target to attenuate or reverse the progression of heart failure. STATEMENT OF SIGNIFICANCE: Heart failure is a significant global health problem that affects more than 25 million people worldwide and increases in prevalence as the population ages. Heart failure has been studied excessively at various scales; yet, there is no compelling concept to connect knowledge from the subcellular, cellular, and organ level across the scales. Here we combined a chronic animal study, continuum growth modeling, and machine learning to quantify correlations between sarcomere dynamics, myocyte morphology, and ventricular dilation. We found that the serial sarcomere number explained 88% of myocyte lengthening, which, in turn, explained 54% of cardiac dilation. Our results show that sarcomere number and myocyte length are closely correlated and constitute the major determinants of dilated heart failure. This suggests that altering the sarcomere turnover-and with it myocyte morphology and ventricular dimensions-could be a potential therapeutic target to attenuate or reverse heart failure.

Effect of intra-myocardial Algisyl-LVR™ injectates on fibre structure in porcine heart failure.

Recent preclinical trials have shown that alginate injections are a promising treatment for ischemic heart disease. Although improvements in heart function and global structure have been reported following alginate implants, the underlying structure is poorly understood. Using high resolution ex vivo MRI and DT-MRI of the hearts of normal control swine (n = 8), swine with induced heart failure (n = 5), and swine with heart failure and alginate injection treatment (n = 6), we visualized and quantified the fibre distribution and implant material geometry. Our findings show that the alginate injectates form solid ellipsoids with a retention rate of 68.7% ±â€¯21.3% (mean ±â€¯SD) and a sphericity index of 0.37 ±â€¯0.03. These ellipsoidal shapes solidified predominantly at the mid-wall position with an inclination of -4.9°â€¯±â€¯31.4° relative to the local circumferential direction. Overall, the change to left ventricular wall thickness and myofiber orientation was minor and was associated with heart failure and not the presence of injectates. These results show that alginate injectates conform to the pre-existing tissue structure, likely expanding along directions of least resistance as mass is added to the injection sites. The alginate displaces the myocardial tissue predominantly in the longitudinal direction, causing minimal disruption to the surrounding myofiber orientations.

Microstructure-based constitutive model of coronary artery with active smooth muscle contraction.

Currently, there is no full three-dimensional (3D) microstructural mechanical model of coronary artery based on measured microstructure including elastin, collagen and smooth muscle cells. Many structural models employ mean values of vessel microstructure, rather than continuous distributions of microstructure, to predict the mechanical properties of blood vessels. Although some models show good agreements on macroscopic vessel responses, they result in a lower elastin stiffness and earlier collagen recruitment. Hence, a full microstructural constitutive model is required for better understanding vascular biomechanics in health and disease. Here, a 3D microstructural model that accounts for all constituent microstructure is proposed to predict macroscopic and microscopic responses of coronary arteries. Coronary artery microstructural parameters were determined based on previous statistical measurements while mechanical testing of arteries (n = 5) were performed in this study to validate the computational predictions. The proposed model not only provides predictions of active and passive stress distributions of vessel wall, but also enables reliable estimations of material parameters of individual fibers and cells and thus predicts microstructural stresses. The validated microstructural model of coronary artery sheds light on vascular biomechanics and can be extend to diseased vessels for better understanding of initiation, progression and clinical treatment of vascular disease.

3D reconstruction of elastin fibres in coronary adventitia.

A 3D reconstruction of individual fibres in vascular tissue is necessary to understand the microstructure properties of the vessel wall.  The objective of this study is to determine the 3D microstructure of elastin fibres in the adventitia of coronary arteries.  Quantification of fibre geometry is challenging due to the complex interwoven structure of the fibres.  In particular, accurate linking of gaps remains a significant challenge, and complex features such as long gaps and interwoven fibres have not been adequately addressed by current fibre reconstruction algorithms.  We use a novel line Laplacian deformation method, which better deals with fibre shape uncertainty to reconstruct elastin fibres in the coronary adventitia of five swine. A cost function, based on entropy and Euler Spiral, was used in the shortest path search. We find that mean diameter of elastin fibres is 1.67 ± 1.42 µm and fibre orientation is clustered around two major angles of 8.9˚ and 81.8˚.  Comparing with CT-FIRE, we find that our method gives more accurate estimation of fibre width.  To our knowledge, the measurements obtained using our algorithm represent the first investigation focused on the reconstruction of full elastin fibre length.  Our data provide a foundation for a 3D microstructural model of the coronary adventitia to elucidate the structure-function relationship of elastin fibres.

Editor's Choice - Fluid-Structure Interaction Simulations of Aortic Dissection with Bench Validation.

INTRODUCTION: The blood flow and stresses in the flap in aortic dissections are not well understood. Validated fluid-structure interaction (FSI) simulations of the interactions between the blood flow and the flap will provide insight into the dynamics of aortic dissections and may lead to developments of novel therapeutic approaches. METHODS: A coupled, two-way blood flow and flap wall computational model was developed. The Arbitrary Lagrange-Eulerian method was used, which allowed the fluid mesh to deform. Inflow velocity waveforms from a pulse duplicator system were used in the simulations. RESULTS: The velocities for true lumen (TL) and false lumen (FL) were not significantly different between bench and simulation. The dynamics of the TL % cross-sectional area (CSA) during the cycle was similar between the bench and computational simulations, with the TL %CSA being most reduced near peak systole of the cycle. The experimental distal measurements had significantly lower velocities, likely due to the spatially heterogeneous flow distally. The conservation of mass and validity of simulations were confirmed. Additionally, regions of stress concentrations were found on the flap leading edge, towards the corners, and through the entire vessel wall. The pressure gradient across the FL results in a net force on the flap. CONCLUSION: The FSI flow velocities in the TL and the FL as well as the dynamics of the CSA during the cardiac cycle were validated by bench experiments. The validated FSI model may provide insights into aortic dissection including the stresses on the dissection flap and related flow disturbance, which may be subdued by novel therapeutic approaches. Simulations of more realistic human aortic dissections and the effects of current therapeutic approaches such as stent-graft can be developed in the future using the validated computational platform provided in the present study.

Mathematical modeling of cardiac growth and remodeling.

This review provides an overview of the current state of mathematical models of cardiac growth and remodeling (G&R). We concisely describe the experimental observations associated with cardiac G&R and discuss existing mathematical models that describe this process. To facilitate the discussion, we have organized the G&R models in terms of (1) the physical focus (biochemical vs mechanical) and (2) the process that they describe (myocyte hypertrophy vs extracellular matrix remodeling). The review concludes with a discussion of some possible directions that can advance the existing state of cardiac G&R mathematical modeling. WIREs Syst Biol Med 2016, 8:211-226. doi: 10.1002/wsbm.1330 For further resources related to this article, please visit the WIREs website.

Heterogeneous growth-induced prestrain in the heart.

Even when entirely unloaded, biological structures are not stress-free, as shown by Y.C. Fung׳s seminal opening angle experiment on arteries and the left ventricle. As a result of this prestrain, subject-specific geometries extracted from medical imaging do not represent an unloaded reference configuration necessary for mechanical analysis, even if the structure is externally unloaded. Here we propose a new computational method to create physiological residual stress fields in subject-specific left ventricular geometries using the continuum theory of fictitious configurations combined with a fixed-point iteration. We also reproduced the opening angle experiment on four swine models, to characterize the range of normal opening angle values. The proposed method generates residual stress fields which can reliably reproduce the range of opening angles between 8.7±1.8 and 16.6±13.7 as measured experimentally. We demonstrate that including the effects of prestrain reduces the left ventricular stiffness by up to 40%, thus facilitating the ventricular filling, which has a significant impact on cardiac function. This method can improve the fidelity of subject-specific models to improve our understanding of cardiac diseases and to optimize treatment options.

Chronic villitis of unknown etiology and massive chronic intervillositis have similar immune cell composition.

INTRODUCTION: Chronic villitis of unknown etiology (CVUE) and massive chronic intervillositis (MCI) are placental lesions associated with infiltration of mononuclear cells in the chorionic villi and the intervillous spaces, respectively. It is not well known whether immune cells in CVUE and MCI have similar phenotypic characteristics. METHODS: A cross-sectional study of third trimester placentas was conducted to identify immune cell subpopulations in CVUE and MCI (n = 17/group). CVUE was diagnosed with H&E staining and antibody to CD3 in serial sections; and MCI, by the presence of massive infiltration of mononuclear cells in the intervillous spaces. Immune cells, ICAM-1 expression and nuclear factor κB (NF-κB) activation were determined immunohistochemically. RESULTS: CVUE and MCI showed similar infiltrates, mainly CD68+ and CD3+ cells. Most cells (>80%) were CD45RB+, and one third were CD45RO+ in both lesions. There were slightly more CD8+ than CD4+ cells in both CVUE and MCI. More than 90% of cells in CVUE and MCI were ICAM-1+ with NFκB nuclear localization. Syncytiotrophoblast ICAM-1 expression was significantly (p < 0.001) higher in MCI (mean of 81.0; range of 71.6-86.0) than in CVUE (52.4; 36.4-59.4) or normal placentas (0.2; 0.0-0.6). Both, failure of physiologic transformation of spiral arteries and placental atherosclerosis-like lesions of atherosis were significantly more frequent in MCI than in CVUE or normal placentas (p = 0.044 and p = 0.007, respectively). DISCUSSION: These finding suggest that MCI and CVUE have very similar infiltration of immune cells although MCI has more severe placental lesions.

Characterization of a bioprosthetic bicuspid venous valve hemodynamics: implications for mechanism of valve dynamics.

BACKGROUND: Chronic venous insufficiency (CVI) of the lower extremities is a common clinical problem. Although bioprosthetic valves have been proposed to treat severe reflux, clinical success has been limited due to thrombosis and neointima overgrowth of the leaflets that is, in part, related to the hemodynamics of the valve. A bioprosthetic valve that mimics native valve hemodynamics is essential. METHODS: A computational model of the prosthetic valve based on realistic geometry and mechanical properties was developed to simulate the interaction of valve structure (fluid-structure interaction, FSI) with the surrounding flow. The simulation results were validated by experiments of a bioprosthetic bicuspid venous valve using particle image velocimetry (PIV) with high spatial and temporal resolution in a pulse duplicator (PD). RESULTS: Flow velocity fields surrounding the valve leaflets were calculated from PIV measurements and comparisons to the FSI simulation results were made. Both the spatial and temporal results of the simulations and experiments were in agreement. The FSI prediction of the transition point from equilibrium phase to valve-closing phase had a 7% delay compared to the PD measurements, while the PIV measurements matched the PD exactly. FSI predictions of reversed flow were within 10% compared to PD measurements. Stagnation or stasis regions were observed in both simulations and experiments. The pressure differential across the valve and associated forces on the leaflets from simulations showed the valve mechanism to be pressure driven. CONCLUSIONS: The flow velocity simulations were highly consistent with the experimental results. The FSI simulation and force analysis showed that the valve closure mechanism is pressure driven under the test conditions. FSI simulation and PIV measurements demonstrated that the flow behind the leaflet was mostly stagnant and a potential source for thrombosis. The validated FSI simulations should enable future valve design optimizations that are needed for improved clinical outcome.

Role of sinus in prosthetic venous valve.

BACKGROUND: The majority of bioprosthetic venous valves do not have a sinus pocket and, in practice, they are often placed in non-sinus segments of the veins. The aim of this study is to investigate the effect of the sinus pocket on the flow dynamics in a prosthetic valve. METHODS: A bench top in vitro experiment was set up at physiological flow conditions to simulate the flow inside a venous system. Bicuspid bioprosthetic valves with different leaflet lengths (5 and 10 mm) were tested in tubes with and without a sinus pocket and the flows around the valve were visualized by particle image velocimetry (PIV). Velocity data measurements were made and the vorticity was calculated in the with- and without-sinus set-ups. RESULTS: PIV measurements showed that vortex structure was maintained by the sinus. For the 10-mm leaflet length design with sinus, the jet width at the exit of the valve was 59% of that without sinus. For the 5-mm design with sinus, the jet width was 73% of the valve without sinus. Flow from the sinus region was entrained into the main jet observed near the exit of the sinus and altered the flow at the near wall region. CONCLUSIONS: The sinus pocket alters the flow around the valve and functions as flow regulator to smooth the flow pattern around the valve. The vortical structure inside the sinus is maintained at the valve leaflet tip during the valve cycle. For the prosthetic valve designated to be placed without a sinus, a shorter leaflet length is preferable and performs more closely to the valve with sinus.

Role of distension on duodenal and colonic contractility in mice: a novel myograph for intestines.

BACKGROUND: The role of mechanical distension (stretch and tension) on intestinal contractility is poorly understood. METHODS: We introduce a novel isovolumic myograph to quantify the intestinal contractility in response to mechanical stimulation. To evaluate the role of distension on contractility, an external restraint was used to restrict intestinal distension or stretch induced by inflation pressure. The amplitude of intraluminal pressure at isovolumic condition was defined as an index of intestinal contractility. KEY RESULTS: The in situ maximal contraction (1.42 ± 0.39 mmHg) of duodenum in response to inflation pressure was similar to the in vitro maximal contraction (1.39 ± 0.37 mmHg). As the pressure was increased, the in situ duodenal contraction attenuated faster than the in vitro one. The in situ maximal contraction (4.86 ± 1.32 mmHg) of distal colon in response to inflation pressure was significantly larger than the in vitro maximal contraction (2.31 ± 0.67 mmHg). With increase of pressure, the in situ colonic contractility (1.82 ± 0.87 mmHg) became similar to the in vitro counterpart (1.61 ± 0.98 mmHg). With restraint, the maximal contraction of duodenum and distal colon decreased from 4.86 ± 1.32 and 1.42 ± 0.39 mmHg to 2.91 ± 0.87 and 0.97 ± 0.29 mmHg, respectively. Finally, a significant linear relation was found between strain and amplitude of contraction for both duodenum and colon which became non-significant with restraint. CONCLUSIONS & INFERENCES: Our results suggest that distension is an important stimulus for intestinal contractility and nervous regulation is implicated in the intestinal contractility response to mechanical stimulus.

A linearized and incompressible constitutive model for arteries.

In many biomechanical studies, blood vessels can be modeled as pseudoelastic orthotropic materials that are incompressible (volume-preserving) under physiological loading. To use a minimum number of elastic constants to describe the constitutive behavior of arteries, we adopt a generalized Hooke's law for the co-rotational Cauchy stress and a recently proposed logarithmic-exponential strain. This strain tensor absorbs the material nonlinearity and its trace is zero for volume-preserving deformations. Thus, the relationships between model parameters due to the incompressibility constraint are easy to analyze and interpret. In particular, the number of independent elastic constants reduces from ten to seven in the orthotropic model. As an illustratory study, we fit this model to measured data of porcine coronary arteries in inflation-stretch tests. Four parameters, n (material nonlinearity), Young's moduli E1 (circumferential), E2 (axial), and E3 (radial) are necessary to fit the data. The advantages and limitations of this model are discussed.

New method to measure coronary velocity and coronary flow reserve.

Coronary flow reserve (CFR) is an important index of coronary microcirculatory function. The objective of this study was to validate the reproducibility and accuracy of intravascular conductance catheter-based method for measurements of baseline and hyperemic coronary flow velocity (and hence CFR). The absolute coronary blood velocity was determined by measuring the time of transit of a saline injection between two pairs of electrodes (known distance) on a conductance catheter during a routine saline injection without the need for reference flow. In vitro validation was made in the velocity range of 5 to 70 cm/s in reference to the volume collection method. In 10 swine, velocity measurements were compared with those from a flow probe in coronary arteries at different CFR attained by microsphere embolization. In vitro, the mean difference between the proposed method and volume collection was 0.7 ± 1.34 cm/s for steady flow and -0.77 ± 2.22 cm/s for pulsatile flow. The mean difference between duplicate measurements was 0 ± 1.4 cm/s. In in vivo experiments, the flow (product of velocity and lumen cross-sectional area that is also measured by the conductance catheter) was determined in both normal and stenotic vessels and the mean difference between the proposed method and flow probe was -1 ± 12 ml/min (flow ranged from 10 to 130 ml/min). For CFR, the mean difference between the two methods was 0.06 ± 0.28 (range of 1 to 3). Our results demonstrate the reproducibility and accuracy of velocity and CFR measurements with a conductance catheter by use of a standard saline injection. The ability of the combined measurement of coronary lumen area (as previously validated) and current velocity and CFR measurements provides an integrative diagnostic tool for interventional cardiology.

Impact of surgical ventricular restoration on ventricular shape, wall stress, and function in heart failure patients.

Surgical ventricular restoration (SVR) was designed to treat patients with aneurysms or large akinetic walls and dilated ventricles. Yet, crucial aspects essential to the efficacy of this procedure like optimal shape and size of the left ventricle (LV) are still debatable. The objective of this study is to quantify the efficacy of SVR based on LV regional shape in terms of curvedness, wall stress, and ventricular systolic function. A total of 40 patients underwent magnetic resonance imaging (MRI) before and after SVR. Both short-axis and long-axis MRI were used to reconstruct end-diastolic and end-systolic three-dimensional LV geometry. The regional shape in terms of surface curvedness, wall thickness, and wall stress indexes were determined for the entire LV. The infarct, border, and remote zones were defined in terms of end-diastolic wall thickness. The LV global systolic function in terms of global ejection fraction, the ratio between stroke work (SW) and end-diastolic volume (SW/EDV), the maximal rate of change of pressure-normalized stress (dσ*/dt(max)), and the regional function in terms of surface area change were examined. The LV end-diastolic and end-systolic volumes were significantly reduced, and global systolic function was improved in ejection fraction, SW/EDV, and dσ*/dt(max). In addition, the end-diastolic and end-systolic stresses in all zones were reduced. Although there was a slight increase in regional curvedness and surface area change in each zone, the change was not significant. Also, while SVR reduced LV wall stress with increased global LV systolic function, regional LV shape and function did not significantly improve.