Cardiac Assist With a Twist: Apical Torsion as a Means to Improve Failing Heart Function

2011 ◽  
Vol 133 (10) ◽  
Author(s):  
Dennnis R. Trumble ◽  
Walter E. McGregor ◽  
Roy C. P. Kerckhoffs ◽  
Lewis K. Waldman

Changes in muscle fiber orientation across the wall of the left ventricle (LV) cause the apex of the heart to turn 10–15 deg in opposition to its base during systole and are believed to increase stroke volume and lower wall stress in healthy hearts. Studies show that cardiac torsion is sensitive to various disease states, which suggests that it may be an important aspect of cardiac function. Modern imaging techniques have sparked renewed interest in cardiac torsion dynamics, but no work has been done to determine whether mechanically augmented apical torsion can be used to restore function to failing hearts. In this report, we discuss the potential advantages of this approach and present evidence that turning the cardiac apex by mechanical means can displace a clinically significant volume of blood from failing hearts. Computational models of normal and reduced-function LVs were created to predict the effects of applied apical torsion on ventricular stroke work and wall stress. These same conditions were reproduced in anesthetized pigs with drug-induced heart failure using a custom apical torsion device programmed to rotate over various angles during cardiac systole. Simulations of applied 90 deg torsion in a prolate spheroidal computational model of a reduced-function pig heart produced significant increases in stroke work (25%) and stroke volume with reduced fiber stress in the epicardial region. These calculations were in substantial agreement with corresponding in vivo measurements. Specifically, the computer model predicted torsion-induced stroke volume increases from 13.1 to 14.4 mL (9.9%) while actual stroke volume in a pig heart of similar size and degree of dysfunction increased from 11.1 to 13.0 mL (17.1%). Likewise, peak LV pressures in the computer model rose from 85 to 95 mm Hg (11.7%) with torsion while maximum ventricular pressures in vivo increased in similar proportion, from 55 to 61 mm Hg (10.9%). These data suggest that: (a) the computer model of apical torsion developed for this work is a fair and accurate predictor of experimental outcomes, and (b) supra-physiologic apical torsion may be a viable means to boost cardiac output while avoiding blood contact that occurs with other assist methods.

2000 ◽  
Vol 279 (6) ◽  
pp. H3101-H3112 ◽  
Author(s):  
Giovanni Esposito ◽  
L. F. Santana ◽  
Keith Dilly ◽  
Jader Dos Santos Cruz ◽  
Lan Mao ◽  
...  

Heart failure and dilated cardiomyopathy develop in mice that lack the muscle LIM protein (MLP) gene (MLP−/−). The character and extent of the heart failure that occurs in MLP−/− mice were investigated using echocardiography and in vivo pressure-volume (P-V) loop measurements. P-V loop data were obtained with a new method for mice (sonomicrometry) using two pairs of orthogonal piezoelectric crystals implanted in the endocardial wall. Sonomicrometry revealed right-shifted P-V loops in MLP−/−mice, depressed systolic contractility, and additional evidence of heart failure. Cellular changes in MLP−/− mice were examined in isolated single cells using patch-clamp and confocal Ca2+ concentration ([Ca2+]) imaging techniques. This cellular investigation revealed unchanged Ca2+ currents and Ca2+ spark characteristics but decreased intracellular [Ca2+] transients and contractile responses and a defect in excitation-contraction coupling. Normal cellular and whole heart function was restored in MLP−/− mice that express a cardiac-targeted transgene, which blocks the function of β-adrenergic receptor (β-AR) kinase-1 (βARK1). These data suggest that, despite the persistent stimulus to develop heart failure in MLP−/− mice (i.e., loss of the structural protein MLP), downregulation and desensitization of the β-ARs may play a pivotal role in the pathogenesis. Furthermore, this work suggests that the inhibition of βARK1 action may prove an effective therapy for heart failure.


2020 ◽  
Vol 318 (2) ◽  
pp. H366-H377
Author(s):  
Jonathan Gold ◽  
Yohei Akazawa ◽  
Mei Sun ◽  
Kendall S. Hunter ◽  
Mark K. Friedberg

Right ventricle (RV) pressure loading can lead to RV fibrosis and dysfunction. We previously found increased RV, septal hinge-point and left ventricle (LV) fibrosis in experimental RV pressure loading. However, the relation of RV wall stress to biventricular fibrosis and dysfunction is incompletely defined. Rabbits underwent progressive pulmonary artery banding (PAB) over 3 wk with hemodynamics, echocardiography, and myocardial samples obtained at a terminal experiment at 6 wk. An additional group received PAB and treatment with an endothelin receptor antagonist. The endocardial and epicardial borders of short-axis echo images were traced and analyzed with invasive pressures to yield regional end-diastolic (ED) and end-systolic (ES) wall stress. To increase clinical translation, computer model-derived wall stress was compared with Laplace wall stress. The relation of wall stress with fibrosis (picrosirius red staining) and ventricular function was analyzed. ED wall stress in all regions and RV and LV free-wall ES wall stress were increased in PAB rabbits versus sham animals. Laplace wall stress correlated well with computational models. In PAB, fibrosis was highest in the RV free wall, then septal hinge regions, and lowest in the septum and LV free wall. Fibrosis was moderately related to ED ( r = 0.47, P = 0.0011), but not ES wall stress. RV ED wall stress was strongly related to echo indexes of function (strain rate: r = 0.71, P = 0.048; E′, r = −0.75, P = 0.0077; tricuspid annular plane systolic excursion: r = 0.85, P = 0.0038) and RV fractional area change ( r = 0.77, P = 0.027). ED, more than ES, wall stress is related moderately to fibrosis and strongly to function in experimental RV pressure loading, especially at the septal hinge-point regions, where fibrosis is prominent. This suggests that wall stress partially links RV pressure loading, fibrosis, and dysfunction and may be useful to follow clinically. NEW & NOTEWORTHY Biventricular fibrosis and dysfunction impact outcomes in RV pressure loading, but their relation to wall stress is poorly defined. Using a pulmonary artery band rabbit model, we entered echocardiography and catheter data into a computer model to yield regional end-diastolic (EDWS) and end-systolic (ESWS) wall stress. EDWS, more than ESWS, correlated with fibrosis and dysfunction, especially at the fibrosis-intense septal hinge-point regions. Thus, wall stress may be clinically useful in linking RV pressure loading to regional fibrosis and dysfunction.


Author(s):  
Xueying Huang ◽  
Chun Yang ◽  
Jie Zheng ◽  
Richard Bach ◽  
David Muccigrosso ◽  
...  

Atherosclerotic plaque rupture is the primary cause of cardiovascular clinical events such as heart attack and stroke. It is commonly believed that plaque rupture may be linked to critical mechanical conditions. Image-based computational models of vulnerable plaques have been introduced seeking critical mechanical indicators which may be used to identify potential sites of rupture [1–5]. A recent study by Tang et al. [4] using in vivo MRI-based 3D fluid-structure interaction (FSI) models for human carotid plaques with and without rupture reported that higher critical plaque wall stress (CPWS) values were associated with plaques with rupture, compared to those without rupture. However, existing computational plaque models are mostly for carotid plaques based on MRI data. Comparable similar studies for coronary plaques are lacking in the current literature. In this study, 3D computational multi-component models with FSI were constructed to identified 3D critical plaque wall stress, critical flow shear stress (CFSS) based on ex vivo MRI data of coronary plaques acquired from 10 patients. The patients were split into 2 groups: patients died in carotid artery disease (CAD, Group 1, 6 patients) and non CAD (Group 2, 4 patients). The possible link between CPWS and death in CAD was investigated by comparing the CPWS values from the two groups.


Author(s):  
Qingyu Wang ◽  
Dalin Tang ◽  
Liang Wang ◽  
Akiko Meahara ◽  
David Molony ◽  
...  

AbstractSeveral image-based computational models have been used to perform mechanical analysis for atherosclerotic plaque progression and vulnerability investigations. However, differences of computational predictions from those models have not been quantified at multi-patient level. In vivo intravascular ultrasound (IVUS) coronary plaque data were acquired from seven patients. Seven 2D/3D models with/without circumferential shrink, cyclic bending and fluid–structure interactions (FSI) were constructed for the seven patients to perform model comparisons and quantify impact of 2D simplification, circumferential shrink, FSI and cyclic bending plaque wall stress/strain (PWS/PWSn) and flow shear stress (FSS) calculations. PWS/PWSn and FSS averages from seven patients (388 slices for 2D and 3D thin-layer models) were used for comparison. Compared to 2D models with shrink process, 2D models without shrink process overestimated PWS by 17.26%. PWS change at location with greatest curvature change from 3D FSI models with/without cyclic bending varied from 15.07% to 49.52% for the seven patients (average = 30.13%). Mean Max-FSS, Min-FSS and Ave-FSS from the flow-only models under maximum pressure condition were 4.02%, 11.29% and 5.45% higher than those from full FSI models with cycle bending, respectively. Mean PWS and PWSn differences between FSI and structure-only models were only 4.38% and 1.78%. Model differences had noticeable patient variations. FSI and flow-only model differences were greater for minimum FSS predictions, notable since low FSS is known to be related to plaque progression. Structure-only models could provide PWS/PWSn calculations as good approximations to FSI models for simplicity and time savings in calculation.


2017 ◽  
Vol 114 (32) ◽  
pp. E6660-E6668 ◽  
Author(s):  
Francisco J. Flores ◽  
Katharine E. Hartnack ◽  
Amanda B. Fath ◽  
Seong-Eun Kim ◽  
Matthew A. Wilson ◽  
...  

General anesthesia (GA) is a reversible drug-induced state of altered arousal required for more than 60,000 surgical procedures each day in the United States alone. Sedation and unconsciousness under GA are associated with stereotyped electrophysiological oscillations that are thought to reflect profound disruptions of activity in neuronal circuits that mediate awareness and cognition. Computational models make specific predictions about the role of the cortex and thalamus in these oscillations. In this paper, we provide in vivo evidence in rats that alpha oscillations (10–15 Hz) induced by the commonly used anesthetic drug propofol are synchronized between the thalamus and the medial prefrontal cortex. We also show that at deep levels of unconsciousness where movement ceases, coherent thalamocortical delta oscillations (1–5 Hz) develop, distinct from concurrent slow oscillations (0.1–1 Hz). The structure of these oscillations in both cortex and thalamus closely parallel those observed in the human electroencephalogram during propofol-induced unconsciousness. During emergence from GA, this synchronized activity dissipates in a sequence different from that observed during loss of consciousness. A possible explanation is that recovery from anesthesia-induced unconsciousness follows a “boot-up” sequence actively driven by ascending arousal centers. The involvement of medial prefrontal cortex suggests that when these oscillations (alpha, delta, slow) are observed in humans, self-awareness and internal consciousness would be impaired if not abolished. These studies advance our understanding of anesthesia-induced unconsciousness and altered arousal and further establish principled neurophysiological markers of these states.


Author(s):  
Federica Boschetti ◽  
Elena Di Martino ◽  
Giancarlo Gioda

Computational models, developed to study abdominal aortic aneurysm (AAA) biomechanics, demonstrated that the presence of an intraluminal thrombus (ILT) can significantly alter the wall stress distribution in the degenerated vessel wall [1,2]. ILT is a soft hydrated tissue constituted of 90% of water. The solid porous matrix is made of a fibrin lattice entrapping solid aggregates, mostly platelets [3].. Although the ILT is subjected to compression in vivo, up to now ILT constitutive models have been based on parameters derived from tensile testing of ILT specimens [1]. The aim of this study was to define the biomechanical properties of ILT under compressive loads, using a combined experimental-numerical approach. ILT samples were tested for unconfined compression and permeation. A poroviscoelastic model was implemented to interpret the experimental data.


1986 ◽  
Vol 251 (1) ◽  
pp. R174-R180 ◽  
Author(s):  
E. A. Rhode ◽  
R. Elsner ◽  
T. M. Peterson ◽  
K. B. Campbell ◽  
W. Spangler

The mechanical properties of the radially enlarged proximal segment of the aorta of diving marine mammals was studied on 15 excised aortas of harbor seals and five aortas of Weddell seals. This was done by recording static pressure-volume relationships for the whole thoracic aorta, the aortic bulb, and the descending thoracic aorta and passive length-tension measurements of aortic strips. Aortic bulb volume distensibility was found to be much greater than that of the descending thoracic aorta or of an equivalent aortic segment of terrestrial mammals. The consequences were that the total potential energy and volume that may be stored within the aortic bulb is very large, with a capacity for storage of the stroke work of more than two normal heart beats and a volume of more than three times normal stroke volume. The aortic bulb has an average radius and wall thickness twice that of the descending aorta, but at any level of distension the wall stress (g/cm2) is the same throughout. The static mechanical properties of aortic strips from the bulb and descending thoracic aortas were not markedly different, so that the differences in the pressure-volume relationships are explained by differences in geometry of the two sections. The expanded aortic bulb functions through energy and volume storage actions and through uncoupling actions to maintain arterial pressures and stroke volume at near predive levels during a dive.


2020 ◽  
Vol 26 (18) ◽  
pp. 2167-2181
Author(s):  
Tatielle do Nascimento ◽  
Melanie Tavares ◽  
Mariana S.S.B. Monteiro ◽  
Ralph Santos-Oliveira ◽  
Adriane R. Todeschini ◽  
...  

Background: Cancer is a set of diseases formed by abnormal growth of cells leading to the formation of the tumor. The diagnosis can be made through symptoms’ evaluation or imaging tests, however, the techniques are limited and the tumor detection may be late. Thus, pharmaceutical nanotechnology has emerged to optimize the cancer diagnosis through nanostructured contrast agent’s development. Objective: This review aims to identify commercialized nanomedicines and patents for cancer diagnosis. Methods: The databases used for scientific articles research were Pubmed, Science Direct, Scielo and Lilacs. Research on companies’ websites and articles for the recognition of commercial nanomedicines was performed. The Derwent tool was applied for patent research. Results: This article aimed to research on nanosystems based on nanoparticles, dendrimers, liposomes, composites and quantum dots, associated to imaging techniques. Commercialized products based on metal and composite nanoparticles, associated with magnetic resonance and computed tomography, have been observed. The research conducted through Derwent tool displayed a small number of patents using nanotechnology for cancer diagnosis. Among these patents, the most significant number was related to the use of systems based on metal nanoparticles, composites and quantum dots. Conclusion: Although few systems are found in the market and patented, nanotechnology appears as a promising field for the development of new nanosystems in order to optimize and accelerate the cancer diagnosis.


2013 ◽  
Vol 28 (5) ◽  
pp. 1101-1116 ◽  
Author(s):  
Zhican Wang ◽  
Yvonne S Lin ◽  
Leslie J Dickmann ◽  
Emma-Jane Poulton ◽  
David L Eaton ◽  
...  

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