Computational modeling of the thermal effects of flow on radio frequency-induced heating of peripheral vascular stents during MRI.

Purpose. The goal of this study was to develop and validate a computational model that can accurately predict the influence of flow on the temperature rise near a peripheral vascular stent during magnetic resonance imaging (MRI).Methods. Computational modeling and simulation of radio frequency (RF) induced heating of a vascular stent during MRI at 3.0 T was developed and validated with flow phantom experiments. The maximum temperature rise of the stent was measured as a function of physiologically relevant flow rates.Results. A significant difference was not identified between the experiment and simulation (P > 0.05). The temperature rise of the stent during MRI was over 10 °C without flow, and was reduced by 5 °C with a flow rate of only 58 ml min-1, corresponding to a reduction of CEM43from 45 min to less than 1 min.Conclusion. The computer model developed in this study was validated with experimental measurements, and accurately predicted the influence of flow on the RF-induced temperature rise of a vascular stent during MRI. Furthermore, the results of this study demonstrate that relatively low flow rates significantly reduce the temperature rise of a stent and the surrounding medium during RF-induced heating under typical scanning power and physiologically relevant conditions.

A mechanistic motor-clutch model that explains cell shape dynamics to cyclic stretch.

Many cells in the body experience cyclic mechanical loading, which can impact cellular processes and morphology. In vitro studies often report that cells reorient in response to cyclic stretch of their substrate. To explore cellular mechanisms involved in this reorientation, a computational model was developed by adapting previous computational models of the actin-myosin-integrin motor-clutch system developed by others. The computational model predicts that under most conditions, actin bundles align perpendicular to the direction of applied cyclic stretch, but under specific conditions, such as low substrate stiffness, actin bundles align parallel to the direction of stretch. The model also predicts that stretch frequency impacts the rate of reorientation and that proper myosin function is critical in the reorientation response. These computational predictions are consistent with reports from the literature and new experimental results presented here. The model suggests that the impact of different stretching conditions (stretch type, amplitude, frequency, substrate stiffness, etc.) on the direction of cell alignment can largely be understood by considering their impact on cell-substrate detachment events, specifically whether detachments preferentially occur during stretching or relaxing of the substrate.

Coronary remodeling and biomechanics: Are we going with the flow in 2020?

Under normal conditions, coronary blood flow (CBF) provides critical blood supply to the myocardium so that it can appropriately meet the metabolic demands of the body. Dogmatically, there exist several known regulators and modulators of CBF that include local metabolites and neurohormonal factors that can influence the function of the coronary circulation. In disease states such as diabetes and myocardial ischemia, these regulators are impaired or shifted such that CBF is reduced. Although functional considerations have been and continued to be well studied, more recent evidence builds upon established studies that collectively suggest that the relative roles of coronary structure, biomechanics, and the influence of cardiac biomechanics via extravascular compression may also play a significant role in dictating CBF. In this mini review, we discuss these regulators of CBF under normal and pathophysiological conditions and their potential influence on the control of CBF.

ßIV-Spectrin/STAT3 complex regulates fibroblast phenotype, fibrosis, and cardiac function.

Increased fibrosis is a characteristic remodeling response to biomechanical and neurohumoral stress and a determinant of cardiac mechanical and electrical dysfunction in disease. Stress-induced activation of cardiac fibroblasts (CFs) is a critical step in the fibrotic response, although the precise sequence of events underlying activation of these critical cells in vivo remain unclear. Here, we tested the hypothesis that a ßIV-spectrin/STAT3 complex is essential for maintenance of a quiescent phenotype (basal nonactivated state) in CFs. We reported increased fibrosis, decreased cardiac function, and electrical impulse conduction defects in genetic and acquired mouse models of ßIV-spectrin deficiency. Loss of ßIV-spectrin function promoted STAT3 nuclear accumulation and transcriptional activity, and it altered gene expression and CF activation. Furthermore, we demonstrate that a quiescent phenotype may be restored in ßIV-spectrin-deficient fibroblasts by expressing a ßIV-spectrin fragment including the STAT3-binding domain or through pharmacological STAT3 inhibition. We found that in vivo STAT3 inhibition abrogates fibrosis and cardiac dysfunction in the setting of global ßIV-spectrin deficiency. Finally, we demonstrate that fibroblast-specific deletion of ßIV-spectrin is sufficient to induce fibrosis and decreased cardiac function. We propose that the ßIV-spectrin/STAT3 complex is a determinant of fibroblast phenotype and fibrosis, with implications for remodeling response in cardiovascular disease (CVD).

Biomechanics and Mechanobiology of Saphenous Vein Grafts.

Within several weeks of use as coronary artery bypass grafts (CABG), saphenous veins (SV) exhibit significant intimal hyperplasia (IH). IH predisposes vessels to thrombosis and atherosclerosis, the two major modes of vein graft failure. The fact that SV do not develop significant IH in their native venous environment coupled with the rapidity with which they develop IH following grafting into the arterial circulation suggests that factors associated with the isolation and preparation of SV and/or differences between the venous and arterial environments contribute to disease progression. There is strong evidence suggesting that mechanical trauma associated with traditional techniques of SV preparation can significantly damage the vessel and might potentially reduce graft patency though modern surgical techniques reduces these injuries. In contrast, it seems possible that modern surgical technique, specifically endoscopic vein harvest, might introduce other mechanical trauma that could subtly injure the vein and perhaps contribute to the reduced patency observed in veins harvested using endoscopic techniques. Aspects of the arterial mechanical environment influence remodeling of SV grafted into the arterial circulation. Increased pressure likely leads to thickening of the medial wall but its role in IH is less clear. Changes in fluid flow, including increased average wall shear stress, may reduce IH while disturbed flow likely increase IH. Nonmechanical stimuli, such as exposure to arterial levels of oxygen, may also have a significant but not widely recognized role in IH. Several potentially promising approaches to alter the mechanical environment to improve graft patency are including extravascular supports or altered graft geometries are covered.