Numerical predictions of shear stress and cyclic stretch in pulmonary hypertension due to left heart failure

Bartolo, M; Qureshi, M. Umar; Colebank, Mitchel J.; Chesler, Naomi C.; Olufsen, Mette S.

doi:10.1007/s10237-021-01538-1

Cited by 19 publications

(15 citation statements)

References 71 publications

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“…Patients suffering from vascular disease such as PH could be at risk because pulmonary circulation, and especially ECs, are possible primary targets of inhaled NPs [36]. EC are subjected to hemodynamic forces, including shear stress and CS, which are increased in pulmonary arteries affected by PH [37]. Moreover, previous studies have shown that ECs are exposed to hypoxia, leading to endothelial dysfunction in hypoxemic PH [38].…”

Section: Discussionmentioning

confidence: 99%

NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction

et al. 2022

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The development and use of nanomaterials, especially of nickel oxide nanoparticles (NiONPs), is expected to provide many benefits but also has raised concerns about the potential human health risks. Inhaled NPs are known to exert deleterious cardiovascular side effects, including pulmonary hypertension. Consequently, patients with pulmonary hypertension (PH) could be at increased risk for morbidity. The objective of this study was to compare the toxic effects of NiONPs on human pulmonary artery endothelial cells (HPAEC) under physiological and pathological conditions. The study was conducted with an in vitro model mimicking the endothelial dysfunction observed in PH. HPAEC were cultured under physiological (static and normoxic) or pathological (20% cycle stretch and hypoxia) conditions and exposed to NiONPs (0.5–5 μg/cm2) for 4 or 24 h. The following endpoints were studied: (i) ROS production using CM-H2DCF-DA and MitoSOX probes, (ii) nitrite production by the Griess reaction, (iii) IL-6 secretion by ELISA, (iv) calcium signaling with a Fluo-4 AM probe, and (v) mitochondrial dysfunction with TMRM and MitoTracker probes. Our results evidenced that under pathological conditions, ROS and nitrite production, IL-6 secretions, calcium signaling, and mitochondria alterations increased compared to physiological conditions. Human exposure to NiONPs may be associated with adverse effects in vulnerable populations with cardiovascular risks.

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Section: Discussionmentioning

confidence: 99%

NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction

et al. 2022

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“…Recent computational modeling simulations from Bartolo et al suggest that physiological cyclic stretch is 15% to 20% in the pulmonary arteries and <5% in the capillaries and veins; in the setting of Ipc‐PH (an increase in LAP from 2 to 20 mm Hg), cyclic stretch is predicted to increase to up to 60% in the arteries, 10% in the capillaries, and 40% in the veins. 35 To understand the impact of these mechanical stimuli on biological changes in each cell type in the pulmonary vasculature, below we review key findings from in vitro studies examining the impact of cyclic stretch on ECs, SMCs, and fibroblasts, with the caveat that most of these studies use nonpulmonary cell sources. Table 1 provides the subset of these study results conducted using pulmonary vascular ECs, SMCs, and fibroblasts.…”

Section: Mechanotransduction Of Cyclic Stretch and Wssmentioning

confidence: 99%

“… 58 Bartolo et al predicted a 50% or more decrease in WSS in PH‐LHF from 10 to 25 dyn/cm 2 (in the healthy state) to 2 to 5 dyn/cm 2 (in PH‐LHF) using a computational fluid dynamics model. 35 Moreover, in humans with PH, computational fluid dynamics and phase‐contrast cardiac magnetic resonance imaging have demonstrated lower WSS in the proximal arteries than controls. 89 Pathological alterations in WSS activate EC mechanotransduction pathways, leading to a chronic proinflammatory state characterized by disorganized alignment, vasoconstriction, increased vascular permeability, and maladaptive ECM remodeling.…”

Section: Mechanotransduction Of Cyclic Stretch and Wssmentioning

confidence: 99%

Biomechanical and Mechanobiological Drivers of the Transition From PostCapillary Pulmonary Hypertension to Combined Pre−/PostCapillary Pulmonary Hypertension

Allen

Frye

Ramanathan

et al. 2023

JAHA

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Combined pre−/postcapillary pulmonary hypertension (Cpc‐PH), a complication of left heart failure, is associated with higher mortality rates than isolated postcapillary pulmonary hypertension alone. Currently, knowledge gaps persist on the mechanisms responsible for the progression of isolated postcapillary pulmonary hypertension (Ipc‐PH) to Cpc‐PH. Here, we review the biomechanical and mechanobiological impact of left heart failure on pulmonary circulation, including mechanotransduction of these pathological forces, which lead to altered biological signaling and detrimental remodeling, driving the progression to Cpc‐PH. We focus on pathologically increased cyclic stretch and decreased wall shear stress; mechanotransduction by endothelial cells, smooth muscle cells, and pulmonary arterial fibroblasts; and signaling‐stimulated remodeling of the pulmonary veins, capillaries, and arteries that propel the transition from Ipc‐PH to Cpc‐PH. Identifying biomechanical and mechanobiological mechanisms of Cpc‐PH progression may highlight potential pharmacologic avenues to prevent right heart failure and subsequent mortality.

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“…We compute wall shear stress (WSS) in the large vessels, i.e., the stress the fluid exerts on the vessel wall, denoted τ w (g/cm/s 2 ), by using the Stokes boundary layer given in equation ( 5) [4]. This results in the following equations:…”

Section: Wall Shear Stressmentioning

confidence: 99%

A computational study of aortic reconstruction in single ventricle patients

Taylor-LaPole¹,

Colebank²,

Weigand³

et al. 2022

Preprint

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Patients with hypoplastic left heart syndrome (HLHS) are born with an underdeveloped left heart. They typically receive a sequence of surgeries that result in a single ventricle physiology called the Fontan circulation. While these patients usually survive into early adulthood, they are at risk for medical complications, partially due to their lower than normal cardiac output, which leads to insufficient cerebral and gut perfusion. While clinical imaging data can provide detailed insight into cardiovascular function within

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Numerical predictions of shear stress and cyclic stretch in pulmonary hypertension due to left heart failure

Cited by 19 publications

References 71 publications

NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction

NiONP-Induced Oxidative Stress and Mitochondrial Impairment in an In Vitro Pulmonary Vascular Cell Model Mimicking Endothelial Dysfunction

Biomechanical and Mechanobiological Drivers of the Transition From PostCapillary Pulmonary Hypertension to Combined Pre−/PostCapillary Pulmonary Hypertension

A computational study of aortic reconstruction in single ventricle patients

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