Journal articles: 'Pulmonary artery stiffne'

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LI, LIN, LIN HUA, HAIXIA ZHANG, and ZHICHENG LIU. "DIFFERENCES BETWEEN PULMONARY ARTERIAL AND AORTIC MATERIAL PROPERTIES." Journal of Mechanics in Medicine and Biology 15, no. 03 (June 2015): 1550019. http://dx.doi.org/10.1142/s0219519415500190.

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To investigate the differences of mechanical responses between pulmonary artery and aorta to different biaxial loading conditions, we simulated the process of human pulmonary artery and aorta subjected to biaxial loading based on four-family fiber strain density function model determined from uniaxial extension data of arterial walls. It was shown that different stress–strain curves of pulmonary artery and aorta under biaxial loading conditions: different loading ratios between the loads in two perpendicular directions and displacement-controlled equibiaxial stretch. Tissue stiffness, defined as the first derivative of the stress–strain response at a strain point, of human pulmonary artery and aorta were obtained when they were subjected to biaxial loads (systemic pressure). The two-dimensional mechanical response of artery can be acquired by determination of the four-family fiber strain density function model of the tissue based on uniaxial extensile data. There are differences between material properties of pulmonary artery and aorta: aorta is stiffer circumferentially than longitudinally, and pulmonary artery is more compliant circumferentially than longitudinally.

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Lammers, Steven R., Phil H. Kao, H. Jerry Qi, Kendall Hunter, Craig Lanning, Joseph Albietz, Stephen Hofmeister, Robert Mecham, Kurt R. Stenmark, and Robin Shandas. "Changes in the structure-function relationship of elastin and its impact on the proximal pulmonary arterial mechanics of hypertensive calves." American Journal of Physiology-Heart and Circulatory Physiology 295, no. 4 (October 2008): H1451—H1459. http://dx.doi.org/10.1152/ajpheart.00127.2008.

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Extracellular matrix remodeling has been proposed as one mechanism by which proximal pulmonary arteries stiffen during pulmonary arterial hypertension (PAH). Although some attention has been paid to the role of collagen and metallomatrix proteins in affecting vascular stiffness, much less work has been performed on changes in elastin structure-function relationships in PAH. Such work is warranted, given the importance of elastin as the structural protein primarily responsible for the passive elastic behavior of these conduit arteries. Here, we study structure-function relationships of fresh arterial tissue and purified arterial elastin from the main, left, and right pulmonary artery branches of normotensive and hypoxia-induced pulmonary hypertensive neonatal calves. PAH resulted in an average 81 and 72% increase in stiffness of fresh and digested tissue, respectively. Increase in stiffness appears most attributable to elevated elastic modulus, which increased 46 and 65%, respectively, for fresh and digested tissue. Comparison between fresh and digested tissues shows that, at 35% strain, a minimum of 48% of the arterial load is carried by elastin, and a minimum of 43% of the change in stiffness of arterial tissue is due to the change in elastin stiffness. Analysis of the stress-strain behavior revealed that PAH causes an increase in the strains associated with the physiological pressure range but had no effect on the strain of transition from elastin-dominant to collagen-dominant behavior. These results indicate that mechanobiological adaptations of the continuum and geometric properties of elastin, in response to PAH, significantly elevate the circumferential stiffness of proximal pulmonary arterial tissue.

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Mulchrone, A., H. Moulton, M. W. Eldridge, and N. C. Chesler. "Susceptibility to high-altitude pulmonary edema is associated with increased pulmonary arterial stiffness during exercise." Journal of Applied Physiology 128, no. 3 (March 1, 2020): 514–22. http://dx.doi.org/10.1152/japplphysiol.00153.2019.

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High-altitude pulmonary edema (HAPE), a reversible form of capillary leak, is a common consequence of rapid ascension to high altitude and a major cause of death related to high-altitude exposure. Individuals with a prior history of HAPE are more susceptible to future episodes, but the underlying risk factors remain uncertain. Previous studies have shown that HAPE-susceptible subjects have an exaggerated pulmonary vasoreactivity to acute hypoxia, but incomplete data are available regarding their vascular response to exercise. To examine this, seven HAPE-susceptible subjects and nine control subjects (HAPE-resistant) were studied at rest and during incremental exercise at sea level and at 3,810 m altitude. Studies were conducted in both normoxic (inspired Po2 = 148 Torr) and hypoxic (inspired Po2 = 91 Torr) conditions at each location. Here, we report an expanded analysis of previously published data, including a distensible vessel model that showed that HAPE-susceptible subjects had significantly reduced small distal artery distensibility at sea level compared with HAPE-resistant control subjects [0.011 ± 0.001 vs. 0.021 ± 0.002 mmHg−1; P < 0.001). Moreover, HAPE-susceptible subjects demonstrated constant distensibility over all conditions, suggesting that distal arteries are maximally distended at rest. Consistent with having increased distal artery stiffness, HAPE-susceptible subjects had greater increases in pulmonary artery pulse pressure with exercise, which suggests increased proximal artery stiffness. In summary, HAPE-susceptible subjects have exercise-induced increases in proximal artery stiffness and baseline increases in distal artery stiffness, suggesting increased pulsatile load on the right ventricle. NEW & NOTEWORTHY In comparison to subjects who appear resistant to high-altitude pulmonary edema, those previously symptomatic show greater increases in large and small artery stiffness in response to exercise. These differences in arterial stiffness may be a risk factor for the development of high-altitude pulmonary edema or evidence that consequences of high-altitude pulmonary edema are long-lasting after return to sea level.

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Stack, Alice, Frederik J. Derksen, Kurt J. Williams, N. Edward Robinson, and William F. Jackson. "Lung region and racing affect mechanical properties of equine pulmonary microvasculature." Journal of Applied Physiology 117, no. 4 (August 15, 2014): 370–76. http://dx.doi.org/10.1152/japplphysiol.00314.2014.

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Exercise-induced pulmonary hemorrhage is a performance-limiting condition of racehorses associated with severe pathology, including small pulmonary vein remodeling. Pathology is limited to caudodorsal (CD) lung. Mechanical properties of equine pulmonary microvasculature have not been studied. We hypothesized that regional differences in pulmonary artery and vein mechanical characteristics do not exist in control animals, and that racing and venous remodeling impact pulmonary vein mechanical properties in CD lung. Pulmonary arteries and veins [range of internal diameters 207–386 ± 67 μm (mean ± SD)] were harvested from eight control and seven raced horses. With the use of wire myography, CD and cranioventral (CV) vessels were stretched in 10-μm increments. Peak wall tension was plotted against changes in diameter (length). Length-tension data were compared between vessel type, lung region, and horse status (control and raced). Pulmonary veins are stiffer walled than arteries. CD pulmonary arteries are stiffer than CV arteries, whereas CV veins are stiffer than CD veins. Racing is associated with increased stiffness of CD pulmonary veins and, to a lesser extent, CV arteries. For example, at 305 μm, tension in raced and control CD veins is 27.74 ± 2.91 and 19.67 ± 2.63 mN/mm (means ± SE; P < 0.05, Bonferroni's multiple-comparisons test after two-way ANOVA), and 16.12 ± 2.04 and 15.07 ± 2.47 mN/mm in raced and control CV arteries, respectively. This is the first report of an effect of region and/or exercise on mechanical characteristics of small pulmonary vessels. These findings may implicate pulmonary vein remodeling in exercise-induced pulmonary hemorrhage pathogenesis.

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Nemes, Attila, and Tamás Forster. "Evaluation of pulmonary arterial stiffness using routine clinical imaging methods." Orvosi Hetilap 154, no. 49 (December 2013): 1931–33. http://dx.doi.org/10.1556/oh.2013.29767.

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Recently, there has been much debate about pulmonary hypertension due to modern therapeutic options available. Arterial hypertension is frequently associated with stiffening of a given artery. The aim of the present review is to present clinical imaging methods for the evaluation of the function and stiffness of the pulmonary artery. Orv. Hetil., 154(49), 1931–1933.

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Su, Junjing, Alun D. Hughes, Ulf Simonsen, Jens Erik Nielsen-Kudsk, Kim H. Parker, Luke S. Howard, and Soren Mellemkjaer. "Impact of pulmonary endarterectomy on pulmonary arterial wave propagation and reservoir function." American Journal of Physiology-Heart and Circulatory Physiology 317, no. 3 (September 1, 2019): H505—H516. http://dx.doi.org/10.1152/ajpheart.00181.2019.

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High wave speed and large wave reflection in the pulmonary artery have previously been reported in patients with chronic thromboembolic pulmonary hypertension (CTEPH). We assessed the impact of pulmonary endarterectomy (PEA) on pulmonary arterial wave propagation and reservoir function in patients with CTEPH. Right heart catheterization was performed using a combined pressure and Doppler flow sensor-tipped guidewire to obtain simultaneous pressure and flow velocity measurements in the pulmonary artery in eight patients with CTEPH before and 3 mo after PEA. Wave intensity and reservoir-excess pressure analyses were then performed. Following PEA, mean pulmonary arterial pressure (PAPm; ∼49 vs. ∼32 mmHg), pulmonary vascular resistance (PVR; ∼11.1 vs. ∼5.1 Wood units), and wave speed (∼16.5 vs. ∼8.1 m/s), i.e., local arterial stiffness, markedly decreased. The changes in the intensity of the reflected arterial wave and wave reflection index (pre: ∼28%; post: ∼22%) were small, and patients post-PEA with and without residual pulmonary hypertension (i.e., PAPm ≥ 25 mmHg) had similar wave reflection index (∼20 vs. ∼23%). The reservoir and excess pressure decreased post-PEA, and the changes were associated with improved right ventricular afterload, function, and size. In conclusion, although PVR and arterial stiffness decreased substantially following PEA, large wave reflection persisted, even in patients without residual pulmonary hypertension, indicating lack of improvement in vascular impedance mismatch. This may continue to affect the optimal ventriculoarterial interaction, and further studies are warranted to determine whether this contributes to persistent symptoms in some patients. NEW & NOTEWORTHY We performed wave intensity analysis in the pulmonary artery in patients with chronic thromboembolic pulmonary hypertension before and 3 mo after pulmonary endarterectomy. Despite substantial reduction in pulmonary arterial pressures, vascular resistance, and arterial stiffness, large pulmonary arterial wave reflection persisted 3 mo postsurgery, even in patients without residual pulmonary hypertension, suggestive of lack of improvement in vascular impedance mismatch.

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Woodcock, Chen-Shan Chen, Neha Hafeez, Adam Handen, Ying Tang, Lloyd D. Harvey, Leonard E. Estephan, Gil Speyer, Seungchan Kim, Thomas Bertero, and Stephen Y. Chan. "Matrix stiffening induces a pathogenic QKI-miR-7-SRSF1 signaling axis in pulmonary arterial endothelial cells." American Journal of Physiology-Lung Cellular and Molecular Physiology 320, no. 5 (May 1, 2021): L726—L738. http://dx.doi.org/10.1152/ajplung.00407.2020.

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Pulmonary arterial hypertension (PAH) refers to a set of heterogeneous vascular diseases defined by elevation of pulmonary arterial pressure (PAP) and pulmonary vascular resistance (PVR), leading to right ventricular (RV) remodeling and often death. Early increases in pulmonary artery stiffness in PAH drive pathogenic alterations of pulmonary arterial endothelial cells (PAECs), leading to vascular remodeling. Dysregulation of microRNAs can drive PAEC dysfunction. However, the role of vascular stiffness in regulating pathogenic microRNAs in PAH is incompletely understood. Here, we demonstrated that extracellular matrix (ECM) stiffening downregulated miR-7 levels in PAECs. The RNA-binding protein quaking (QKI) has been implicated in the biogenesis of miR-7. Correspondingly, we found that ECM stiffness upregulated QKI, and QKI knockdown led to increased miR-7. Downstream of the QKI-miR-7 axis, the serine and arginine-rich splicing factor 1 (SRSF1) was identified as a direct target of miR-7. Correspondingly, SRSF1 was reciprocally upregulated in PAECs exposed to stiff ECM and was negatively correlated with miR-7. Decreased miR-7 and increased QKI and SRSF1 were observed in lungs from patients with PAH and PAH rats exposed to SU5416/hypoxia. Lastly, miR-7 upregulation inhibited human PAEC migration, whereas forced SRSF1 expression reversed this phenotype, proving that miR-7 depended upon SRSF1 to control migration. In aggregate, these results define the QKI-miR-7-SRSF1 axis as a mechanosensitive mechanism linking pulmonary arterial vascular stiffness to pathogenic endothelial function. These findings emphasize implications relevant to PAH and suggest the potential benefit of developing therapies that target this miRNA-dependent axis in PAH.

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Gan, C. Tji-Joong, Jan-Willem Lankhaar, Nico Westerhof, J. Tim Marcus, Annemarie Becker, Jos W. R. Twisk, Anco Boonstra, Pieter E. Postmus, and Anton Vonk-Noordegraaf. "Noninvasively Assessed Pulmonary Artery Stiffness Predicts Mortality in Pulmonary Arterial Hypertension." Chest 132, no. 6 (December 2007): 1906–12. http://dx.doi.org/10.1378/chest.07-1246.

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Dodson, R. Blair, Matthew R. Morgan, Csaba Galambos, Kendall S. Hunter, and Steven H. Abman. "Chronic intrauterine pulmonary hypertension increases main pulmonary artery stiffness and adventitial remodeling in fetal sheep." American Journal of Physiology-Lung Cellular and Molecular Physiology 307, no. 11 (December 1, 2014): L822—L828. http://dx.doi.org/10.1152/ajplung.00256.2014.

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Persistent pulmonary hypertension of the newborn (PPHN) is a clinical syndrome that is characterized by high pulmonary vascular resistance due to changes in lung vascular growth, structure, and tone. PPHN has been primarily considered as a disease of the small pulmonary arteries (PA), but proximal vascular stiffness has been shown to be an important predictor of morbidity and mortality in other diseases associated with pulmonary hypertension (PH). The objective of this study is to characterize main PA (MPA) stiffness in experimental PPHN and to determine the relationship of altered biomechanics of the MPA with changes in extracellular matrix (ECM) content and orientation of collagen and elastin fibers. MPAs were isolated from control and PPHN fetal sheep model and were tested by planar biaxial testing to measure stiffness in circumferential and axial vessel orientations. Test specimens were fixed for histological assessments of the vascular wall ECM constituents collagen and elastin. MPAs from PPHN sheep had increased mechanical stiffness ( P < 0.05) and altered ECM remodeling compared with control MPA. A constitutive mathematical model and histology demonstrated that PPHN vessels have a smaller contribution of elastin and a greater role for collagen fiber engagement compared with the control arteries. We conclude that exposure to chronic hemodynamic stress in late-gestation fetal sheep increases proximal PA stiffness and alters ECM remodeling. We speculate that proximal PA stiffness further contributes to increased right ventricular impedance in experimental PPHN, which contributes to abnormal transition of the pulmonary circulation at birth.

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Stevens, Gerin R., Ana Garcia-Alvarez, Sheila Sahni, Mario J. Garcia, Valentin Fuster, and Javier Sanz. "RV Dysfunction In Pulmonary Hypertension Is Independently Related To Pulmonary Artery Stiffness." JACC: Cardiovascular Imaging 5, no. 4 (April 2012): 378–87. http://dx.doi.org/10.1016/j.jcmg.2011.11.020.

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Sanz, Javier, Mbabazi Kariisa, Santo Dellegrottaglie, Susanna Prat-González, Mario J. Garcia, Valentin Fuster, and Sanjay Rajagopalan. "Evaluation of Pulmonary Artery Stiffness in Pulmonary Hypertension With Cardiac Magnetic Resonance." JACC: Cardiovascular Imaging 2, no. 3 (March 2009): 286–95. http://dx.doi.org/10.1016/j.jcmg.2008.08.007.

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Şahinli, Hayriye, Mustafa Gökhan Vural, and Göksal Keskin. "Evaluation of pulmonary artery stiffness patients with Behcet's disease." Ortadoğu Tıp Dergisi 11, no. 1 (March 31, 2019): 22–26. http://dx.doi.org/10.21601/ortadogutipdergisi.433615.

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Alberti, Elena, Luca Stucchi, Chiara Maria Lo Feudo, Francesco Ferrucci, and Enrica Zucca. "Feasibility of Echocardiographic Estimation of Pulmonary Artery Stiffness in Horses." Journal of Equine Veterinary Science 112 (May 2022): 103921. http://dx.doi.org/10.1016/j.jevs.2022.103921.

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Huang, FeiQiong, and Tan Ru San. "GW24-e0413 Pulmonary artery stiffness in patients with heart failure." Heart 99, Suppl 3 (August 2013): A214.1—A214. http://dx.doi.org/10.1136/heartjnl-2013-304613.598.

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Luehrs, Rachel E., John D. Newell, Alejandro P. Comellas, Eric A. Hoffman, Kelsey Warner, Anna Croghan, Lyndsey E. DuBose, et al. "CT-measured lung air-trapping is associated with higher carotid artery stiffness in individuals with chronic obstructive pulmonary disease." Journal of Applied Physiology 125, no. 6 (December 1, 2018): 1760–66. http://dx.doi.org/10.1152/japplphysiol.00580.2018.

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Early stages of chronic obstructive pulmonary disease (COPD) are characterized by the loss and narrowing of terminal bronchioles in the lung, resulting in “air-trapping,” often occurring before overt emphysema manifests. Individuals with an airway-predominant phenotype of COPD display extensive lung air-trapping and are at greater cardiovascular disease (CVD) risk than COPD patients with an emphysema-predominant phenotype. We hypothesized that the degree of computed tomography (CT)-quantified lung air-trapping would be associated with greater aortic and carotid artery stiffness and lower endothelial function, known biomarkers of CVD risk. Lung air-trapping was associated with greater aortic stiffness (carotid femoral pulse wave velocity, CFPWV) ( r = 0.60, P = 0.007) and carotid β-stiffness ( r = 0.75, P = 0.0001) among adults with ( n = 10) and without ( n = 9) a clinical diagnosis of COPD and remained significant after adjusting for blood pressure (BP) and smoking history (pack-years) (carotid β-stiffness: r = 0.68, P < 0.01; CFPWV r = 0.53, P = 0.03). The association between lung air-trapping and carotid β-stiffness remained significant after additionally adjusting for age and forced expiratory volume 1(FEV1) ( r = 0.64, P = 0.01). In the COPD group only ( n = 10), lung air-trapping remained associated with carotid β-stiffness ( r = 0.82, P = 0.05) after adjustment for age, pack-years, and FEV1. In contrast, no association was observed between CFPWV and lung air-trapping after adjustment for BP, pack-years, age, and FEV1 ( r = 0.12, P = 0.83). Lung air-trapping was not associated with endothelial function (brachial artery flow-mediated dilation) in the entire cohort ( P = 0.80) or in patients with COPD only ( P = 0.71). These data suggest that carotid artery stiffness may be a mechanism explaining the link between airway-predominant phenotypes of COPD and high CVD risk. NEW & NOTEWORTHY Previous cross-sectional studies have demonstrated greater large elastic artery stiffness and lower endothelium-dependent dilation in chronic obstructive pulmonary disease (COPD) patients compared with controls. Furthermore, COPD patients with emphysema have greater aortic stiffness than non-COPD controls, and the degree of stiffness is associated with emphysema severity. The present study is the first to demonstrate that even before overt emphysema manifests, lung air-trapping is associated with carotid artery stiffness in COPD patients independent of blood pressure, age, or smoking history.

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Lau, Edmund M. T., Nithin Iyer, Rahn Ilsar, Brian P. Bailey, Mark R. Adams, and David S. Celermajer. "Abnormal Pulmonary Artery Stiffness in Pulmonary Arterial Hypertension: In Vivo Study with Intravascular Ultrasound." PLoS ONE 7, no. 3 (March 30, 2012): e33331. http://dx.doi.org/10.1371/journal.pone.0033331.

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Thenappan, Thenappan, Stephen Y. Chan, and E. Kenneth Weir. "Role of extracellular matrix in the pathogenesis of pulmonary arterial hypertension." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 5 (November 1, 2018): H1322—H1331. http://dx.doi.org/10.1152/ajpheart.00136.2018.

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Pulmonary arterial hypertension (PAH) is characterized by remodeling of the extracellular matrix (ECM) of the pulmonary arteries with increased collagen deposition, cross-linkage of collagen, and breakdown of elastic laminae. Extracellular matrix remodeling occurs due to an imbalance in the proteolytic enzymes, such as matrix metalloproteinases, elastases, and lysyl oxidases, and tissue inhibitor of matrix metalloproteinases, which, in turn, results from endothelial cell dysfunction, endothelial-to-mesenchymal transition, and inflammation. ECM remodeling and pulmonary vascular stiffness occur early in the disease process, before the onset of the increase in the intimal and medial thickness and pulmonary artery pressure, suggesting that the ECM is a cause rather than a consequence of distal pulmonary vascular remodeling. ECM remodeling and increased pulmonary arterial stiffness promote proliferation of pulmonary vascular cells (endothelial cells, smooth muscle cells, and adventitial fibroblasts) through mechanoactivation of various signaling pathways, including transcriptional cofactors YAP/TAZ, transforming growth factor-β, transient receptor potential channels, Toll-like receptor, and NF-κB. Inhibition of ECM remodeling and mechanotransduction prevents and reverses experimental pulmonary hypertension. These data support a central role for ECM remodeling in the pathogenesis of the PAH, making it an attractive novel therapeutic target.

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Nakanishi, Toshio, Nobuo Momoi, Hirohide Kobayashi, Toshio Nishikawa, Makoto Nakazawa, Yasuharu Imai, and Kazuo Momma. "Mechanical properties of the pulmonary arteries after the arterial switch operation for complete transposition." Cardiology in the Young 7, no. 3 (July 1997): 266–76. http://dx.doi.org/10.1017/s1047951100004157.

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AbstractThis study was designed to determine, first, the stiffness of the pulmonary arteries and, second, the relationship between the stiffness of the pulmonary arteries and the success rate of balloon angioplasty in patients with complete transposition after an arterial switch operation. Indexes of pulmonary arterial wall stiffness, percent change in the radius during a cardiac cycle and the pressure elastic modulus, were calculated from the pulmonary arterial pressure and radius measured from a cineangiogram. Of the patients, 13 had no significant stenosis, while 25 had significant stenoses and, therefore, underwent balloon angioplasty. In all, we dilated 33 stenotic lesions. In the presence or absence of postoperative pulmonary stenosis, the percent change in the radius of the pulmonary trunk was significantly less than the normal value. The pressure elastic modulus of the trunk and its branches was significantly greater than normal, and increased significantly with time after the operation. In patients without pulmonary stenosis, the systolic pulmonary arterial pressure increased concomitantly with the pressure elastic modulus. Balloon dilation was successful at 17 locations and unsuccessful at 16 locations. The percent change in radius was significantly less for the failures than for the successes. Prior to 3.5 years after the operation, the pressure elastic modulus was < 400 g/cm2at most locations and balloon dilation was successful in 88%. More than 3.5 years after the operation, the pressure elastic modulus was < 400 g/cm2in 11 of 15 locations, and balloon dilation was successful in only one location. The increased stiffness of the pulmonary artery may result in increased pulmonary systolic pressure in patients without pulmonary stenosis, and result in a low success rate for balloon angioplasty in patients with pulmonary stenosis.

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Wessels, Jeroen N., and Frances S. de Man. "Possible use of pulmonary artery stiffness in screening for portopulmonary hypertension." Journal of Clinical Ultrasound 50, no. 6 (July 2022): 756–58. http://dx.doi.org/10.1002/jcu.23240.

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Kang, Ki-Woon, Hyuk-Jae Chang, Young-Jin Kim, Byoung-Wook Choi, Hye Sun Lee, Woo-In Yang, Chi-Young Shim, Jongwon Ha, and Namsik Chung. "Cardiac Magnetic Resonance Imaging-Derived Pulmonary Artery Distensibility Index Correlates With Pulmonary Artery Stiffness and Predicts Functional Capacity in Patients With Pulmonary Arterial Hypertension." Circulation Journal 75, no. 9 (2011): 2244–51. http://dx.doi.org/10.1253/circj.cj-10-1310.

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Betticher, D. C., W. H. Reinhart, and J. Geiser. "Effect of RBC shape and deformability on pulmonary O2 diffusing capacity and resistance to flow in rabbit lungs." Journal of Applied Physiology 78, no. 3 (March 1, 1995): 778–83. http://dx.doi.org/10.1152/jappl.1995.78.3.778.

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Isolated rabbit lungs were perfused with washed and resuspended human red blood cells (RBCs) in the presence of drugs known to change the shape and deformability of RBCs. With sodium salicylate (0.5–2 g/l), which causes echinocytosis and increases RBC deformability, lung diffusing capacity for O2 (DLO2) increased by 21%. When chlorpromazine, which induces stomatocytosis and stiffens RBCs, was given (50 mg/l), DLO2 decreased by 18%. With sodium salicylate, the mean pulmonary artery pressure dropped by 14% from control values, whereas it increased by 18% under chlorpromazine. Comparative experiments with hemoglobin solutions did not reveal any effect of those two drugs either on DLO2 or on pulmonary arterial pressure, which indicates that the effects of sodium salicylate and chlorpromazine were due to changes in RBC shape and deformability. It is concluded that RBC shape and deformability affect pulmonary artery pressure and oxygen diffusing capacity, which may have an influence on oxygen transfer to tissue and hence be of clinical relevance.

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Dieffenbach, Paul B., Christina Mallarino Haeger, Anna Maria F. Coronata, Kyoung Moo Choi, Xaralabos Varelas, Daniel J. Tschumperlin, and Laura E. Fredenburgh. "Arterial stiffness induces remodeling phenotypes in pulmonary artery smooth muscle cells via YAP/TAZ-mediated repression of cyclooxygenase-2." American Journal of Physiology-Lung Cellular and Molecular Physiology 313, no. 3 (September 1, 2017): L628—L647. http://dx.doi.org/10.1152/ajplung.00173.2017.

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Pulmonary arterial stiffness is an independent risk factor for mortality in pulmonary hypertension (PH) and plays a critical role in PH pathophysiology. Our laboratory has recently demonstrated arterial stiffening early in experimental PH, along with evidence for a mechanobiological feedback loop by which arterial stiffening promotes further cellular remodeling behaviors (Liu F, Haeger CM, Dieffenbach PB, Sicard D, Chrobak I, Coronata AM, Suárez Velandia MM, Vitali S, Colas RA, Norris PC, Marinković A, Liu X, Ma J, Rose CD, Lee SJ, Comhair SA, Erzurum SC, McDonald JD, Serhan CN, Walsh SR, Tschumperlin DJ, Fredenburgh LE. JCI Insight 1: e86987, 2016). Cyclooxygenase-2 (COX-2) and prostaglandin signaling have been implicated in stiffness-mediated regulation, with prostaglandin activity inversely correlated to matrix stiffness and remodeling behaviors in vitro, as well as to disease progression in rodent PH models. The mechanism by which mechanical signaling translates to reduced COX-2 activity in pulmonary vascular cells is unknown. The present work investigated the transcriptional regulators Yes-associated protein (YAP) and WW domain-containing transcription regulator 1 (WWTR1, a.k.a., TAZ), which are known drivers of downstream mechanical signaling, in mediating stiffness-induced changes in COX-2 and prostaglandin activity in pulmonary artery smooth muscle cells (PASMCs). We found that YAP/TAZ activity is increased in PAH PASMCs and experimental PH and is necessary for the development of stiffness-dependent remodeling phenotypes. Knockdown of YAP and TAZ markedly induces COX-2 expression and downstream prostaglandin production by approximately threefold, whereas overexpression of YAP or TAZ reduces COX-2 expression and prostaglandin production to near undetectable levels. Together, our findings demonstrate a stiffness-dependent YAP/TAZ-mediated positive feedback loop that drives remodeling phenotypes in PASMCs via reduced COX-2 and prostaglandin activity. The ability to interrupt this critical mechanobiological feedback loop and enhance local prostaglandin activity via manipulation of YAP/TAZ signaling presents a highly attractive novel strategy for the treatment of PH.

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Hunter, Kendall S., Joseph A. Albietz, Po-Feng Lee, Craig J. Lanning, Steven R. Lammers, Stephen H. Hofmeister, Philip H. Kao, H. Jerry Qi, Kurt R. Stenmark, and Robin Shandas. "In vivo measurement of proximal pulmonary artery elastic modulus in the neonatal calf model of pulmonary hypertension: development and ex vivo validation." Journal of Applied Physiology 108, no. 4 (April 2010): 968–75. http://dx.doi.org/10.1152/japplphysiol.01173.2009.

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Developing clinical work suggests that vascular stiffening plays a role in the progression of pulmonary hypertension (PH), while recent studies in animal models of hypoxic PH have found significant proximal vascular stiffening in the diseased population. Here, we develop and validate a minimally invasive, clinically realizable method to estimate the local elastic modulus of the proximal pulmonary arteries from pressure-diameter (PD) data. PD measurements were made in the main pulmonary arteries of 16 calves; lumen diameter was assessed using color M-mode tissue Doppler imaging ultrasound, while pressure was measured via catheter. Two methods corresponding to thin-walled pressure vessel theory (“thin”) and Lame's equation for a thick-walled cylinder (“thick”) were used to approximate the artery elastic modulus from PD measurements. The harvested arteries were tested independently to determine their “true” ex vivo elastic modulus and stiffness. Both approximations displayed excellent correlation with ex vivo elastic modulus of the calf main pulmonary artery (thin r2 = 0.811; thick r2 = 0.844; both P < 0.01). Bland-Altman analysis indicated that the thick-walled approximation has better overall agreement with ex vivo modulus. The approximations displayed quantitatively distinct regression slopes that were statistically different ( P = 0.02). The elastic modulus of the main pulmonary artery can be reasonably estimated from combined color M-mode tissue Doppler imaging ultrasound and catheter pressure measurements in calves. Such measurements may be a valuable tool in the diagnosis and treatment of human PH.

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Kobs, Ryan W., Nidal E. Muvarak, Jens C. Eickhoff, and Naomi C. Chesler. "Linked mechanical and biological aspects of remodeling in mouse pulmonary arteries with hypoxia-induced hypertension." American Journal of Physiology-Heart and Circulatory Physiology 288, no. 3 (March 2005): H1209—H1217. http://dx.doi.org/10.1152/ajpheart.01129.2003.

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Right heart failure due to pulmonary hypertension causes significant morbidity and mortality. To study the linked vascular mechanical and biological changes that are induced by pulmonary hypertension, we mechanically tested isolated left main pulmonary arteries from mice exposed to chronic hypobaric hypoxia and performed histological assays on contralateral vessels. In isolated vessel tests, hypoxic vessels stretched less in response to pressure than controls at all pressure levels. Given the short length and large diameter of the pulmonary artery, the tangent Young's modulus could not be measured; instead, an effective elastic modulus was calculated that increased significantly with hypoxia [(280 kPa (SD 53) and 296 kPa (SD 50) for 10 and 15 days, respectively, vs. 222 kPa (SD 35) for control; P < 0.02)]. Hypoxic vessels also had higher damping coefficients [(0.063 (SD 0.017) and 0.054 (SD 0.014) for 10 and 15 days, respectively, vs. 0.033 (SD 0.016) for control; P < 0.002)], indicating increased energy dissipation. The increased stiffness with hypoxia correlated with an increase in collagen thickness (percent collagen multiplied by wall thickness) as well as the sum of elastin and collagen thicknesses measured histologically in the artery wall. These results highlight the mechanobiological changes in the pulmonary vasculature that occur in response to hypoxia-induced pulmonary hypertension. Furthermore, they demonstrate significant vascular mechanical and biological changes that would increase pulmonary vascular impedance, leading to right heart failure.

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Stevens, Gerin Rachel, Ana Garcia-Alvarez, Sean Pinney, Mario J. Garcia, Valentin Fuster, and Javier Sanz. "PULMONARY ARTERY STIFFNESS IS INDEPENDENTLY ASSOCIATED WITH THE DEGREE OF RIGHT VENTRICULAR DYSFUNCTION IN PULMONARY HYPERTENSION." Journal of the American College of Cardiology 55, no. 10 (March 2010): A154.E1446. http://dx.doi.org/10.1016/s0735-1097(10)61447-7.

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Kantzis, Marinos, Christoph M. Happel, and Nikolaus A. Haas. "Is mesocardia with left-sided caval vein draining to coronary sinus a contraindication for a percutaneous pulmonary valve implantation? A case description." Cardiology in the Young 28, no. 2 (October 4, 2017): 229–33. http://dx.doi.org/10.1017/s1047951117001743.

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AbstractIntroductionAlthough the right jugular vein approach for percutaneous pulmonary valve implantation is well described, there are no reports that describe a percutaneous pulmonary valve implantation through a left superior caval vein to coronary sinus pathway.CaseA 14-year-old female with tetralogy of Fallot, mesocardia, left superior caval vein draining into the coronary sinus, and hemiazygos continuation of the inferior caval vein underwent ventricular septal defect closure, with homograft insertion from the right ventricle to the pulmonary artery, patch augmentation of the left pulmonary artery, and creation of an atrial communication. Thereafter followed numerous catheterisations and interventions with stent implantation for stenosis of the left pulmonary artery and the homograft, as did device closure of the atrial communication. When she was a 12-year-old, the indications for a percutaneous pulmonary valve implantation were fulfilled and she underwent implantation of a 22 mm Melody® valve through the left superior caval vein. The extra-stiff exchange wire was pre-formed into a “U-spiral”-type configuration, according to the underlying anatomy, in order to provide a smooth route for the delivery of stents, to create the landing zone, and for the implantation of the Melody “ensemble”. The procedure was performed under deep sedation according to our standard protocol. The duration of the procedure was 172 min and the radiation time was 24.9 min.ConclusionOn the basis of this unique experience, percutaneous pulmonary valve implantation is safe and feasible even in patients with unusual anatomy. Crucial is the “U-spiral” shaped configuration of the guide wire.

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Chambers, Megan J., Mitchel J. Colebank, M. Umar Qureshi, Rachel Clipp, and Mette S. Olufsen. "Structural and hemodynamic properties of murine pulmonary arterial networks under hypoxia-induced pulmonary hypertension." Proceedings of the Institution of Mechanical Engineers, Part H: Journal of Engineering in Medicine 234, no. 11 (July 28, 2020): 1312–29. http://dx.doi.org/10.1177/0954411920944110.

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Detection and monitoring of patients with pulmonary hypertension, defined as a mean blood pressure in the main pulmonary artery above 25 mmHg, requires a combination of imaging and hemodynamic measurements. This study demonstrates how to combine imaging data from microcomputed tomography images with hemodynamic pressure and flow waveforms from control and hypertensive mice. Specific attention is devoted to developing a tool that processes computed tomography images, generating subject-specific arterial networks in which one-dimensional fluid dynamics modeling is used to predict blood pressure and flow. Each arterial network is modeled as a directed graph representing vessels along the principal pathway to ensure perfusion of all lobes. The one-dimensional model couples these networks with structured tree boundary conditions representing the small arteries and arterioles. Fluid dynamics equations are solved in this network and compared to measurements of pressure in the main pulmonary artery. Analysis of microcomputed tomography images reveals that the branching ratio is the same in the control and hypertensive animals, but that the vessel length-to-radius ratio is significantly lower in the hypertensive animals. Fluid dynamics predictions show that in addition to changed network geometry, vessel stiffness is higher in the hypertensive animal models than in the control models.

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Altıparmak, Ibrahim Halil, Muslihittin Emre Erkus, Mustafa Polat, Zafer Hasan Ali Sak, Funda Yalcın, Ozgur Gunebakmaz, Yusuf Sezen, Zekeriya Kaya, and Recep Demirbag. "Evaluation of Pulmonary Artery Stiffness in Patients with Obstructive Sleep Apnea Syndrome." Echocardiography 33, no. 3 (October 29, 2015): 362–71. http://dx.doi.org/10.1111/echo.13098.

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Baysal, Sadettin Selçuk, and Mehmet Has. "Evaluation of pulmonary artery stiffness in newly diagnosed adult patients with asthma." Echocardiography 36, no. 5 (March 18, 2019): 870–76. http://dx.doi.org/10.1111/echo.14309.

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Ozdogru, I., I. Gul, M. Kaya, A. Dogan, M. Inanc, N. Kalay, R. Topsakal, N. Eryol, and A. Oguzhan. "ACUTE EFFECTS OF PASSIVE SMOKING ON PULMONARY ARTERY STIFFNESS IN HEALTHY VOLUNTEERS." Atherosclerosis Supplements 9, no. 1 (May 2008): 124. http://dx.doi.org/10.1016/s1567-5688(08)70500-2.

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Hidayet, Şıho, Adil Bayramoğlu, Emine Hidayet, Zeynep Ulutaş, Fırat Dağtekin, Fatih Güven, Yücel Karaca, Yakup Yiğit, Muhammed Yasin Adigüzel, and Hasan Pekdemir. "The relationship between bioelectrical impedance parameters and pulmonary artery stiffness in obese subjects." Echocardiography 39, no. 3 (February 9, 2022): 490–95. http://dx.doi.org/10.1111/echo.15320.

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Çelik, M., U. Ç. Yüksel, Y. Gökoğlan, E. Yalçınkaya, B. Buğan, S. Yaşar, M. Demir, H. K. Kabul, and A. İyisoy. "OP-096 Evaluation of Pulmonary Artery Stiffness in Patients with Chronic Heart Failure." American Journal of Cardiology 113, no. 7 (April 2014): S25. http://dx.doi.org/10.1016/j.amjcard.2014.01.071.

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Kuhr, Frank K., Kimberly A. Smith, Michael Y. Song, Irena Levitan, and Jason X.-J. Yuan. "New mechanisms of pulmonary arterial hypertension: role of Ca2+ signaling." American Journal of Physiology-Heart and Circulatory Physiology 302, no. 8 (April 15, 2012): H1546—H1562. http://dx.doi.org/10.1152/ajpheart.00944.2011.

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Pulmonary arterial hypertension (PAH) is a severe and progressive disease that usually culminates in right heart failure and death if left untreated. Although there have been substantial improvements in our understanding and significant advances in the management of this disease, there is a grim prognosis for patients in the advanced stages of PAH. A major cause of PAH is increased pulmonary vascular resistance, which results from sustained vasoconstriction, excessive pulmonary vascular remodeling, in situ thrombosis, and increased pulmonary vascular stiffness. In addition to other signal transduction pathways, Ca2+ signaling in pulmonary artery smooth muscle cells (PASMCs) plays a central role in the development and progression of PAH because of its involvement in both vasoconstriction, through its pivotal effect of PASMC contraction, and vascular remodeling, through its stimulatory effect on PASMC proliferation. Altered expression, function, and regulation of ion channels and transporters in PASMCs contribute to an increased cytosolic Ca2+ concentration and enhanced Ca2+ signaling in patients with PAH. This review will focus on the potential pathogenic role of Ca2+ mobilization, regulation, and signaling in the development and progression of PAH.

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Jankowich, Matthew, Siddique A. Abbasi, Alexander Vang, and Gaurav Choudhary. "Right Ventricular Fibrosis Is Related to Pulmonary Artery Stiffness in Pulmonary Hypertension: A Cardiac Magnetic Resonance Imaging Study." American Journal of Respiratory and Critical Care Medicine 200, no. 6 (September 15, 2019): 776–79. http://dx.doi.org/10.1164/rccm.201903-0580le.

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PELED, NIR, DAVID SHITRIT, BENJAMIN D. FOX, DEKEL SHLOMI, ANAT AMITAL, DANIELE BENDAYAN, and MORDECHAI R. KRAMER. "Peripheral Arterial Stiffness and Endothelial Dysfunction in Idiopathic and Scleroderma Associated Pulmonary Arterial Hypertension." Journal of Rheumatology 36, no. 5 (April 15, 2009): 970–75. http://dx.doi.org/10.3899/jrheum.081088.

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Objective.Pulmonary endothelial dysfunction and increased reflection of pulmonary pressure waves have been reported in pulmonary arterial hypertension (PAH). However, the systemic vascular involvement is not fully understood. Our study focused on the systemic arterial stiffness and endothelial involvement in idiopathic and scleroderma associated PAH.Methods.Peripheral arterial stiffness and endothelial function were evaluated in 38 patients with idiopathic (n = 28) and scleroderma associated (n = 10) PAH, and 21 control subjects (13 healthy; 8 with scleroderma and normal pulmonary pressure). All participants underwent clinical and cardiopulmonary evaluation. Arterial stiffness was measured through the fingertip tonometry derived augmentation index (AI), which is the boost increase in the late systolic pressure wave after the initial systolic shoulder. Endothelial function was measured by forearm blood flow dilatation response to brachial artery occlusion by a noninvasive plethysmograph (EndoPAT 2000), which is associated with nitric oxide-dependent vasodilatation and yields a peripheral arterial tone (PAT) ratio.Results.Mean systolic pulmonary pressure was 70.5 ± 21.6 mm Hg (idiopathic-PAH) and 69.3 ± 20 mm Hg (scleroderma-PAH). AI was higher in scleroderma patients (10.5% ± 19.6% in healthy controls, 9.0% ± 21.5% in idiopathic-PAH, 20.1% ± 19.1% in scleroderma-PAH, and 24.4% ± 18.9% in scleroderma-controls; nonsignificant). PAT ratio was significantly lower (p < 0.05) than control values in idiopathic-PAH and scleroderma-PAH (PAT ratio: control 2.20 ± 0.25; idiopathic 1.84 ± 0.51; scleroderma 1.66 ± 0.66). AI was not correlated to endothelial dysfunction. There were no differences between the 2 PAH patient groups in age, body mass index, New York Heart Association classification, or 6-min walk test.Conclusion.Our study shows a trend towards increased arterial stiffness in scleroderma (nonsignificant), and also peripheral endothelial dysfunction in idiopathic-PAH and in scleroderma-PAH. These findings suggest involvement of different vessels in scleroderma-PAH compared to idiopathic-PAH.

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Triantafyllidi, Helen, Dionysia Birmpa, Dimitrios Benas, Ignatios Ikonomidis, Antonis Schoinas, Paraskevi Trivilou, Frantzeska Frantzeskaki, and Stylianos E. Orfanos. "May We Use Non-Invasive Indices of Aortic Stiffness and Endothelial Glycocalyx as Biomarkers for Idiopathic Pulmonary Artery Hypertension Follow-Up?" Medicina 57, no. 6 (June 1, 2021): 558. http://dx.doi.org/10.3390/medicina57060558.

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Idiopathic pulmonary arterial hypertension (IPAH) initial evaluation and follow-up, a rare and incurable disease if left untreated, is based on a multiparametric approach (functional status of the patient, biomarkers, hemodynamic parameters and imaging evaluation of right heart impairment). Arterial stiffness (AS) and endothelial glycocalyx are indices of systemic circulation. We present the 3-years follow-up of a female IPAH patient. We propose aortic stiffness and endothelial glycocalyx indices as non-invasive markers of either improvement or deterioration of IPAH disease.

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Silva, Gonçalo Teixeira de Almeida, Bruce B. Guest, Diego E. Gomez, Martine McGregor, Laurent Viel, M. Lynne O’Sullivan, John Runciman, and Luis G. Arroyo. "Development of a technique for determination of pulmonary artery pulse wave velocity in horses." Journal of Applied Physiology 122, no. 5 (May 1, 2017): 1088–94. http://dx.doi.org/10.1152/japplphysiol.00962.2016.

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Calcification of the tunica media of the axial pulmonary arteries (PA) has been reported in a large proportion of racehorses. In humans, medial calcification is a significant cause of arterial stiffening and is implicated in the pathogenesis of cardiac, cerebral, and renal microvascular diseases. Pulse wave velocity (PWV) provides a measure of arterial stiffness. This study aimed to develop a technique to determine PA-PWV in horses and, secondarily, to investigate a potential association between PA-PWV and arterial fibro-calcification. A dual-pressure sensor catheter (PSC) was placed in the main PA of 10 sedated horses. The pressure waves were used to determine PWV along the PA, using the statistical phase offset method. Histological analysis of the PA was performed to investigate the presence of fibro-calcified lesions. The mean (±SD) PWV was 2.3 ± 0.7 m/s in the proximal PA trunk and 1.1 ± 0.1 m/s further distal (15 cm) in a main PA branch. The mean (±SD) of mean arterial pressures in the proximal PA trunk was 30.1 ± 5.2 mmHg, and 22.0 ± 6.0 mmHg further distal (15 cm) within the main PA branch. The mean (±SD) pulse pressure in the proximal PA trunk was 15.0 ± 4.7 mmHg, and 13.5 ± 3.3 mmHg further distal (15 cm) within the main PA branch. Moderate to severe lesions of the tunica media of the PAs were observed in seven horses, but a correlation with PWV could not be established yet. Pulmonary artery PWV may be determined in standing horses. The technique described may allow further investigation of the effect of calcification of large PAs in the pathogenesis of equine pulmonary circulatory disorders. NEW & NOTEWORTHY Pulmonary artery pulse wave velocity was determined safely in standing sedated horses. The technique described may allow further investigation of the effect of calcification of large pulmonary arteries in the pathogenesis of pulmonary circulatory disorders in horses.

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Mahfouz, Ragab A., Ashraf Dewedar, Amr Abdelmoneim, and Ekhlas M. Hossien. "Aortic and Pulmonary Artery Stiffness and Cardiac Function in Children at Risk for Obesity." Echocardiography 29, no. 8 (June 14, 2012): 984–90. http://dx.doi.org/10.1111/j.1540-8175.2012.01736.x.

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Ibrahim, El-Sayed H., Jean M. Shaffer, and Richard D. White. "Assessment of pulmonary artery stiffness using velocity-encoding magnetic resonance imaging: evaluation of techniques." Magnetic Resonance Imaging 29, no. 7 (September 2011): 966–74. http://dx.doi.org/10.1016/j.mri.2011.04.012.

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Shibata, Shigeki, Jeff L. Hastings, Anand Prasad, Qi Fu, Paul S. Bhella, Eric Pacini, Felix Krainski, M. Dean Palmer, Rong Zhang, and Benjamin D. Levine. "Congestive heart failure with preserved ejection fraction is associated with severely impaired dynamic Starling mechanism." Journal of Applied Physiology 110, no. 4 (April 2011): 964–71. http://dx.doi.org/10.1152/japplphysiol.00826.2010.

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Sedentary aging leads to increased cardiovascular stiffening, which can be ameliorated by sufficient amounts of lifelong exercise training. An even more extreme form of cardiovascular stiffening can be seen in heart failure with preserved ejection fraction (HFpEF), which comprises ∼40∼50% of elderly patients diagnosed with congestive heart failure. There are two major interrelated hypotheses proposed to explain heart failure in these patients: 1) increased left ventricular (LV) diastolic stiffness and 2) increased arterial stiffening. The beat-to-beat dynamic Starling mechanism, which is impaired with healthy human aging, reflects the interaction between ventricular and arterial stiffness and thus may provide a link between these two mechanisms underlying HFpEF. Spectral transfer function analysis was applied between beat-to-beat changes in LV end-diastolic pressure (LVEDP; estimated from pulmonary artery diastolic pressure with a right heart catheter) and stroke volume (SV) index. The dynamic Starling mechanism (transfer function gain between LVEDP and the SV index) was impaired in HFpEF patients ( n = 10) compared with healthy age-matched controls ( n = 12) (HFpEF: 0.23 ± 0.10 ml·m−2·mmHg−1 and control: 0.37 ± 0.11 ml·m−2·mmHg−1, means ± SD, P = 0.008). There was also a markedly increased (3-fold) fluctuation of LV filling pressures (power spectral density of LVEDP) in HFpEF patients, which may predispose to pulmonary edema due to intermittent exposure to higher pulmonary capillary pressure (HFpEF: 12.2 ± 10.4 mmHg2 and control: 3.8 ± 2.9 mmHg2, P = 0.014). An impaired dynamic Starling mechanism, even more extreme than that observed with healthy aging, is associated with marked breath-by-breath LVEDP variability and may reflect advanced ventricular and arterial stiffness in HFpEF, possibly contributing to reduced forward output and pulmonary congestion.

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Schäfer, Michal, Neil Wilson, D. Dunbar Ivy, Richard Ing, Steven Abman, Lorna P. Browne, Gareth Morgan, et al. "Noninvasive wave intensity analysis predicts functional worsening in children with pulmonary arterial hypertension." American Journal of Physiology-Heart and Circulatory Physiology 315, no. 4 (October 1, 2018): H968—H977. http://dx.doi.org/10.1152/ajpheart.00227.2018.

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The purpose of the present study was to characterize pulmonary vascular stiffness using wave intensity analysis (WIA) in children with pulmonary arterial hypertension (PAH), compare the WIA indexes with catheterization- and MRI-derived hemodynamics, and assess the prognostic ability of WIA-derived biomarkers to predict the functional worsening. WIA was performed in children with PAH ( n = 40) and healthy control subjects ( n = 15) from phase-contrast MRI-derived flow and area waveforms in the main pulmonary artery (MPA). From comprehensive WIA spectra, we collected and compared with healthy control subjects forward compression waves (FCW), backward compression waves (BCW), forward decompression waves (FDW), and wave propagation speed ( c-MPA). There was no difference in the magnitude of FCW between PAH and control groups (88 vs. 108 mm5·s−1·ml−1, P = 0.239). The magnitude of BCW was increased in patients with PAH (32 vs. 5 mm5·s−1·ml−1, P < 0.001). There was no difference in magnitude of indexed FDW (32 vs. 28 mm5·s−1·ml−1, P = 0.856). c-MPA was increased in patients with PAH (3.2 vs. 1.6 m/s, P < 0.001). BCW and FCW correlated with mean pulmonary arterial pressure, right ventricular volumes, and ejection fraction. Elevated indexed BCW [heart rate (HR) = 2.91, confidence interval (CI): 1.18–7.55, P = 0.019], reduced indexed FDW (HR = 0.34, CI: 0.11–0.90, P = 0.030), and increased c-MPA (HR = 3.67, CI: 1.47–10.20, P = 0.004) were strongly associated with functional worsening of disease severity. Our results suggest that noninvasively derived biomarkers of pulmonary vascular resistance and stiffness may be helpful for determining prognosis and monitoring disease progression in children with PAH. NEW & NOTEWORTHY Wave intensity analysis (WIA) studies are lacking in children with pulmonary arterial hypertension (PAH) partially because WIA, which is necessary to assess vascular stiffness, requires an invasive pressure-derived waveform along with simultaneous flow measurements. We analyzed vascular stiffness using WIA in children with PAH who underwent phase-contrast MRI and observed significant differences in WIA indexes between patients with PAH and control subjects. Furthermore, WIA indexes were predictive of functional worsening and were associated with standard catheterization measures.

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Korurek, Mehmet, Mustafa Yildiz, Ayhan Yüksel, and Alparslan Şahin. "Simulation of Eisenmenger syndrome with ventricular septal defect using equivalent electronic system." Cardiology in the Young 22, no. 3 (September 26, 2011): 301–6. http://dx.doi.org/10.1017/s1047951111001478.

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AbstractBackground: In this study, we aim to investigate the simulation of the cardiovascular system using an electronic circuit model under normal and pathological conditions, especially the Eisenmenger syndrome. Methods and Results: The Eisenmenger syndrome includes a congenital communication between the systemic and pulmonary circulation, with resultant pulmonary arterial hypertension and right-to-left reversal of flow through the defect. When pulmonary vascular resistance exceeds systemic vascular resistance, it results in hypoxaemia and cyanosis. The Westkessel model including Resistor-Inductance-Capacitance pi-segments was chosen in order to simulate both systemic and pulmonary circulation. The left and right heart are represented by trapezoidal shape stiffness for better simulation results. The Eisenmenger syndrome is simulated using a resistance (septal resistance) connected between the left ventricle and right ventricle points of the model. Matlab® is used for the model implementation. In this model, although there is a remarkable increase in the pulmonary artery pressure and right ventricle pressure, left ventricle pressure, aortic pressure, aortic flow, and pulmonary compliance decrease in the Eisenmenger syndrome. In addition, left-to-right septal flow reversed in these diseases. Conclusion: Our model is effective and available for simulating normal cardiac conditions and cardiovascular diseases, especially the Eisenmenger syndrome.

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Tian, Lian, Steven R. Lammers, Philip H. Kao, Mark Reusser, Kurt R. Stenmark, Kendall S. Hunter, H. Jerry Qi, and Robin Shandas. "Linked opening angle and histological and mechanical aspects of the proximal pulmonary arteries of healthy and pulmonary hypertensive rats and calves." American Journal of Physiology-Heart and Circulatory Physiology 301, no. 5 (November 2011): H1810—H1818. http://dx.doi.org/10.1152/ajpheart.00025.2011.

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Understanding how arterial remodeling changes the mechanical behavior of pulmonary arteries (PAs) is important to the evaluation of pulmonary vascular function. Early and current efforts have focused on the arteries' histological changes, their mechanical properties under in vitro mechanical testing, and their zero-stress and no-load states. However, the linkage between the histology and mechanical behavior is still not well understood. To explore this linkage, we investigated the geometry, residual stretch, and histology of proximal PAs in both adult rat and neonatal calf hypoxic models of pulmonary hypertension (PH), compared their changes due to chronic hypoxia across species, and proposed a two-layer mechanical model of artery to relate the opening angle to the stiffness ratio of the PA outer to inner layer. We found that the proximal PA remodeling in calves was quite different from that in rats. In rats, the arterial wall thickness, inner diameter, and outer layer thickness fraction all increased dramatically in PH and the opening angle decreased significantly, whereas in calves, only the arterial wall thickness increased in PH. The proposed model predicted that the stiffness ratio of the calf proximal PAs changed very little from control to hypertensive group, while the decrease of opening angle in rat proximal PAs in response to chronic hypoxia was approximately linear to the increase of the stiffness ratio. We conclude that the arterial remodeling in rat and calf proximal PAs is different and the change of opening angle can be linked to the change of the arterial histological structure and mechanics.

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Maniar, Hersh S., Sunil M. Prasad, Sydney L. Gaynor, Celeste M. Chu, Paul Steendijk, and Marc R. Moon. "Impact of pericardial restraint on right atrial mechanics during acute right ventricular pressure load." American Journal of Physiology-Heart and Circulatory Physiology 284, no. 1 (January 1, 2003): H350—H357. http://dx.doi.org/10.1152/ajpheart.00444.2002.

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Optimization of right atrial (RA) mechanics is important for maintaining right ventricular (RV) filling and global cardiac output. However, the impact of pericardial restraint on RA function and the compensatory role of the right atrium to changes in RV afterload remain poorly characterized. In eight open-chest sheep, RA elastance (contractility) and chamber stiffness were measured (RA pressure-volume relations) at baseline and during partial pulmonary artery (PA) occlusion. Data were collected before and after pericardiotomy. With the pericardium intact and partial PA occlusion, RA elastance increased by 28% ( P < 0.04), whereas RA stiffness tended to rise ( P = 0.08). However, after pericardiotomy, there was a significant fall in both RA elastance (54%, P < 0.04) and stiffness (39%, P < 0.04), and subsequent PA occlusion failed to induce a change in elastance ( P > 0.19) or stiffness ( P > 0.84). After pericardiotomy, RA elastance and stiffness fell dramatically, and the compensatory response of the right atrium to elevated RV afterload was lost. The ability of the right atrium to respond to changes in RV hemodynamics is highly dependent on pericardial integrity.

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Su, Zhenbi, Wei Tan, Robin Shandas, and Kendall S. Hunter. "Influence of Distal Resistance and Proximal Stiffness on Hemodynamics and RV Afterload in Progression and Treatments of Pulmonary Hypertension: A Computational Study with Validation Using Animal Models." Computational and Mathematical Methods in Medicine 2013 (2013): 1–12. http://dx.doi.org/10.1155/2013/618326.

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We develop a simple computational model based on measurements from a hypoxic neonatal calf model of pulmonary hypertension (PH) to investigate the interplay between vascular and ventricular measures in the setting of progressive PH. Model parameters were obtained directly fromin vivoandex vivomeasurements of neonatal calves. Seventeen sets of model-predicted impedance and mean pulmonary arterial pressure (mPAP) show good agreement with the animal measurements, thereby validating the model. Next, we considered a predictive model in which three parameters, PVR, elastic modulus (EM), and arterial thickness, were varied singly from one simulation to the next to study their individual roles in PH progression. Finally, we used the model to predict the individual impacts of clinical (vasodilatory) and theoretical (compliance increasing) PH treatments on improving pulmonary hemodynamics. Our model (1) displayed excellent patient-specific agreement with measured global pulmonary parameters; (2) quantified relationships between PVR and mean pressure and PVS and pulse pressure, as well as studiying the right ventricular (RV) afterload, which could be measured as a hydraulic load calculated from spectral analysis of pulmonary artery pressure and flow waves; (3) qualitatively confirmed the derangement of vascular wall shear stress in progressive PH; and (4) established that decreasing proximal vascular stiffness through a theoretical treatment of reversing proximal vascular remodeling could decrease RV afterload.

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Agroyannis, B., A. Dalamangas, H. Tzanatos, C. Fourtounas, I. Kopelias, and D. Koutsikos. "Echinocytic transformation and aggregation of red cells in uremic patients." Journal of Applied Physiology 80, no. 2 (February 1, 1996): 711–12. http://dx.doi.org/10.1152/jappl.1996.80.2.711.

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Isolated rabbit lungs were perfused with washed and resuspended human red blood cells (RBCs) in the presence of drugs known to change the shape and deformability of RBCs. With sodium salicylate (0.5-2 g/l), which causes echinocytosis and increases RBC deformability, lung diffusing capacity for O2 (DLO2) increased by 21%. When chlorpromazine, which induces stomatocytosis and stiffens RBCs, was given (50 mg/l), DLO2 decreased by 18% under chlorpromazine. Comparative experiments with hemoglobin solutions did not reveal any effect of those two drugs either on DLO2 or on pulmonary arterial pressure, which indicates that the effects of sodium salicylate and chlorpromazine were due to changes in RBC shape and deformability. It is concluded that RBC shape and deformability affect pulmonary artery pressure and oxygen diffusing capacity, which may have an influence on oxygen transfer to tissue and hence be of clinical relevance.

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Zhang, Yanhang, Martin L. Dunn, Kendall S. Hunter, Craig Lanning, D. Dunbar Ivy, Lori Claussen, S. James Chen, and Robin Shandas. "Application of A Microstructural Constitutive Model of the Pulmonary Artery to Patient-Specific Studies: Validation and Effect of Orthotropy." Journal of Biomechanical Engineering 129, no. 2 (August 22, 2006): 193–201. http://dx.doi.org/10.1115/1.2485780.

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We applied a statistical mechanics based microstructural model of pulmonary artery mechanics, developed from our previous studies of rats with pulmonary arterial hypertension (PAH), to patient-specific clinical studies of children with PAH. Our previous animal studies provoked the hypothesis that increased cross-linking density of the molecular chains may be one biological remodeling mechanism by which the PA stiffens in PAH. This study appears to further confirm this hypothesis since varying molecular cross-linking density in the model allows us to simulate the changes in the P‐D loops between normotensive and hypertensive conditions reasonably well. The model was combined with patient-specific three-dimensional vascular anatomy to obtain detailed information on the topography of stresses and strains within the proximal branches of the pulmonary vasculature. The effect of orthotropy on stress∕strain within the main and branch PAs obtained from a patient was explored. This initial study also puts forward important questions that need to be considered before combining the microstructural model with complex patient-specific vascular geometries.

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Su, Junjing, Charmilie C. Logan, Alun D. Hughes, Kim H. Parker, Niti M. Dhutia, Carl Christian Danielsen, and Ulf Simonsen. "Impact of chronic hypoxia on proximal pulmonary artery wave propagation and mechanical properties in rats." American Journal of Physiology-Heart and Circulatory Physiology 314, no. 6 (June 1, 2018): H1264—H1278. http://dx.doi.org/10.1152/ajpheart.00695.2017.

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Arterial stiffness and wave reflection are important components of the ventricular afterload. Therefore, we aimed to assess the arterial wave characteristics and mechanical properties of the proximal pulmonary arteries (PAs) in the hypoxic pulmonary hypertensive rat model. After 21 days in normoxic or hypoxic chambers (24 animals/group), animals underwent transthoracic echocardiography and PA catheterization with a dual-tipped pressure and Doppler flow sensor wire. Wave intensity analysis was performed. Artery rings obtained from the pulmonary trunk, right and left PAs, and aorta were subjected to a tensile test to rupture. Collagen and elastin content were determined. In hypoxic rats, proximal PA wall thickness, collagen content, tensile strength per unit collagen, maximal elastic modulus, and wall viscosity increased, whereas the elastin-to-collagen ratio and arterial distensibility decreased. Arterial pulse wave velocity was also increased, and the increase was more prominent in vivo than ex vivo. Wave intensity was similar in hypoxic and normoxic animals with negligible wave reflection. In contrast, the aortic maximal elastic modulus remained unchanged, whereas wall viscosity decreased. In conclusion, there was no evidence of altered arterial wave propagation in proximal PAs of hypoxic rats while the extracellular matrix protein composition was altered and collagen tensile strength increased. This was accompanied by altered mechanical properties in vivo and ex vivo. NEW & NOTEWORTHY In rats exposed to chronic hypoxia, we have shown that pulse wave velocity in the proximal pulmonary arteries increased and pressure dependence of the pulse wave velocity was steeper in vivo than ex vivo leading to a more prominent increase in vivo.

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Grignola, Juan C., Enric Domingo, Carlos Bravo, Rio Aguilar, Manuel Lopez-Messeguer, Manuel Vazquez, and Antonio Roman. "LOCAL PULMONARY ARTERY STIFFNESS INDEXES ARE CORRELATED WITH STEADY AND PULSATILE COMPONENTS OF RIGHT VENTRICULAR AFTERLOAD IN PULMONARY ARTERIAL HYPERTENSION." Journal of the American College of Cardiology 55, no. 10 (March 2010): A172.E1613. http://dx.doi.org/10.1016/s0735-1097(10)61614-2.

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Liu, Chia-Ying, Megha Parikh, David A. Bluemke, Pallavi Balte, James Carr, Stephen Dashnaw, Hooman D. Poor, et al. "Pulmonary artery stiffness in chronic obstructive pulmonary disease (COPD) and emphysema: The Multi-Ethnic Study of Atherosclerosis (MESA) COPD Study." Journal of Magnetic Resonance Imaging 47, no. 1 (May 10, 2017): 262–71. http://dx.doi.org/10.1002/jmri.25753.

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Journal articles on the topic 'Pulmonary artery stiffne'

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