scholarly journals Atherosclerosis and the Capillary Network; Pathophysiology and Potential Therapeutic Strategies

Cells ◽  
2019 ◽  
Vol 9 (1) ◽  
pp. 50 ◽  
Author(s):  
Tilman Ziegler ◽  
Farah Abdel Rahman ◽  
Victoria Jurisch ◽  
Christian Kupatt
Keyword(s):  
Vessel Wall ◽  
Prolonged Exposure ◽  
Vascular System ◽  
Therapeutic Strategies ◽  
Atherosclerotic Plaques ◽  
Pathological Changes ◽  
Vessel Disease ◽  
Disease States ◽  
Disease Entities ◽  
Key Drivers

Atherosclerosis and associated ischemic organ dysfunction represent the number one cause of mortality worldwide. While the key drivers of atherosclerosis, arterial hypertension, hypercholesterolemia and diabetes mellitus, are well known disease entities and their contribution to the formation of atherosclerotic plaques are intensively studied and well understood, less effort is put on the effect of these disease states on microvascular structure an integrity. In this review we summarize the pathological changes occurring in the vascular system in response to prolonged exposure to these major risk factors, with a particular focus on the differences between these pathological alterations of the vessel wall in larger arteries as compared to the microcirculation. Furthermore, we intend to highlight potential therapeutic strategies to improve microvascular function during atherosclerotic vessel disease.

scholarly journals Endothelial cell–oligodendrocyte interactions in small vessel disease and aging

2017 ◽  
Vol 131 (5) ◽  
pp. 369-379 ◽  
Author(s):  
Rikesh M. Rajani ◽  
Anna Williams
Keyword(s):  
Endothelial Cells ◽  
Endothelial Cell ◽  
Neurological Disease ◽  
Small Vessel Disease ◽  
Cell Types ◽  
Cerebral Small Vessel Disease ◽  
Small Vessel ◽  
Pathological Changes ◽  
Vessel Disease ◽  
Disease States

Cerebral small vessel disease (SVD) is a prevalent, neurological disease that significantly increases the risk of stroke and dementia. The main pathological changes are vascular, in the form of lipohyalinosis and arteriosclerosis, and in the white matter (WM), in the form of WM lesions. Despite this, it is unclear to what extent the key cell types involved–the endothelial cells (ECs) of the vasculature and the oligodendrocytes of the WM–interact. Here, we describe the work that has so far been carried out suggesting an interaction between ECs and oligodendrocytes in SVD. As these interactions have been studied in more detail in other disease states and in development, we explore these systems and discuss the role these mechanisms may play in SVD.

scholarly journals Real-world long-term outcomes based on three therapeutic strategies in very old patients with three-vessel disease

2021 ◽  
Vol 21 (1) ◽  
Author(s):  
Deshan Yuan ◽  
Sida Jia ◽  
Ce Zhang ◽  
Lin Jiang ◽  
Lianjun Xu ◽  
...  
Keyword(s):  
Real World ◽  
Cardiac Death ◽  
Artery Bypass ◽  
Therapeutic Strategies ◽  
Old Patients ◽  
Very Old ◽  
Vessel Disease ◽  
Significant Difference ◽  
Very Old Patients

Abstract Background There are relatively limited data regarding real-world outcomes in very old patients with three-vessel disease (3VD) receiving different therapeutic strategies. This study aimed to perform analysis of long-term clinical outcomes of medical therapy (MT), coronary artery bypass grafting (CABG), and percutaneous coronary intervention (PCI) in this population. Methods We included 711 patients aged ≥ 75 years from a prospective cohort of patients with 3VD. Consecutive enrollment of these patients began from April 2004 to February 2011 at Fu Wai Hospital. Patients were categorized into three groups (MT, n = 296; CABG, n = 129; PCI, n = 286) on the basis of different treatment strategies. Results During a median follow-up of 7.25 years, 262 deaths and 354 major adverse cardiac and cerebrovascular events (MACCE) occurred. Multivariate Cox analysis showed that the risk of cardiac death was significantly lower for CABG compared with PCI (adjusted hazard ratio [HR] = 0.475, 95% confidence interval [CI] 0.232–0.974, P = 0.042). Additionally, MACCE appeared to show a trend towards a better outcome for CABG (adjusted HR = 0.759, 95% CI 0.536–1.074, P = 0.119). Furthermore, CABG was significantly superior in terms of unplanned revascularization (adjusted HR = 0.279, 95% CI 0.079–0.982, P = 0.047) and myocardial infarction (adjusted HR = 0.196, 95% CI 0.043–0.892, P = 0.035). No significant difference in all-cause death between CABG and PCI was observed. MT had a higher risk of cardiac death than PCI (adjusted HR = 1.636, 95% CI 1.092–2.449, P = 0.017). Subgroup analysis showed that there was a significant interaction between treatment strategy (PCI vs. CABG) and sex for MACCE (P = 0.026), with a lower risk in men for CABG compared with that of PCI, but not in women. Conclusions CABG can be performed with reasonable results in very old patients with 3VD. Sex should be taken into consideration in therapeutic decision-making in this population.

scholarly journals Exploring the Relationships Between Hemodynamic Stresses in the Carotid Arteries

2021 ◽  
Vol 7 ◽  
Author(s):  
Magnus Ziegler ◽  
Jesper Alfraeus ◽  
Elin Good ◽  
Jan Engvall ◽  
Ebo de Muinck ◽  
...  
Keyword(s):  
Vessel Wall ◽  
Carotid Arteries ◽  
Carotid Bifurcation ◽  
Vessel Diameter ◽  
Atherosclerotic Plaques ◽  
Shear Stresses ◽  
Strongly Correlated ◽  
4D Flow ◽  
Bifurcation Angle

Background: Atherosclerosis manifests as a focal disease, often affecting areas with complex hemodynamics such as the carotid bifurcation. The magnitude and regularity of the hemodynamic shear stresses acting on the vessel wall are thought to generate risk patterns unique to each patient and play a role in the pathogenesis of atherosclerosis. The involvement of different expressions of shear stress in the pathogenesis of carotid atherosclerosis highlights the need to characterize and compare the differential impact of the various expressions of shear stress in the atherosclerotic carotid bifurcation. Therefore, the aim of this study is to characterize and compare hemodynamic wall shear stresses (WSS) in the carotid arteries of subjects with asymptomatic atherosclerotic plaques. Shear stresses were also compared against vessel diameter and bifurcation angle to examine the relationships with the geometry of the carotid bifurcation.Methods: 4D Flow MRI and contrast-enhanced MRA data were acquired for 245 subjects with atherosclerotic plaques of at least 2.7 mm in conjunction with the Swedish CArdioPulmonary bioImage Study (SCAPIS). Following automatic segmentation and geometric analysis, time-resolved WSS and near-wall turbulent kinetic energy (nwTKE) were derived from the 4D Flow data. Whole-cycle parameters including time-averaged WSS and nwTKE, and the oscillatory shear index (OSI) were calculated. Pairwise Spearman rank-correlation analyses were used to investigate relationships among the hemodynamic as well as geometric parameters.Results: One hundred and seventy nine subjects were successfully segmented using automated tools and subsequently geometric and hemodynamic analyses were performed. Temporally resolved WSS and nwTKE were strongly correlated, ρ = 0.64. Cycle-averaged WSS and nwTKE were moderately correlated, ρ = 0.57. Cycle-average nwTKE was weakly correlated to OSI (ρ = −0.273), revealing that nwTKE provides information about disturbed flow on the vessel wall that OSI does not. In this cohort, there was large inter-individual variation for both WSS and nwTKE. Both WSS and nwTKE varied most within the external carotid artery. WSS, nwTKE, and OSI were weakly correlated to vessel diameter and bifurcation angle.Conclusion: The turbulent and mean component of WSS were examined together in vivo for the first time, and a strong correlation was found between them. nwTKE presents the opportunity to quantify turbulent wall stresses in vivo and gain insight into the effects of disturbed flow on the vessel wall. Neither vessel diameter nor bifurcation angle were found to be strongly correlated to the turbulent or mean component of WSS in this cohort.

scholarly journals High Plasma Levels of Soluble Talin-1 in Patients with Coronary Artery Disease

2020 ◽  
Vol 2020 ◽  
pp. 1-8
Author(s):  
Masayuki Aoyama ◽  
Yoshimi Kishimoto ◽  
Emi Saita ◽  
Yukinori Ikegami ◽  
Reiko Ohmori ◽  
...  
Keyword(s):  
Coronary Artery Disease ◽  
Coronary Artery ◽  
Coronary Vessels ◽  
Focal Adhesions ◽  
High Plasma ◽  
Blood Levels ◽  
Atherosclerotic Plaques ◽  
Vessel Disease ◽  
Artery Disease

Aims. Talin-1 is a cytoskeletal protein that binds integrin, thereby leading to integrin activation and affecting focal adhesions. Recently, talin-1 expression was reported to be downregulated in human atherosclerotic plaques. However, blood levels of soluble talin-1 (sTalin-1) in patients with atherosclerotic disease, such as coronary artery disease (CAD), have not been elucidated. Methods. We measured plasma sTalin-1 levels in 349 patients undergoing elective coronary angiography. The severity of CAD was represented as the number of stenotic coronary vessels and segments. Results. Of the 349 study patients, CAD was found in 194 patients, of whom 88 had 1-vessel disease (1-VD), 60 had 2-vessel disease (2-VD), and 46 had 3-vessel disease (3-VD). Plasma sTalin-1 levels were higher in 194 patients with CAD than in 155 without CAD (CAD(-) group) (median 0.30 vs. 0.23 ng/mL, P<0.005). A stepwise increase in sTalin-1 levels was found depending on the number of >50% stenotic coronary vessels: 0.23 in CAD(-), 0.29 in 1-VD, 0.30 in 2-VD, and 0.32 ng/mL in 3-VD group, respectively, (P<0.05). High sTalin-1 level (>0.28 ng/mL) was found in 36% of CAD(-), 51% of 1-VD, 53% of 2-VD, and 59% of 3-VD group (P<0.025). sTalin-1 levels also correlated with the number of >50% stenotic segments (r=0.14, P<0.02). The multivariate analysis revealed that sTalin-1 levels were independently associated with CAD. The odds ratio for CAD was 1.83 (95%CI=1.14−2.93) for high sTalin-1 level (>0.28 ng/mL) (P<0.02). Conclusions. Plasma sTalin-1 levels in patients with CAD were found to be high and to be associated with the presence and severity of CAD, suggesting a role of sTalin-1 in the progression of coronary atherosclerosis.

Can O2Dysregulation Induce Premature Aging?

Physiology ◽  
2008 ◽  
Vol 23 (6) ◽  
pp. 333-349 ◽  
Author(s):  
Robert M. Douglas ◽  
Gabriel G. Haddad
Keyword(s):  
Intermittent Hypoxia ◽  
Molecular Mechanisms ◽  
Cell Injury ◽  
Prolonged Exposure ◽  
Cumulative Effect ◽  
Premature Aging ◽  
Cell Integrity ◽  
Catecholamine Biosynthesis ◽  
Disease States ◽  
Episodic Hypoxia

Chronic intermittent or episodic hypoxia, as occurs during a number of disease states, can have devastating effects, and prolonged exposure to this hypoxia can result in cell injury or cell death. Indeed, intermittent hypoxia activates a number of signaling pathways that are involved in oxygen sensing, oxidative stress, metabolism, catecholamine biosynthesis, and immune responsiveness. The cumulative effect of these processes over time can undermine cell integrity and lead to a decline in function. Furthermore, the ability to respond adequately to various stressors is hampered, and this is traditionally defined as premature aging or senescence. This review highlights recent advances in our understanding of the cellular and molecular mechanisms that are involved in the response to intermittent hypoxia and the potential interplay among various pathways that may accelerate the aging process.

High-Resolution Arterial Pressure-Area Loops in Rats

2009 ◽  
Author(s):  
Craig Fancourt ◽  
Yuzhuo Su ◽  
Jeffrey R. Sachs ◽  
Michelle Bunzel ◽  
Barry R. Campbell ◽  
...  
Keyword(s):  
High Resolution ◽  
Arterial Pressure ◽  
Pressure Pulse ◽  
Vascular System ◽  
Artery Wall ◽  
Pharmacological Interventions ◽  
Disease States ◽  
Pressure Area ◽  
Cardio Vascular ◽  
Contracting Heart

The artery wall is compliant and stretches in response to the traveling pressure pulse generated by the contracting heart. The dynamics of this motion are known to convey important information about the health of the artery and cardio-vascular system. For example, compliance, a measure of artery flexibility, decreases due to aging, as well as disease states such as hypertension and atherosclerosis. It also exhibits acute and chronic changes under pharmacological interventions.

scholarly journals Ligneous Conjunctivitis in Plasminogen-Deficient Mice

Blood ◽  
1998 ◽  
Vol 91 (5) ◽  
pp. 1616-1624 ◽  
Author(s):  
A.F. Drew ◽  
A.H. Kaufman ◽  
K.W. Kombrinck ◽  
M.J.S. Danton ◽  
C.C. Daugherty ◽  
...  
Keyword(s):  
Genetic Background ◽  
Direct Evidence ◽  
Therapeutic Strategies ◽  
Pathological Changes ◽  
Rare Form ◽  
Lesion Development ◽  
Ligneous Conjunctivitis ◽  
Plasminogen Deficiency ◽  
Human And Mouse ◽  
Deficient Mice

Abstract Ligneous conjunctivitis is a rare form of chronic pseudomembranous conjunctivitis that is associated with systemic membranous pathological changes. A probable link between plasminogen and ligneous conjunctivitis has been indicated by the recent diagnoses of plasminogen deficiency in five patients suffering from ligneous conjunctivitis. The current study reports that plasminogen-deficient mice develop conjunctival lesions indistinguishable from human ligneous conjunctivitis in both appearance and histology. Both human and mouse lesions contain acellular material rich in fibrin, and aberrant or disrupted epithelium. The incidence of lesion development in mice increases with age and is strongly influenced by genetic background. Interestingly, ligneous conjunctivitis was not observed in plasminogen-deficient mice simultaneously lacking fibrinogen. This study provides direct evidence that plasminogen deficiency is one cause of ligneous conjunctivitis and suggests that plasminogen-deficient mice may be an excellent model for the development of therapeutic strategies for the treatment of this debilitating disease.

Numerical Simulation of Blood Flow in the Renal Arteries: Influence of the Ostium Flow Diverter

2013 ◽  
Author(s):  
Scott Albert ◽  
Jenn Stroud Rossmann ◽  
Robert Balaban
Keyword(s):  
Shear Stress ◽  
Vessel Wall ◽  
Flow Diverter ◽  
Atherosclerotic Plaques ◽  
Residence Times ◽  
Branch Points ◽  
Tissue Microenvironment ◽  
Low Shear Stress ◽  
Arterial Branch ◽  
Low Shear

The tendency of atherosclerotic plaques to develop at arterial branch points is likely due to both the hemodynamics and macromolecular environment associated with these branch points. Arterial branches experience flow separation, which results in regions of low shear stress[1–3], and contributes to longer residence times that may allow for deposition of pro-atherogenic material in the vessel wall [2]. In addition, low shear stress itself may provide cellular signals that alter the tissue microenvironment in favor of atherogenesis [3, e.g.].

Airway epithelium and bronchial reactivity

1987 ◽  
Vol 65 (3) ◽  
pp. 448-450 ◽  
Author(s):  
P. M. Vanhoutte
Keyword(s):  
Epithelial Cells ◽  
Airway Epithelium ◽  
Vessel Wall ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Blood Vessel Wall ◽  
Respiratory Epithelial Cells ◽  
Relaxing Factor ◽  
Respiratory Epithelial

Damage to or dysfunction of respiratory epithelial cells may contribute to the etiology of bronchial hyperreactivity in asthma and airway infection. In the vascular system, endogenous neurohumoral mediators can cause either relaxation or contraction of the smooth muscle of the blood vessel wall because they cause the release of relaxing or contracting factor(s), respectively, from the vascular endothelial cells. This brief overview summarizes data from the author's laboratory, which suggests that release of relaxing factor(s) from epithelial cells contributes to the regulation of bronchomotor tone.

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