Explore chapters and articles related to this topic
Future Developments in Human Thermography
Published in James Stewart Campbell, M. Nathaniel Mead, Human Medical Thermography, 2023
James Stewart Campbell, M. Nathaniel Mead
Atherosclerosis entails the buildup of fatty plaque in the artery walls, ultimately restricting blood flow or flaking off as emboli. Atherosclerosis is a chronic inflammatory process.53 The inflammation is both local and systemic, with both the innate and adaptive immune systems playing key roles in its initiation and progression.54 Arteries are generally located too deep anatomically to be detected by thermal imaging (except during surgery), but they can be studied by other thermological methods.
Cardiovascular disease
Published in Sally Robinson, Priorities for Health Promotion and Public Health, 2021
Blood pressure is the pressure inside the arteries. It rises (systolic pressure) when the heart contracts and falls (diastolic pressure) when the heart relaxes. Hypertension means the pressure is too high. The heart is needing to work hard to move the blood, and the pressure in the arteries causes them to bulge (aneurysm), which damages the artery walls. This is more likely to happen if the arteries are already narrowed by atherosclerosis. It is a vicious circle. At some point an artery may burst/haemorrhage. High blood pressure tires the heart and encourages poor blood flow which leads to tissue and organ damage. The causes, symptoms and prevalence of high blood pressure are summarised in Tables 13.8 and 13.9.
Features of Lipid Metabolism in Diabetes Mellitus and Ischemic Heart Disease
Published in E.I. Sokolov, Obesity and Diabetes Mellitus, 2020
In persons with an increased level of total cholesterol in the blood serum (especially of LDLP) and a reduced content of HDLP, disorders in the lipid transportation system and a liability of atherosclerosis are noted. Numerous clinical studies showed that LDLP are the most dangerous. They carry cholesterol into the tissues, including an artery wall. They concentrate two-thirds of the cholesterol content in the blood serum.
Recent advances in treating hypertriglyceridemia in patients at high risk of cardiovascular disease with apolipoprotein C-III inhibitors
Published in Expert Opinion on Pharmacotherapy, 2023
Catherine M Spagnuolo, Robert A Hegele
The European Atherosclerosis Society recently published a consensus statement that critically appraises the current understanding of the metabolism of triglyceride-rich lipoproteins (TRL) and the pathophysiological mechanisms by which they contribute to atherosclerotic cardiovascular disease (ASCVD) [3]. The TRL metabolism produces TRL remnants less than 70 nm in diameter, such as chylomicron remnants, very low-density lipoprotein (VLDL) remnants and intermediate-density lipoprotein (IDL). Due to their small size, these particles can cross the endothelial layer and enter the subendothelial space of the artery wall. Elevated plasma levels of these TRL remnants can lead to accumulation of these particles in the subendothelial space and persistence within the artery wall. This process contributes to lesion initiation and progression through cholesterol deposition, endothelial dysfunction and inflammation, and prothrombotic effects. An unstable complex plaque eventually forms that is at risk of thrombus formation, plaque rupture, and occlusion of the arterial lumen [3].
The pulsatile 3D-Hemodynamics in a doubly afflicted human descending abdominal artery with iliac branching
Published in Computer Methods in Biomechanics and Biomedical Engineering, 2023
Sumit Kumar, S. K. Rai, B.V. Rathish Kumar, Om Shankar
The spatial discretization of the velocity-pressure coupling is carried out following the SIMPLE algorithm with a second-order upwind scheme for convective terms and a cell-based approximation for pressure gradients. A workstation of 48 cores with 64 GB RAM and an 8 GB graphics card is used to carry out the CFD simulations. For precise controls of velocity field near the artery walls, a fine grid with a thickness of 0.1 mm and a growth rate of 1.2 is used near the vessel wall. A localized meshing technique with 0.25 mm element size is used at various local coordinates. The transient flow analysis is carried out using the first-order implicit Euler method with a time step of size 0.01 ms. The convergence threshold values for the residuals are set at 10−4 for all equations, and it provided well-converged results at each of the time steps. All the simulations in the present work are carried out for at least three cardiac cycles till a periodic state in the solution has been reached. Flow simulation results for one complete cycle is presented and discussed in the next section.
Molecular and cellular biology of PCSK9: impact on glucose homeostasis
Published in Journal of Drug Targeting, 2022
Sègbédé E. R. Tchéoubi, Casimir D. Akpovi, Frédérique Coppée, Anne-Emilie Declèves, Sophie Laurent, Clément Agbangla, Carmen Burtea
Cardiovascular diseases are the main macrovascular complications of T2DM, involving atherosclerosis. Atherosclerosis is now considered as a chronic inflammation disease of the artery wall. Several studies showed that PCSK9 is an important player in atherosclerosis development. At a systemic level, serum PCSK9 promotes liver LDLR degradation and induces hypercholesterolaemia and elevated oxidised LDL (OxLDL), well-known atherosclerosis determinants. Serum PCSK9 level is thus considered as a cardiovascular disease biomarker [85, 154] and correlated positively with severity of artery lesions as well [155]. PCSK9 is involved in atherosclerosis by other non-canonical pathways as well [156]. At a local level, PCSK9 is secreted by vascular and blood cells involved in atherosclerotic plaque development: macrophages, endothelial cells and vascular smooth muscle cells. Intraplaque PCSK9 enhances oxLDL and foam cells production, and triggers local inflammation [32, 115, 156]. As far as PCSK9 genetic variants are concerned, LOF mutations or polymorphisms characterised by low level of LDL-c are associated with marked reduction of cardiovascular risk [157] whereas GOF variants are associated with high level of LDL-c and high risk of atherosclerotic cardiovascular diseases [9].