Atherosclerosis | definition of atherosclerosis by …
Coronary heart disease is a common term for the in the heart’s arteries that could lead to heart attack. But what about coronary artery disease? Is there a difference?
The short answer is often no — health professionals frequently use the terms interchangeably.
However, coronary heart disease , or CHD, is actually a result of coronary artery disease, or CAD, said Edward A. Fisher, M.D., Ph.D., M.P.H., an American Heart Association volunteer who is the Leon H. Charney Professor of Cardiovascular Medicine and also of the Marc and Ruti Bell Vascular Biology and Disease Program at the NYU School of Medicine.
With coronary artery disease, plaque first grows within the walls of the coronary arteries until the blood flow to the heart’s muscle is limited. . This is also called . It may be chronic, narrowing of the coronary artery over time and limiting of the blood supply to part of the muscle. Or it can be acute, resulting from a sudden rupture of a plaque and formation of a thrombus or blood clot.
The traditional risk factors for coronary artery disease are high , low , , family history, , , being post-menopausal for women and being older than 45 for men, according to Fisher. may also be a risk factor.
atherosclerosis explanation free
The endothelium is a single layer of cells thatlines the interior of the vascular system and has thus a strategicposition between the blood and the surrounding tissues. Endothelialcells are involved in a wide range of physiological processes, suchas the regulation of vascular tone, vascular permeability, bloodcoagulation/fibrinolysis and inflammation, which are required tomaintain proper vascular functioning () (). Endothelial dysfunction has beenobserved in patients with atherosclerosis and in patients thatexhibit CVD risk factors such as smoking, dyslipidaemia, obesityand diabetes mellitus (),and is considered one of the first indicators of futurecardiovascular morbidity and mortality (–). It should be noted that theendothelium is regarded as a critical target for radiation-inducedCVD.
With low doses and dose rates of radiation theresponse warrants further investigation. Mitchel exposed ApoE mice to low doses of radiation(0.025–0.5 Gy) at either the high (150 mGy/min) or low (1 mGy/min)dose rate (). The mice wereexposed at an early stage of atherosclerotic disease (2 months old)or at a late stage of atherosclerotic disease (8 months old). Dosesof 0.025–0.050 Gy, administered at both the low- and high-doserate, induced a protective effect by attenuating the formation ofnew lesions and the increase in the size of existing lesions, inmice exposed at an early stage. High-dose rate exposure however,increased the progression of lesion severity. The effect for miceexposed at a late stage of atherosclerotic disease with low-doserate was similar as that for mice exposed at an early stage. On theother hand, high-dose rate exposures protected against theprogression of lesion severity, opposite to what was observed inmice exposed at an early stage. Additional experiments withApoE mice with reduced p53 functionality(Trp53) revealed an important role for p53 inatherosclerosis progression (). For example, protective effects oflow-dose radiation delivered at both low and high dose rate wereobserved in Trp53 normal mice exposed at a late stage ofatherosclerotic disease. On the other hand, with the sameirradiation procedure, detrimental effects were observed inTrp53 mice exposed at a late stage of atheroscleroticdisease. Overall, these findings raised the importance of dose-rateeffects and p53 functionality on the development ofatherosclerosis. Furthermore, their findings point out that alinear extrapolation of the effects at high doses to low doses isnot appropriate.
Atherosclerosis — An Inflammatory Disease | NEJM
In this review article, Göran Hansson, a pioneer in the study of the role of inflammation in atherosclerosis and coronary artery disease, summarizes new ideas on the pathogenesis of acute coronary syndromes.
Atherosclerosis is an inflammatory disease
Irreparable DSB can cause cellular apoptosis, orpremature senescence (described below). Endothelial apoptosis hasimplications on both the micro- and macrovascular. Namely,endothelial cell death in the microvasculature leads to a decreasein capillary density. In addition, endothelial apoptosis has beenrelated to the development of atherosclerosis (,) as it may compromise theregulation of vascular tone, and increase the proliferation andmigration of vascular smooth muscle cells (VSMCs) (). Furthermore, thrombosis, themajor complication of atherosclerosis, can be triggered byendothelial cell death ().It should be noted that radiation-induced endothelial cellapoptosis is not solely a consequence of DNA damage. Indeed,ionizing radiation can act on the cellular membrane of endothelialcells as well, generating ceramide which can induce apoptosis().
Atherosclerosis: Basic Mechanisms | Circulation
Of course, endothelial models,although useful, are not fully representative for the situation. Yet, advances have been made, such as thedevelopment of co-culture models where endothelial cells arecultured with vascular smooth muscle cells to study theatherosclerotic process (,). In addition, 3-D cultures, whereendothelial cells are grown in a matrix allowing the formation oftubule-like structures are increasingly used to study angiogenesis(,). A recent review described indetail the use of these co-culture and 3-D culture models inradiation research ().