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Coronary Arterial and Venous Disease
Published in Paul Schoenhagen, Frank Dong, Cardiac CT Made Easy, 2023
Atherosclerotic plaque accumulation in the vessel wall begins long before the development of angiographic stenosis. Most acute coronary events are initiated by rupture or erosion of mildly stenotic but vulnerable (high-risk) lesions.85 Modern atherosclerosis imaging therefore evaluates overall plaque burden and plaque characteristics as predictors of future cardiovascular risk. Non-enhanced CT imaging (CT calcium scoring) only allows for the assessment of calcified plaque, while contrast-enhanced CTA allows differentiation of calcified and non-calcified plaque.
Non-DR Retinal Vascular Diseases
Published in Ching-Yu Cheng, Tien Yin Wong, Ophthalmic Epidemiology, 2022
Sobha Sivaprasad, Luke Nicholson, Shruti Chandra
Elevated cholesterol levels are responsible for atherosclerotic plaque build-up in the blood vessels. These plaques eventually throw microemboli responsible for retinal arterial occlusion. It is essential to note that high body mass index and triglycerides have a less important role in the atherogenic pathogenesis of retinal artery occlusion, while the low-density lipoproteins is the fraction that has a more potent role in the etiology.
Endarterectomy for Asymptomatic Carotid Artery Stenosis
Published in Juan Carlos Jimenez, Samuel Eric Wilson, 50 Landmark Papers Every Vascular and Endovascular Surgeon Should Know, 2020
Juan Carlos Jimenez, Samuel Eric Wilson
Finally, medical management, as a form of primary prevention, has clearly improved over the years. The introduction of statin therapy to reduce LDL levels has had a remarkable impact upon atherosclerotic plaque stabilization and now figures prominently in primary prevention. This has led to a re-examination of the role of CEA in patients with asymptomatic carotid stenosis with the advent of the CREST 2 study. CREST 2 is a two-track, prospective, randomized, controlled trial that is designed to compare the benefit of either carotid stent/angioplasty (CAS) plus intensive medical management or CEA plus intensive medical management versus intensive medical management alone. Intensive medical management includes 325 mgm aspirin daily, the use of a statin drug to keep LDL cholesterol below 70 mgm/dcL, and medical management to keep systolic blood pressure below 130 mmHg. For diabetic patients it means careful control to maintain their HbA1c below 7%. Intensive medical management also includes an exercise program supervised to accommodate a patient's tolerance, as well as a program to help those still using tobacco products, to quit. At this time, the study enrollment is at about the halfway mark. Once enrollment is complete and the last patient has had 2 years of follow-up, we will know whether or not ACAS is still relevant.6,7
The impact of baseline calcified plaque volume on coronary rapid plaque progression by serial coronary computed tomography angiography in patients with type 2 diabetes
Published in Annals of Medicine, 2023
Zhijie Jian, Guolin Yao, Huafeng Guo, Hui Liu, Bolin Li, Bolang Yu, Jian Yang, Lele Cheng
To understand how plaque composition can be mapped, some important pathophysiological aspects of atherosclerotic disease should first be highlighted. Atherosclerotic plaque is composed of extracellular lipid particles, foam cells, and debris that accumulates in the intima of the arterial wall, forming a lipid or necrotic core. The core is surrounded by a layer of collagen-rich matrix and smooth muscle cells covered by endothelial cells, known as the fibrous cap [1]. During their evolution, many atherosclerotic plaques develop regions of calcification that arise from dysregulation of deposition and impaired clearance [2]. Many factors have an impact on the occurrence and development of plaque, most notably cholesterol, inflammation, and endothelium, which are involved in the formation of various plaque components [3]. Therefore, the content of different components of plaque can affect the progression and outcome of plaque.
Optimisation of individual cardiovascular risk assessment in a German coronary artery disease cohort using a commercial test for genetic polymorphisms – a pilot study
Published in Acta Cardiologica, 2023
Jona B. Krohn, Clemens Neubauer, Simon Fischer, Christian Oberkanins, Hugo A. Katus, Christian A. Gleissner
Coronary artery disease (CAD) is a leading cause of death worldwide [1], posing a significant risk to the ageing population of the Western world. Despite major advances in diagnosis and therapeutic strategies in past decades, a worrisome global trend toward an increasing number of cardiovascular deaths attributed to CAD has been reported [2]. As of today, CAD has been generally recognised as an inflammatory disease of the arterial wall propagated by a number of colluding cardiovascular risk factors [3]. Among these, arterial hypertension, hyperlipidaemia, diabetes mellitus, obesity or a history of tobacco consumption are known to effectuate atherosclerotic plaque genesis and growth. Moreover, a number of additional risk factors such as genetics [4] or a residual inflammatory risk [5] have emerged in past decades, further complicating the multidimensional approach to cardiovascular risk estimation.
Predictive value of HDL function in patients with coronary artery disease: relationship with coronary plaque characteristics and clinical events
Published in Annals of Medicine, 2022
Marco Magnoni, Daniele Andreini, Angela Pirillo, Patrizia Uboldi, Roberto Latini, Alberico L. Catapano, Aldo P. Maggioni, Giuseppe D. Norata
Can this finding be explained by the correlation between SR-BI-mediated cholesterol efflux and atherosclerotic plaque features? We have previously shown that quantitative parameters of CCTA plaque assessment, more specifically the coronary plaque volume, and particularly the non-calcified plaque volume, are the most powerful predictors of cardiovascular events at follow-up, even beyond lumen stenosis and clinical risk profile [32]. Therefore, we tested the correlation between SR-BI- and ABCA-1-mediated cholesterol efflux and coronary plaque features, on the premise that improved cholesterol efflux should reduce cholesterol burden in the arteries and thus improve plaque features. Unexpectedly, total plaque volume was only slightly reduced in patients in the highest quartile of SR-BI-mediated cholesterol efflux. Furthermore, the prevalence of patients with severe lumen stenosis, arterial remodelling, plaque burden, napkin ring sign, or spotty calcification did not differ among quartiles of SR-BI-mediated cholesterol efflux. Similar observations were reported for other markers of atherosclerotic plaque quality and burden. These observations suggest that, although HDL function may be a predictor of cardiovascular disease, this role does not appear to be related to improved atherosclerotic plaque characteristics.