Natural History of Diabetic Coronary Atherosclerosis by Quantitative Measurement of Serial Coronary Computed Tomographic Angiography

Kim, Ung; Leipsic, Jonathon; Sellers, Stephanie; Shao, Michael; Blanke, Philipp; Hadamitzky, Martin; Kim, Yong Jin; Conte, Edoardo; Andreini, Daniele; Pontone, Gianluca; Budoff, Matthew J.; Gottlieb, Ilan; Lee, Byoung Kwon; Chun, Eun Ju; Cademartiri, Filippo; Maffei, Erica; Marques, Hugo; Shin, Sanghoon; Choi, Jung Hyun; Virmani, Renu; Samady, Habib; Stone, Peter H.; Berman, Daniel S.; Narula, Jagat; Shaw, Leslee J.; Bax, Jeroen J.; Min, James K.; Chang, Hyuk Jae

doi:10.1016/j.jcmg.2018.04.009

Cited by 70 publications

(54 citation statements)

References 31 publications

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“…Thus, Won et al used coronary computed tomography angiography to demonstrate that atherosclerotic lesion progression is faster in people with diabetes than in those without, despite having lower LDL cholesterol at baseline (124). In a similar study, Kim et al demonstrated that plaque progression (necrotic core expansion), was accelerated in diabetes-again in the absence of elevated LDL cholesterol (125). These studies highlight the concept that diabetes accelerates atherosclerotic lesion progression even in settings in which LDL cholesterol levels are lower or similar as compared with the non-diabetic control cohort.…”

Section: Diabetes Exacerbates Lesion Progression and Necrotic Core Exmentioning

confidence: 99%

Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes

Kanter

Hsu

Bornfeldt

2020

Front. Cardiovasc. Med.

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With the increasing prevalence of diabetes worldwide, vascular complications of diabetes are also on the rise. Diabetes results in an increased risk of macrovascular complications, with atherosclerotic cardiovascular disease (CVD) being the leading cause of death in adults with diabetes. The exact mechanisms for how diabetes promotes CVD risk are still unclear, although it is evident that monocytes and macrophages are key players in all stages of atherosclerosis both in the absence and presence of diabetes, and that phenotypes of these cells are altered by the diabetic environment. Evidence suggests that at least five pro-atherogenic mechanisms involving monocytes and macrophages contribute to the accelerated atherosclerotic lesion progression and hampered lesion regression associated with diabetes. These changes include (1) increased monocyte recruitment to lesions; (2) increased inflammatory activation; (3) altered macrophage lipid accumulation and metabolism; (4) increased macrophage cell death; and (5) reduced efferocytosis. Monocyte and macrophage phenotypes and mechanisms have been revealed mostly by different animal models of diabetes. The roles of specific changes in monocytes and macrophages in humans with diabetes remain largely unknown. There is an ongoing debate on whether the changes in monocytes and macrophages are caused by altered glucose levels, insulin deficiency or insulin resistance, lipid abnormalities, or combinations of these factors. Current research in humans and mouse models suggests that reduced clearance of triglyceride-rich lipoproteins and their remnants is one important mechanism whereby diabetes adversely affects macrophages and promotes atherosclerosis and CVD risk. Although monocytes and macrophages readily respond to the diabetic environment and can be seen as protagonists in diabetes-accelerated atherosclerosis, they are likely not instigators of the increased CVD risk.

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Section: Diabetes Exacerbates Lesion Progression and Necrotic Core Exmentioning

confidence: 99%

Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes

Kanter

Hsu

Bornfeldt

2020

Front. Cardiovasc. Med.

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“…Evidence indicates that DM is associated with significantly higher coronary artery total plaque volume, independent of other CAD risk factors [ 2 ]. In addition, patients with T2DM have greater coronary plaque progression, and in particular significantly greater progression of plaques associated with adverse outcomes [ 3 ]. Risk factors related to plaque progression in patients with T2DM include hypertension [ 2 ], male sex, and mean plaque burden > 75% at baseline [ 3 ].…”

Section: Introductionmentioning

confidence: 99%

Impact of long-term glucose variability on coronary atherosclerosis progression in patients with type 2 diabetes: a 2.3 year follow-up study

Tang

Luo

et al. 2020

Cardiovasc Diabetol

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Background Glycemic variability (GV) confers a risk of cardiovascular events. In this study, we aimed to investigate whether long-term GV has an impact on coronary atherosclerosis progression in patients with type 2 diabetes mellitus (T2DM). Methods A total of 396 patients with T2DM who had coronary computed tomography angiography and laboratory data available at baseline and for follow-up evaluations [median 2.3 (1.8–3.1) years] were included. Fasting plasma glucose (FPG) was measured every 1–3 months, and HbA1c was measured quarterly. The coefficient of variation (CV) of HbA1c and FPG were calculated as measures of GV. Quantitative assessment of coronary plaques was performed by measuring the annual change and progression rate of total plaque volume (TPV). Significant progression was defined as annual TPV progression ≥ 15%. Multivariable regression analyses were used to assess the effects of GV on atherosclerosis progression. Results In the 396 patients, the annual change in TPV was 12.35 ± 14.23 mm3, and annual progression rate was 13.36 ± 12.69%. There were 143 (36.11%) patients with significant progression, and they had a significantly higher CV-HbA1c (P < 0.001) and CV-FPG (P < 0.001) than those without significant progression. In multivariable regression analyses, both CV-HbA1c and CV-FPG were independent predictors of annual change in TPV [CV-HbA1c: β = 0.241 (0.019–0.462), P = 0.034; CV-FPG: β = 0.265 (0.060–0.465), P = 0.012], annual TPV progression [CV-HbA1c: β = 0.214 (0.023–0.405), P = 0.029; CV-FPG: β = 0.218 (0.037–0.399), P = 0.019], and significant atherosclerosis progression [CV-HbA1c: odds ratio [OR] = 1.367 (1.149–1.650), P = 0.010; CV-FPG: OR = 1.321 (1.127–1.634), P = 0.013]. Conclusions Long-term GV is associated with accelerated progression of coronary atherosclerosis independent of conventional risk factors in patients with T2DM. Trial registration ClinicalTrials.gov (NCT02587741), October 27, 2015; retrospectively registered

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“…A therosclerosis is caused by the deposition of fat, thrombi, connective tissue, and calcium carbonate in blood vessels [1][2][3] and includes aortal atherosclerosis, coronary atherosclerosis, cerebral atherosclerosis, renal atherosclerosis, and others. [4][5][6][7] In light of the third report by the World Health Organization (Geneva, Switzerland), 10 million people die of cardiovascular disease caused by atherosclerosis annually around the world. 8 As we all know, atherosclerosis is the main cause of cerebrovascular diseases, and it can lead to thickening and hardening of the arterial wall and stenosis of the vascular lumen.…”

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confidence: 99%

Comparison of the Diagnostic Performances of Ultrasound, High‐Resolution Magnetic Resonance Imaging, and Positron Emission Tomography/Computed Tomography in a Rabbit Carotid Vulnerable Plaque Atherosclerosis Model

Wang

Liu

et al. 2020

J of Ultrasound Medicine

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Objectives-Our study aimed to evaluate the diagnostic performances of 3 routine examination methods for cerebrovascular disease in a rabbit carotid artery atherosclerosis model. Methods-A total of 12 New Zealand rabbits were included: 4 in a control group and 8 in an experimental group. A clinically relevant atherosclerosis rabbit model was induced by left common carotid artery ligation and a 12-week highfat diet. Atherosclerosis was further confirmed by a histopathologic analysis. Then carotid ultrasound (US) imaging, high-resolution magnetic resonance imaging (HRMRI), and positron emission tomography (PET)/computed tomography (CT) were performed on this model to evaluate the diagnostic performances. Results-Carotid US showed plaque formation in the left common carotid artery and little plaque in the right common carotid artery in the experimental group. In addition, HRMRI showed stenosis formation in the left common carotid artery in the experimental group. At the horizontal level, plaques were found in the left common carotid artery, and no plaques were found in the right common carotid artery in the experimental group. Also, PET/CT showed local hypermetabolism and vulnerable plaques in the left common carotid artery of the experimental group, whereas no hypermetabolism was found in the right common carotid artery of the experimental group. Moreover, the soft plaques detected by carotid US were different from the vulnerable plaques detected by PET/CT. The unstable plaques on HRMRI were the same as the hypermetabolic vulnerable plaques on PET/CT. Conclusions-High-resolution MRI is recommended for the evaluation of neck and intracranial vascular stenosis and plaque properties in patients with stroke.

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Natural History of Diabetic Coronary Atherosclerosis by Quantitative Measurement of Serial Coronary Computed Tomographic Angiography

Abstract: People with DM experience greater PP, particularly significantly greater progression in adverse plaque, than those without DM. Male sex and mean plaque burden >75% at baseline were identified as independent risk factors for PP.

Cited by 70 publications

References 31 publications

Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes

Monocytes and Macrophages as Protagonists in Vascular Complications of Diabetes

Impact of long-term glucose variability on coronary atherosclerosis progression in patients with type 2 diabetes: a 2.3 year follow-up study

Comparison of the Diagnostic Performances of Ultrasound, High‐Resolution Magnetic Resonance Imaging, and Positron Emission Tomography/Computed Tomography in a Rabbit Carotid Vulnerable Plaque Atherosclerosis Model

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