Is Obesity a Risk Factor for Carotid Atherosclerotic Disease?—Opportunistic Review

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Abstract

Obesity is a risk factor for coronary atherosclerosis. However, the influence of adipose tissue in carotid atherosclerosis is not completely understood. No systematic review/meta-analysis was previously performed to understand if obesity is a risk factor for carotid atherosclerosis. This paper aims to provide an opportunistic review of the association between obesity and carotid atherosclerosis and define the role of the different adipose tissue depots in the characteristics of carotid stenosis. The databases PubMed and Cochrane Library were searched on 15–27 April and 19 May 2021. A total of 1750 articles published between 1985 and 2019 were identified, 64 were preselected, and 38 papers (35,339 subjects) were included in the final review. The most frequent methods used to determine obesity were anthropometric measures. Carotid plaque was mostly characterized by ultrasound. Overall obesity and visceral fat were not associated with the presence of carotid plaque when evaluated separately. Waist-hip ratio, however, was a significant anthropometric measure associated with the prevalence of carotid plaques. As it reflected the ratio of visceral and subcutaneous adipose tissue, the balance between these depots could impact the prevalence of carotid plaques.

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Inflammation and plaque vulnerability.

G K Hansson, P. Libby, I Tabas (2015)

Atherosclerosis is a maladaptive, nonresolving chronic inflammatory disease that occurs at sites of blood flow disturbance. The disease usually remains silent until a breakdown of integrity at the arterial surface triggers the formation of a thrombus. By occluding the lumen, the thrombus or emboli detaching from it elicits ischaemic symptoms that may be life-threatening. Two types of surface damage can cause atherothrombosis: plaque rupture and endothelial erosion. Plaque rupture is thought to be caused by loss of mechanical stability, often due to reduced tensile strength of the collagen cap surrounding the plaque. Therefore, plaques with reduced collagen content are thought to be more vulnerable than those with a thick collagen cap. Endothelial erosion, on the other hand, may occur after injurious insults to the endothelium instigated by metabolic disturbance or immune insults. This review discusses the molecular mechanisms involved in plaque vulnerability and the development of atherothrombosis.

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The clinical importance of visceral adiposity: a critical review of methods for visceral adipose tissue analysis.

Scott Shuster, M Patlas, M Mourtzakis … (2011)

As a result of the rising epidemic of obesity, understanding body fat distribution and its clinical implications is critical to timely treatment. Visceral adipose tissue is a hormonally active component of total body fat, which possesses unique biochemical characteristics that influence several normal and pathological processes in the human body. Abnormally high deposition of visceral adipose tissue is known as visceral obesity. This body composition phenotype is associated with medical disorders such as metabolic syndrome, cardiovascular disease and several malignancies including prostate, breast and colorectal cancers. Quantitative assessment of visceral obesity is important for evaluating the potential risk of development of these pathologies, as well as providing an accurate prognosis. This review aims to compare different methods of measuring visceral adiposity with emphasis on their advantages and drawbacks in clinical practice.

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Abdominal obesity is associated with accelerated progression of carotid atherosclerosis in men.

Timo Lakka, Hanna-Maaria Lakka, Riitta Salonen … (2001)

Abdominal obesity increases the risk of clinical atherosclerotic diseases, but whether it accelerates the progression of preclinical atherosclerosis is unknown. We studied whether waist-to-hip ratio (WHR) and waist circumference are associated with 4-year increase in indicators of common carotid atherosclerosis, assessed by B-mode ultrasonography, in 774 Finnish men aged 42-60 years without atherosclerotic diseases. Men with WHR of 0.96 (thirds) had increase in maximal intima-media thickness (IMT) of 0.230, 0.255 and 0.281 mm/4 years (P=0.007 for linear trend; P=0.025 for difference) and plaque height of 0.241, 0.254 and 0.291 mm/4 years (P=0.005, P=0.013) adjusting for age, body mass index and technical covariates. Men with waist circumference of 93 cm (thirds) had increase in maximal IMT of 0.227, 0.251 and 0.290 mm/4 years (P=0.011, P=0.035) and plaque height of 0.229, 0.263 and 0.296 mm/4 years (P=0.003, P=0.013). These associations were stronger in men with high (> or =3.8 mmol/l) than lower serum LDL cholesterol (P<0.05 for interaction). This is the first documentation that abdominal obesity is associated with accelerated progression of atherosclerosis, and supports the view that it is an important cardiovascular risk factor. This study emphasizes the role of avoiding abdominal obesity to prevent atherosclerotic diseases.