Key result
Abdominal adiposity, particularly waist-to-height ratio, was significantly associated with the progression of total carotid plaque area (mean change 0.665 mm2 per 1 SD increase), an effect largely mediated by cardiometabolic markers.
Why the study?
Few reports are available on the contribution of general and abdominal obesity to the progression of carotid atherosclerosis in late adulthood.
Does higher adiposity (measured by BMI, WC, WHR, WHtR) increase the progression of carotid atherosclerosis in adults?
Cohort (n=4,345)
No
Does higher adiposity (measured by BMI, WC, WHR, WHtR) increase the progression of carotid atherosclerosis in adults?
Abdominal obesity is more strongly associated with the progression of carotid atherosclerosis than general obesity, an effect that appears largely mediated by traditional cardiometabolic risk factors.
Answers are grounded in this paper and cite their sources.
Supports WHtR for carotid atherosclerosis risk stratification; hypothesis-generating for mediation effects in observational cohorts.
BACKGROUND: Few reports are available on the contribution of general and abdominal obesity to the progression of carotid atherosclerosis in late adulthood. This study investigated the impact of four simple anthropometric measures of general and abdominal obesity on the progression of carotid atherosclerosis and the extent to which the association between adiposity and the progression of plaque burden is mediated by cardiometabolic markers. METHODS: Four thousand three hundred forty-five adults (median age 60) from the population-based Tromsø Study were followed over 7 years from the first carotid ultrasound screening to the next. The progression of carotid atherosclerosis was measured in three ways: incidence of plaques in previously plaque-free participants; change in the number of plaques; and total plaque area (TPA). We used generalised linear models to investigate the association between each adiposity measure - body mass index (BMI), waist circumference (WC), waist-to-hip ratio (WHR), and waist-to-height ratio (WHtR) - and each outcome. Models were adjusted for potential confounders (age, sex, smoking, education, physical activity). The pathways through which any associations observed might operate were investigated by further adjusting for cardiometabolic mediators (systolic blood pressure, cholesterol, and HbA1c). Effect sizes were substantially reduced after the adjustment for potential mediators. CONCLUSIONS: Abdominal obesity indirectly measured with WC seems more strongly associated with the progression of TPA than general obesity. These associations appear to be largely mediated by known cardiometabolic markers.
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Imahori et al. (2020) conducted a cohort in Carotid atherosclerosis (n=4,345). Abdominal adiposity (Waist-to-height ratio) vs. Lower adiposity (per 1 SD decrease) was evaluated on Progression of total plaque area (TPA) (MD 0.665 mm2, 95% CI 0.198, 1.133). Abdominal adiposity, particularly waist-to-height ratio, was significantly associated with the progression of total carotid plaque area (mean change 0.665 mm2 per 1 SD increase), an effect largely mediated by cardiometabolic markers.
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