Abstract
Introduction: The accumulation of visceral abdominal tissue (VAT) seems to be a hallmark feature of abdominal obesity and substantially contributes to metabolic abnormalities. There are numerous factors that make the body-mass index (BMI) a suboptimal measure of adiposity. The visceral adiposity index (VAI) may be considered a simple surrogate marker of visceral adipose tissue dysfunction. However, the evidence comparing general to visceral adiposity in CAD is scarce. Therefore, we have set out to investigate visceral adiposity in relation to general adiposity in patients with stable CAD. Material and methods: A total of 204 patients with stable CAD hospitalized in the Department of Medicine and the Department of Geriatrics entered the study. Based on the VAI-defined adipose tissue dysfunction (ATD) types, the study population (N = 204) was divided into four groups: (1) no ATD (N = 66), (2) mild ATD (N = 50), (3) moderate ATD (N = 48), and (4) severe ATD (N = 40). Nutritional status was assessed using the Controlling Nutritional Status (CONUT) score. Results: Patients with moderate and severe ATD were the youngest (median 67 years), yet their metabolic age was the oldest (median 80 and 84 years, respectively). CONUT scores were similar across all four study groups. The VAI had only a modest positive correlation with BMI (r = 0.59 p < 0.01) and body adiposity index (BAI) (r = 0.40 p < 0.01). There was no correlation between VAI and CONUT scores. There was high variability in the distribution of BMI-defined weight categories across all four types of ATD. A total of 75% of patients with normal nutritional status had some form of ATD, and one-third of patients with moderate or severe malnutrition did not have any ATD (p = 0.008). In contrast, 55–60% of patients with mild, moderate, or severe ATD had normal nutritional status (p = 0.008). ROC analysis demonstrated that BMI and BAI have poor predictive value in determining no ATD. Both BMI (AUC 0.78 p < 0.0001) and BAI (AUC 0.66 p = 0.003) had strong predictive value for determining severe ATD (the difference between AUC 0.12 being p = 0.0002). However, BMI predicted mild ATD and severe ATD better than BAI. Conclusions: ATD and malnutrition were common in patients with CAD. Notably, this study has shown a high rate of misclassification of visceral ATD via BMI and BAI. In addition, we demonstrated that the majority of patients with normal nutritional status had some form of ATD and as much as one-third of patients with moderate or severe malnutrition did not have any ATD. These findings have important clinical ramifications for everyday practice regarding the line between health and disease in the context of malnutrition in terms of body composition and visceral ATD, which are significant for developing an accurate definition of the standards for the intensity of clinical interventions.
Highlights
The accumulation of visceral abdominal tissue (VAT) seems to be a hallmark feature of abdominal obesity and substantially contributes to metabolic abnormalities
A total of 75% of patients with normal nutritional status had some form of adipose tissue dysfunction (ATD), and one-third of patients with moderate or severe malnutrition did not have any ATD (p = 0.008)
We demonstrated that the majority of patients with normal nutritional status had some form of ATD and as much as one-third of patients with moderate or severe malnutrition did not have any ATD
Summary
The accumulation of visceral abdominal tissue (VAT) seems to be a hallmark feature of abdominal obesity and substantially contributes to metabolic abnormalities. The evidence comparing general to visceral adiposity in CAD is scarce. We have set out to investigate visceral adiposity in relation to general adiposity in patients with stable CAD. Adipose tissue has long been viewed as a storage place for fatty acids. This traditional view has been replaced by the theory that adipose tissue is a crucial organ of the endocrine system, which releases various adipokines connected to the pathogenesis of a myriad of obesity-related metabolic disturbances. Visceral adiposity may explain more of the variance in the CVD risk factors than would general obesity [5]
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Disclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.