Coexistence of high visceral fat area and sarcopenia and atherosclerotic markers in older patients with diabetes: Is there an association?

Dear Sir, Sato et al.1 published in the August issue a study titled “Coexistence of high visceral fat area and sarcopenia is associated with atherosclerotic markers in old-old patients with diabetes: A cross-sectional study”. The authors aimed to investigate whether there is an association between sarcopenic obesity and the progression of atherosclerotic lesions in older patients1. In their cross-section study, 118 participants were included, “50 (42.4%) were men and 68 (57.6%) were women, with a median age of 80 years, and 6 (5%) had type 1 diabetes. The median body mass index (BMI) was 24.0 kg/m2, the median HbA1c level was 9.1%, and the median duration of diabetes mellitus was 18 years”1. As surrogate marker for preclinical atherosclerosis, the carotid intima-media thickness (cIMT) was used, measured by sonography1. The authors measured cIMT bilaterally at the common carotid artery (CCA1). The study showed that the cIMT “in the group showing sarcopenia with a high visceral fat area was significantly higher than that in the control group (P = 0.012)”1. The authors concluded, “Although further research is needed to clarify whether sarcopenic obesity should be treated as a risk factor for atherosclerosis, this study suggests that evaluation of both sarcopenia and visceral fat mass is important in the evaluation of older patients with diabetes mellitus because they may serve as markers of atherosclerosis”1. Some comments are here needed to evaluate the cIMT results of this study in a more balanced way. The authors measured only in one segment of the carotid tree, namely the CCA1. A single location cIMT measurement is performed by some authors for technical reasons, namely a higher spatial resolution of the far wall of the CCA2. The disadvantage of a single-site CCA measurement however, given the asymmetric presentation of atherosclerosis, is that it may coincide with a normal segment but of an atherosclerotic affected vessel, providing an inaccurate cIMT measure. Other authors perform therefore a multi-site cIMT data acquisition that considers several sections of the CA tree, for example, far/near walls of CCA, bifurcation, and/or internal CA3. Sato et al.1 did not report further, if cIMT measurement was synchronized with the cardiac cycle (the end-diastolic phase). CIMT values differ during the cardiac cycle, due to changes in vessel diameter with reported mean differences of 0.041 mm4. In summary: If cIMT is used as surrogate marker for preclinical atherosclerosis importantly to mind that submillimetric differences are sufficient to categorize subjects into different cIMT groups. Authors need to have a meticulous measurement protocol in place explaining, in respect of the rigor of scientific reporting, their applied cIMT methodology, to allow the reader for a balanced and full understanding of the obtained results. The cIMT data and conclusions drawn by Sato et al.1 should be analyzed within the context of these above-mentioned methodological limitations and be considered with caution. The author declares no conflict of interest.