Search

ObjectivePericardial fat and lipoprotein abnormalities contribute to increased risk of cardiovascular disease (CVD). We investigated the relationship between pericardial fat volume and lipoprotein distribution, and whether the association of pericardial fat volume with subclinical atherosclerosis and incident CVD events differs according to lipoprotein distribution.MethodsWe analyzed data from 5407 participants from the Multi-Ethnic Study of Atherosclerosis who had measurements of pericardial fat volume, lipoprotein distribution, carotid intima-media thickness (IMT), and coronary artery calcium (CAC). All participants were free of clinically apparent CVD at baseline. Incident CVD was defined as any adjudicated CVD event.ResultsAfter adjusting for demographic factors, traditional risk factors, and biomarkers of inflammation and hemostasis, a larger pericardial fat volume was associated with higher large VLDL particle (VLDL-P) concentration and small HDL particle (HDL-P) concentration, and smaller HDL-P size (regression coefficients = 0.585 nmol/L, 0.366 μmol/L, and -0.025 nm per SD increase in pericardial fat volume respectively, all P 0.05).ConclusionPericardial fat is associated with atherogenic lipoprotein abnormalities. However, its relationship with subclinical atherosclerosis and incident CVD events does not differ according to lipoprotein distribution.

ObjectivePericardial fat may increase the risk of cardiovascular disease (CVD) by increasing circulating levels of inflammation and hemostasis biomarkers. We investigated the associations of pericardial fat with inflammation and hemostasis biomarkers, as well as incident CVD events, and whether there are any ethnic differences in these associations.MethodsWe analyzed results from 6415 participants from the Multi-Ethnic Study of Atherosclerosis who had measurements of pericardial fat volume and circulating levels of C-reactive protein (CRP), fibrinogen, interleukin (IL)-6, factor VIII, D-dimer and plasmin-antiplasmin complex (PAP), and had a mean follow-up period of 9.5 years. Incident CVD event was defined as any adjudicated CVD event.ResultsAfter adjusting for confounding factors, pericardial fat volume was positively associated with natural log (ln) of IL-6 levels, but inversely associated with ln D-dimer and ln PAP levels (β = 0.067, -0.032, and -0.105 respectively, all P < 0.05). Although a larger pericardial fat volume was associated with a higher risk of incident CVD, the association was attenuated to borderline significance after adjusting for traditional cardiovascular risk factors (P = 0.050). There was a borderline significant ethnicity interaction (P = 0.080), whereby the association between pericardial fat volume and incident CVD was significant in Hispanic Americans, even after further adjusting for biomarkers of inflammation and hemostasis (hazard ratio = 1.31 per SD increase, 95% confidence interval 1.09-1.57, P = 0.004).ConclusionPericardial fat was associated with several inflammation and hemostasis biomarkers. The association of pericardial fat with incident CVD events was independent of these biomarkers only among Hispanic Americans.

ObjectiveInsulin resistance may be related to vascular calcification as both are associated with abdominal obesity. We investigated the association of insulin resistance with abdominal aortic calcium (AAC), coronary artery calcium (CAC) and thoracic aortic calcium (TAC), and whether it differs according to different levels of subcutaneous fat area (SFA) and visceral fat area (VFA) in a cross-sectional study design.MethodsWe investigated 1632 participants without diabetes from the Multi-Ethnic Study of Atherosclerosis with valid data on homeostasis model assessment index (HOMA-IR), AAC, CAC, and TAC. Adipocytokines, SFA, and VFA were also determined.ResultsHOMA-IR was associated with the presence of CAC, but not AAC and TAC, and the association remained significant after adjusting for traditional risk factors, adipocytokines, abdominal muscle mass, SFA, and VFA (prevalence ratio = 1.04 per one interquartile range [IQR] increase, P = 0.01). As the strength of the association of HOMA-IR with vascular calcification may differ by abdominal fat composition, subgroup analysis was performed among participants with different tertiles of SFA and VFA. Significant interactions between HOMA-IR with SFA and VFA separately were observed for the presence of TAC, but not AAC and CAC, even after adjusting for confounding factors. The association of HOMA-IR with TAC tended to be stronger in participants with more SFA and VFA.ConclusionsAtherosclerotic calcification, especially in the coronary arteries, is related to insulin resistance. Further studies are needed to delineate the mechanisms by which visceral obesity can lead to vascular calcification.