V. T. Hurst1,2, S. E. Deery1, G. Sharma2, M. D. Coll1,2, M. Tao2, K. Trocha2, A. Longchamp2, C. K. Ozaki2, R. J. Guzman1 1Beth Israel Deaconess Medical Center,Vascular And Endovascular Surgery,Boston, MA, USA 2Brigham And Women’s Hospital,Vascular And Endovascular Surgery,Boston, MA, USA
Introduction: The mechanisms underlying calcification of atherosclerotic plaques remain obscure. Since carotid plaque calcification is associated with stability, and the adipose associated hormone adiponectin underlies multiple vasculo-protective pathways, we hypothesized that human adiponectin would positively correlate with severe carotid plaque calcification in a compartment specific (e.g. perivascular adipose) manner.
Methods: Fifty-five patients who received either a carotid endarterectomy (n=38) or open lower extremity revascularization (n=17) and who had a carotid duplex ultrasound were studied. After informed consent, blood, perivascular and subcutaneous adipose samples, and medical history were obtained. Carotid bulb plaque was assessed via duplex ultrasonography, and patients were stratified into two groups: none/mild or severe calcification. Potentially relevant biomarkers were measured by multiplex bead immunoassay after tissue protein isolation, and data were normalized to initial adipose tissue mass. Wilcoxon Rank Sum testing was used to compare adiponectin levels in none/mild versus severe calcification patients. Categorical variables were presented as counts (percentages); continuous variables were presented as mean (standard deviation) or median (interquartile range), based on the normality of distribution. Differences between those with none/mild calcification and those with severe calcification were assessed using the Fisher’s exact test for categorical variables and either the Student T test or the Mann Whitney U test for continuous variables, where appropriate. All tests were 2-sided, and a P-value of less than 0.05 was considered significant. Statistical analysis was conducted using STATA 14.1.
Results: Of the clinical/biologic factors evaluated, carotid plaque calcification most strongly associated with adiponectin. In all compartments assayed, adiponectin levels positively linked to severe carotid plaque calcification (note log scale).
Conclusion: Human plasma, subcutaneous, and perivascular adiponectin levels positively correlate with carotid plaque calcification. These findings suggest relationships between adipose associated biomediators and vascular calcification. Furthermore, adiponectin based interventions may serve as novel strategies toward vascular plaque stabilization.
