1 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU2 Wharton School of the University of Pennsylvania3 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU
Objectives: Aging is an important independent determinant of plaque biology. This study aimed to investigate the effect of aging on atherosclerotic plaque inflammation and calcification metabolism. Methods: Thirteen healthy volunteers without traditional cardiovascular risk factors were prospectively assessed by 18-FDG (inflammation) and Sodium 18-Fluoride (Na-18F) (calcification metabolism) PET CT imaging. Global aortic uptake of 18-FDG and Na-18F was quantified by subtracting the blood pool SUVmean from the aortic SUVmax (cSUV) [maximum SUVaorta - mean SUVblood pool]. Calculating regression and correlation coefficients summarized the data. Results: A quadratic relationship was observed between aging and aortic 18-FDG and aortic Na-18F avidity. A second order polynomial regression established that aging is a predictor of the degree of aortic plaque inflammation (R = 0.524; F statistic = 4.93; P = 0.036) and aortic calcification metabolism (R = 0.447; F statistic = 3.64; P = 0.069). A strong linear relationship was observed between aortic plaque inflammation and aortic plaque calcification metabolism (Pearson’s r = 0.74 [95% CI; 0.30, 0.92]; t statistic = 3.53; P = 0.005). Conclusions: Based on preliminary data, a quadratic relationship appears to exist between aging and plaque inflammation. Furthermore, a quadratic relationship was observed between aging and plaque calcification metabolism. In line with these observations, a linear relationship was observed between atherosclerotic plaque inflammation and plaque calcification metabolism. These data suggest that vascular calcification metabolism is highly depended on vascular inflammation. Based on these data, we hypothesize that inflammation induces calcification metabolism and that established plaque calcification might counteract the inflammatory component of atherosclerosis.