Blomberg, Björn4; Thomassen, Anders4; Simonsen, Jane Angel4; Hildebrandt, Malene4; Diederichsen, Axel Cosmus Pyndt5; Mickley, Hans5; Alavi, Abass3; Høilund-Carlsen, Poul Flemming4
1 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU2 Cardiology, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU3 Wharton School of the University of Pennsylvania4 Clinical Physiology and Nuclear Medicine, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU5 Cardiology, Department of Clinical Research, Det Sundhedsvidenskabelige Fakultet, SDU
Aim: Aging is an important independent risk factor for the inception and maturation of atherosclerotic plaques. This study aimed to investigate the effect of aging on atherosclerotic plaque inflammation and molecular calcification. Methods: Thirteen healthy volunteers without traditional cardiovascular risk factors were prospectively assessed by 18F-FDG (inflammation) and sodium 18F-fluoride (18F-NaF) (molecular calcification) PET CT imaging. Global aortic uptake of 18F-FDG and 18F-NaF was determined semi-quantitatively by calculating the average blood pool corrected standardized uptake value (cSUV) [Mean SUVAORTA - Mean SUVBLOOD POOL]. Furthermore, the average maximum 18F-NaF cSUV was determined in the coronary arteries. Calculating regression and correlation coefficients summarized the data. Results: A quadratic relationship was observed between aging and aortic 18F-FDG avidity. A second order polynomial regression established that aging is a strong predictor of the degree of aortic plaque inflammation (R2 = 0.71, F statistic = 11.98, P = 0.002). A linear relationship was observed between aging and molecular calcification. Linear regression established that aging is a predictor of both the degree of aortic (R2 = 0.50, F statistic = 10.18, P = 0.001) and coronary artery (R2 = 0.61, F statistic = 15.64, P < 0.001) molecular calcification. A very strong relationship was observed between aortic and coronary molecular calcification (Pearson's r = 0.94 [95% CI; 0.79, 0.98], t -statistic = 8.48, P < 0.001). Conclusions: Based on preliminary data, a quadratic relationship appears to exist between aging and plaque inflammation. In contrast, a linear relationship was observed between aging and plaque molecular calcification. These data reject the existence of a linear relationship between plaque inflammation and calcification. Therefore, we hypothesize that established plaque calcification might counteract the inflammatory component of atherosclerosis.