The effect of aging on atherosclerotic plaque inflammation and molecular calcification: A PET CT imaging study

Research output: Contribution to conference without publisher/journalPosterResearch

Abstract

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.
Original languageEnglish
Publication date2. Jun 2013
Publication statusPublished - 2. Jun 2013
Event81st EAS Congress: European Athrosclerosis Society - Lyon, France
Duration: 2. Jun 20135. Jun 2013

Conference

Conference81st EAS Congress
CountryFrance
CityLyon
Period02/06/201305/06/2013

Cite this

@conference{eec2d817c0814c70b5468c4b5cb15323,
title = "The effect of aging on atherosclerotic plaque inflammation and molecular calcification: A PET CT imaging study",
abstract = "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.",
author = "Bj{\"o}rn Blomberg and Anders Thomassen and Simonsen, {Jane Angel} and Malene Hildebrandt and Diederichsen, {Axel Cosmus Pyndt} and Hans Mickley and Abass Alavi and H{\o}ilund-Carlsen, {Poul Flemming}",
year = "2013",
month = "6",
day = "2",
language = "English",
note = "null ; Conference date: 02-06-2013 Through 05-06-2013",

}

The effect of aging on atherosclerotic plaque inflammation and molecular calcification: A PET CT imaging study. / Blomberg, Björn; Thomassen, Anders; Simonsen, Jane Angel; Hildebrandt, Malene ; Diederichsen, Axel Cosmus Pyndt; Mickley, Hans; Alavi, Abass; Høilund-Carlsen, Poul Flemming.

2013. Poster session presented at 81st EAS Congress, Lyon, France.

Research output: Contribution to conference without publisher/journalPosterResearch

TY - CONF

T1 - The effect of aging on atherosclerotic plaque inflammation and molecular calcification: A PET CT imaging study

AU - Blomberg, Björn

AU - Thomassen, Anders

AU - Simonsen, Jane Angel

AU - Hildebrandt, Malene

AU - Diederichsen, Axel Cosmus Pyndt

AU - Mickley, Hans

AU - Alavi, Abass

AU - Høilund-Carlsen, Poul Flemming

PY - 2013/6/2

Y1 - 2013/6/2

N2 - 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.

AB - 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.

M3 - Poster

ER -