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Prediction of coronary artery calcium progression by FDG uptake of large arteries in asymptomatic individuals. | LitMetric

Purpose: The purpose of this study is to evaluate whether fluorodeoxyglucose (FDG) uptake of the large arteries can predict coronary artery calcium (CAC) progression in asymptomatic individuals.

Methods: Ninety-six asymptomatic individuals who underwent FDG positron emission tomography (PET) and CAC scoring on the same day for health screening and follow-up CAC scoring ≥1 year after baseline studies (mean 4.3 years) were included. Vascular FDG uptake was measured and corrected for blood pool activity to obtain peak and average target-to-blood pool ratios (TBRpeak and TBRavg, respectively) for the carotid arteries, and ascending and abdominal aorta. CAC scores at baseline and follow-up of each individual were measured and absolute CAC change (ΔCAC), annual CAC change (ΔCAC/year), and annual CAC change rate (ΔCAC%/year) were calculated. CAC progression was defined as ΔCAC >0 for individuals with negative baseline CAC; ΔCAC/year ≥10 for those with baseline CAC of 0
Results: Thirty-one subjects showed CAC progression. CAC-progressors showed significantly higher TBRpeak and TBRavg as compared to non-CAC-progressors for all three arteries. TBRpeak of the abdominal aorta was significantly associated with CAC progression in multivariate analysis, with age and baseline CAC. A higher TBRpeak of the abdominal aorta (≥2.11) was associated with CAC progression among subjects with negative baseline CAC only. In subjects with positive baseline CAC, only the amount of baseline CAC was significantly associated with CAC progression. However, the positive predictive value of the TBRpeak of the abdominal aorta was <40 % when age was <58 or baseline CAC was negative.

Conclusions: Higher FDG uptake of the large arteries is associated with an increased risk of CAC progression in asymptomatic subjects with negative baseline CAC. But its clinical application needs further validation.

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http://dx.doi.org/10.1007/s00259-016-3523-1DOI Listing

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