Amr Abdelbaky1, Erin Corsini1, Amparo L Figueroa1, Sharath Subramanian1, Sara Fontanez1, Hamed Emami1, Udo Hoffmann2, Jagat Narula3, Ahmed Tawakol4. 1. Cardiac MR PET CT Program, Massachusetts General Hospital, Boston, MA, USA. 2. Cardiac MR PET CT Program, Massachusetts General Hospital, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Boston, MA, USA. 3. Division of Cardiology, Mount Sinai School of Medicine, New York City, New York. 4. Cardiac MR PET CT Program, Massachusetts General Hospital, Boston, MA, USA; Division of Cardiology, Massachusetts General Hospital, Boston, MA, USA. Electronic address: atawakol@mgh.harvard.edu.
Abstract
OBJECTIVES: Recent data shows a relationship between aortic valve (AV) inflammation and calcification. However, direct evidence linking early valve inflammation (prior to hemodynamic compromise) to subsequent calcium (Ca) deposition is lacking in humans. We sought to test the hypothesis whether local AV inflammation predisposes to subsequent AV Ca deposition. METHODS: We identified 111 individuals (age 60[49, 68], 50.5% male) without active cancer or aortic stenosis who underwent 2 PET/CT studies 1-5 years apart for cancer surveillance. AV inflammation was determined by measuring FDG uptake (maximum standardized uptake value, SUVmax) within the AV on baseline PET/CT. Subsequent deposition of AV Ca was determined by comparing baseline and follow-up CT scans, determined as an increase in AV Ca volume score (CaVS). Patients were classified as "non-progressors" or "progressors" based on Square Root difference in CaVS (using a pre-determined cut-off value of 2.5). CT and PET measurements were conducted by 2 mutually blinded laboratories. RESULTS: During follow-up, AV Ca increased in 23 patients (20.2%) classified as "progressors", of whom 9 (9.2%) demonstrated subsequent 'incident' AV Ca. The AV SUVmax (mean ± SD) was higher in progressors vs. non-progressors (2.03 ± 0.52 vs.1.74 ± 0.36, p = 0.02) and especially in patients with-vs. without-incident AV Ca (2.28 ± 0.42 vs. 1.73 ± 0.36, p < 0.001). Moreover, AV inflammation (AV SUVmax) independently predicted subsequent calcification after adjusting for cardiovascular risk factors [OR (95%CI): 4.99 (1.30-19.15), p = 0.02]. CONCLUSION: The findings suggest that early AV inflammation may predispose to AV sclerosis. The evaluation of valvular metabolic activity may prove useful for developing a better understanding of calcific valve disease.
OBJECTIVES: Recent data shows a relationship between aortic valve (AV) inflammation and calcification. However, direct evidence linking early valve inflammation (prior to hemodynamic compromise) to subsequent calcium (Ca) deposition is lacking in humans. We sought to test the hypothesis whether local AV inflammation predisposes to subsequent AV Ca deposition. METHODS: We identified 111 individuals (age 60[49, 68], 50.5% male) without active cancer or aortic stenosis who underwent 2 PET/CT studies 1-5 years apart for cancer surveillance. AV inflammation was determined by measuring FDG uptake (maximum standardized uptake value, SUVmax) within the AV on baseline PET/CT. Subsequent deposition of AV Ca was determined by comparing baseline and follow-up CT scans, determined as an increase in AV Ca volume score (CaVS). Patients were classified as "non-progressors" or "progressors" based on Square Root difference in CaVS (using a pre-determined cut-off value of 2.5). CT and PET measurements were conducted by 2 mutually blinded laboratories. RESULTS: During follow-up, AV Ca increased in 23 patients (20.2%) classified as "progressors", of whom 9 (9.2%) demonstrated subsequent 'incident' AV Ca. The AV SUVmax (mean ± SD) was higher in progressors vs. non-progressors (2.03 ± 0.52 vs.1.74 ± 0.36, p = 0.02) and especially in patients with-vs. without-incident AV Ca (2.28 ± 0.42 vs. 1.73 ± 0.36, p < 0.001). Moreover, AV inflammation (AV SUVmax) independently predicted subsequent calcification after adjusting for cardiovascular risk factors [OR (95%CI): 4.99 (1.30-19.15), p = 0.02]. CONCLUSION: The findings suggest that early AV inflammation may predispose to AV sclerosis. The evaluation of valvular metabolic activity may prove useful for developing a better understanding of calcific valve disease.
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