Abdelbaky Amr, Corsini Erin, Figueroa Amparo L, Subramanian Sharath, Fontanez Sara, Emami Hamed, Hoffmann Udo, Narula Jagat, Tawakol Ahmed
Cardiac MR PET CT Program, Massachusetts General Hospital, Boston, MA, USA.
Cardiac MR PET CT Program, Massachusetts General Hospital, Boston, MA, USA; Department of Radiology, Massachusetts General Hospital, Boston, MA, USA.
Atherosclerosis. 2015 Feb;238(2):165-72. doi: 10.1016/j.atherosclerosis.2014.11.026. Epub 2014 Dec 2.
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.
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.
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].
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.
近期数据显示主动脉瓣（AV）炎症与钙化之间存在关联。然而，在人类中缺乏将早期瓣膜炎症（在血流动力学受损之前）与随后的钙（Ca）沉积联系起来的直接证据。我们试图检验局部AV炎症是否会导致随后的AV钙沉积这一假设。
我们确定了111名个体（年龄60[49, 68]岁，50.5%为男性），他们没有活动性癌症或主动脉狭窄，为了癌症监测在1至5年的时间间隔内接受了2次PET/CT检查。通过测量基线PET/CT上AV内的FDG摄取（最大标准化摄取值，SUVmax）来确定AV炎症。通过比较基线和随访CT扫描来确定AV钙的后续沉积，以AV钙体积评分（CaVS）的增加来衡量。根据CaVS的平方根差异（使用预先确定的截断值2.5）将患者分为“非进展者”或“进展者”。CT和PET测量由两个相互盲法的实验室进行。
在随访期间，23名被归类为“进展者”的患者（20.2%）的AV钙增加，其中9名（9.2%）出现了随后的“新发”AV钙。进展者的AV SUVmax（平均值±标准差）高于非进展者（2.03±0.52对1.74±0.36，p = 0.02），尤其是有新发AV钙的患者与没有新发AV钙的患者相比（2.28±0.42对1.73±0.36，p < 0.001）。此外，在调整心血管危险因素后，AV炎症（AV SUVmax）独立预测了随后的钙化[比值比（95%置信区间）：4.99（1.30 - 19.15），p = 0.02]。
研究结果表明早期AV炎症可能易导致AV硬化。评估瓣膜代谢活性可能有助于更好地理解钙化性瓣膜病。
