2-[(18)F]FDG PET identifies metabolic substrates of sudden cardiac death in hypertrophic cardiomyopathy

2-[(18)F]FDG PET 可识别肥厚型心肌病中猝死的代谢底物

阅读:2

Abstract

Risk stratification for sudden cardiac death (SCD) in hypertrophic cardiomyopathy (HCM) remains challenging. Enhanced imaging techniques could improve prognostic accuracy. This study investigates myocardial resting perfusion and metabolism using [(13)N]-NH(3) and 2-[(18)F]FDG PET/CT and their correlation with HCM SCD risk scores. Thirty non-obstructive HCM patients (mean age 54 years, 57% male) with a mean SCD risk score of 3.7 ± 2.5% were evaluated. Myocardial 2-[(18)F]FDG metabolism and rest [(13)N]-NH(3) perfusion PET/CT were analyzed. Hypermetabolism (2-[(18)F]FDG uptake with normal perfusion) occurred in 53% of cases (mean extension 11.8 ± 17.2%), while fibrosis (reduced perfusion without 2-[(18)F]FDG uptake) averaged 10.3 ± 10.2%. Mean rest myocardial blood flow (MBF) was 0.75 ± 0.21 ml/min/g, increasing with hypermetabolism extension (0.83 ± 0.32 ml/min/g for ≥ 20%, p = 0.019) but decreasing with SCD scores ≥ 6% (0.58 ± 0.05 ml/min/g, p = 0.034). Hypermetabolism correlated moderately with SCD risk scores (rho = 0.38, p = 0.036), with hypermetabolism peaking at intermediate risk (23.5 ± 27.1%) before declining. Fibrosis extension consistently increased with SCD risk (rho = 0.38, p = 0.039). In conclusion, our findings identify important correlations between myocardial hypermetabolism and fibrosis and SCD risk in HCM. Hypermetabolism peaks in intermediate-risk patients, reflecting earlier disease stages, while fibrosis increases with higher SCD risk, signaling disease progression and structural damage.

特别声明

1、本页面内容包含部分的内容是基于公开信息的合理引用;引用内容仅为补充信息,不代表本站立场。

2、若认为本页面引用内容涉及侵权,请及时与本站联系,我们将第一时间处理。

3、其他媒体/个人如需使用本页面原创内容,需注明“来源:[生知库]”并获得授权;使用引用内容的,需自行联系原作者获得许可。

4、投稿及合作请联系:info@biocloudy.com。