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

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.