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Updated: May 24, 2025

In Vivo Quantitative Assessment of Myocardial Structure, Function, Perfusion and Viability Using Cardiac Micro-computed Tomography
Published on: February 16, 2016
Molecular imaging in hypertrophic cardiomyopathy: an exploratory study with 2-[18F]FDG and [13N]NH3
Maria João Ferreira1,2,3,4, Patrícia Marques-Alves5, Rodolfo Silva1,2,3
1Universidade de Coimbra, Coimbra, Portugal.
Insights
Positron emission tomography-computed tomography (PET-CT) reveals metabolic changes and fibrosis in non-obstructive hypertrophic cardiomyopathy (NOHCM). These findings correlate with increased heart thickness, dysfunction, and sudden cardiac death risk.
Area of Science:
- Cardiology
- Nuclear Medicine
- Medical Imaging
Background:
- Hypertrophic Cardiomyopathy (HCM) is a genetic heart disorder with varied presentations, increasing risks of heart failure and sudden cardiac death.
- Pathological pathways in HCM include inflammation, increased workload, myocyte disarray, apoptosis, and fibrosis.
- The utility of molecular imaging, specifically PET-CT, in assessing these pathways in HCM remains largely unexplored.
Purpose of the Study:
- To investigate the relationship between myocardial metabolism and perfusion in patients with non-obstructive HCM (NOHCM) using PET-CT.
- To explore the association of metabolic and perfusion abnormalities with clinical parameters and risk scores in NOHCM.
Main Methods:
- PET-CT imaging was performed on 30 NOHCM patients using 13N-ammonia for perfusion and 2-18F-FDG for metabolism assessment.
- Key clinical parameters measured included maximal myocardial wall thickness (MMWT), left atrial volume (LAV), NT-proBNP levels, and the sudden cardiac death (SCD) risk score.
- Analysis focused on 2-18F-FDG uptake (inflammatory pattern) and areas of fibrosis (scar pattern) within the left ventricle (LV).
Main Results:
- Increased 2-18F-FDG uptake, indicative of inflammation, was observed in 53% of patients.
- The extent of inflammatory patterns correlated significantly with MMWT, LAV, and NT-proBNP levels.
- Fibrotic patterns (scar) were also identified and correlated with the SCD risk score.
- Higher metabolic activity (TBR) was associated with greater MMWT, elevated NT-proBNP, and increased SCD risk.
Conclusions:
- PET-CT imaging offers valuable insights into myocardial metabolic activity and fibrosis in NOHCM patients.
- These imaging findings are closely linked to myocardial hypertrophy, left ventricular dysfunction, and elevated risk of sudden cardiac death.
Background:
Hypertrophic Cardiomyopathy (HCM), a genetic disorder with diverse phenotypes, is associated with risks of heart failure and sudden cardiac death. While the condition involves multiple pathological pathways, including myocardial inflammation, increased workload, myocyte disarray, apoptosis, and fibrosis, the role of molecular imaging via PET-CT remains unexplored in this context. This study aimed to investigate the relationship between myocardial metabolism and perfusion using PET-CT in patients with non-obstructive HCM (NOHCM).
Results:
Myocardial perfusion and metabolism were assessed using PET-CT with [13N]NH3 and 2-[18F]FDG uptake, respectively, in 30 NOHCM patients. Baseline measurements included maximal myocardial wall thickness (MMWT), left atrial volume (LAV), NT-proBNP levels, and the sudden cardiac death (SCD) risk score. Increased 2-[18F]FDG uptake (Target to Background Ratio - TBR ≥ 1.1) was detected in 53% of patients, with an average TBR of 1.4 ± 0.5. The inflammatory pattern involved 11.8 ± 17.2% of the left ventricle (LV) and correlated with MMWT (rho = 0.49, p = 0.009), LAV (rho = 0.39, p = 0.04), and NT-proBNP levels (rho = 0.63, p = 0.003). The maximum TBR within the LV correlated with MMWT (rho = 0.53, p = 0.004), NT-proBNP (rho = 0.70,p = 0.0008), and the SCD risk score (rho = 0.38,p = 0.04). Additionally, the fibrotic (scar) pattern, involving 10.3 ± 10.2% of the LV, correlated with the SCD score (rho = 0.38,p = 0.04).
Conclusion:
In patients with NOHCM, PET-CT imaging provides valuable insights into myocardial metabolism and fibrosis, which are closely associated with myocardial hypertrophy, left ventricular dysfunction, and the risk of sudden cardiac death.
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