In this work, we address the understanding of the signaling pathways involved in cardiac remodeling in human SCD through molecular imaging analysis with a fibrosis marker. Furthermore, we emphasize characterizing the cardiac remodeling process by analyzing proteomic data from SCD myocardial biopsies and by analyzing the profile of microRNAs associated with hypertrophic cardiomyopathy and their diagnostic and prognostic value.
Adult patients, over 18 years of age;
Diagnosis of Fabry disease
Refusal to participate in the study
Adult patients, over 18 years of age with diagnosis of Fabry disease
Cohort
Cross-sectional
PET scan of 68Ga-FAPI
Procedure/SurgeryTo assess myocardial fibroblast activation, all enrolled patients will undergo positron emission tomography/computed tomography (PET/CT) imaging using the radiotracer \[68Ga\]Ga-FAPI. This tracer binds selectively to the fibroblast activation protein (FAP), expressed predominantly in activated cardiac fibroblasts involved in pathological myocardial remodelling.
Identify and validate novel molecular biomarkers and pathophysiological mechanisms of FD cardiomyopathy, focusing on myocardial fibrosis, inflammation, and cardiac remodelling
The primary objective includes: * Proteomic and metabolomic profiling of myocardial biopsies from FD patients versus controls. * Circulating microRNA (miRNA) analysis in plasma samples from HCM and FD patients to define diagnostic/prognostic miRNA signatures. * Evaluation of fibroblast activation using \[68Ga\]Ga-FAPI PET/CT imaging and its association with myocardial fibrosis and sudden cardiac death risk scores. * Correlation of molecular findings with cardiac imaging and standard biomarkers (NT-proBNP, troponin).
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Núcleo de Apoio à Investigação Clínica - FMUP
Lead sponsor
Universidade do Porto
Sponsor institution
Universidade do Porto
Collaborator
SOFIE
Collaborator
GE Healthcare
Collaborator
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