⁶⁸Ga-FAPI PET/CT for Cardiac Fibrosis in Heart Failure
Trial statusRecruiting
Trial phaseNot listed
Trial typeObservational
Biological sexAll
Age18+
SponsorUniversity of Coimbra
About this trial
Heart failure (HF) is a clinical syndrome with increasing incidence and prevalence, associated with high morbidity, mortality, and economic impact, despite therapeutic advances.
Myocardial fibrosis is a common feature across different pathophysiological processes and plays a key role in HF development, with growing research interest specifically in non-ischemic dilated cardiomyopathy (HFrEF phenotype) and hypertrophic cardiomyopathy (HFpEF phenotype). Given its potential reversibility with certain drugs, fibrosis is an attractive therapeutic target, requiring non-invasive methods to monitor fibrogenesis and treatment efficacy.
Cardiac magnetic resonance imaging (CMR) is the gold standard for detecting fibrosis but cannot distinguish between active and inactive fibrosis or detect early stages, limitations that may be addressed by gallium-68-labeled fibroblast activation protein inhibitor positron emission tomography/computed tomography (68Ga-FAPI PET/CT).
This single-center, prospective, observational pilot study aims primarily to assess myocardial fibrosis in patients with HFrEF (non-ischemic dilated cardiomyopathy) and a subtype of HFpEF (hypertrophic cardiomyopathy) using 68Ga-FAPI PET/CT compared to CMR.
Secondary objectives include developing 68Ga-FAPI uptake assessment methodologies for future anti-fibrotic therapy studies and correlating fibrosis with serum cardiac biomarkers and cardiovascular events.
Eligibility criteria
This trial does not accept healthy volunteersQualifiers
≥ 18 years old;
Signs and symptoms of heart failure (HF);
[Preserved left ventricular ejection fraction (LVEF) (≥50%) and Evidence of structural/functional abnormality consistent with diastolic dysfunction/increased ventricular filling pressures, including elevated natriuretic peptides and Imaging diagnosis of hypertrophic cardiomyopathy and Genetic diagnosis of hypertrophic cardiomyopathy due to sarcomeric gene mutation] OR [Reduced LVEF (≤40%) and Imaging diagnosis of dilated cardiomyopathy: left ventricular end-diastolic diameter >58 mm in men and >52 mm in women, and left ventricular volume ≥75 mL/m² in men and ≥62 mL/m² in women, not explained solely by loading conditions]
Recent transthoracic echocardiogram (< 3 months);
Disqualifiers
Inability to provide informed consent;
Inability to tolerate the supine position;
Hemodynamic instability;
Claustrophobia;
Trial population
Fifteen patients with HFrEF (non-ischemic dilated cardiomyopathy) and Fifteen patients with HFpEF (hypertrophic cardiomyopathy)
Trial design
Design model
Cohort
Time perspective
Prospective
Treatments tested in this trial
68Ga-FAPI PET/CT
Diagnostic testPositron emission tomography/computed tomography (68Ga-FAPI PET/CT)
Treatment groups
30 Participants
are divided into 1 treatment groupGroup A: patients with HFrEF and HFpEF1 intervention
Trial outcomes
Primary outcomes
1
68Ga-FAPI uptake
Comparison of myocardial fibroblast activation identified by 68Ga-FAPI PET/CT with the non-invasive gold standard for fibrosis detection (Cardiac magnetic resonance with late gadolinium enhancement and extracellular volume)
Time frame
BaselineSecondary outcomes
1
68Ga-FAPI uptake
1. Identify suitable methodologies for assessing 68Ga-FAPI uptake for future studies evaluating the efficacy of anti-fibrotic therapies. 2. Correlate myocardial fibroblast activation identified by 68Ga-FAPI PET/CT with serum markers of cardiac pathology. 3. Correlate myocardial fibroblast activation identified by 68Ga-FAPI PET/CT with cardiovascular events over a 2-year follow-up.
Time frame
Baseline (1 & 2) and after 2 years (3)Sponsors and contacts
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University of Coimbra
Lead sponsor
Unidade Local de Saúde de Coimbra, EPE
Collaborator
Source ClinicalTrials.gov