68 Ga-NODAGA-E[c(RGDγK)]2: Positron Emission Tomography Tracer for Imaging of Angiogenesis in Ischemic Heart Disease

Chronic Ischemic Heart Disease Clinical Trial

Official title:

68 Ga-NODAGA-E[c(RGDγK)]2: Positron Emission Tomography Tracer for Imaging of Angiogenesis in Ischemic Heart Disease

Clinical Trial Details — Status: Not yet recruiting

Administrative data

• NCT number: NCT03505346
• Other study ID #: EUDRA-CT: 2017-002712-14
• Status: Not yet recruiting
• Phase: Phase 2
• Start date: January 1, 2024
• Est. completion date: December 1, 2025

Study information

• Verified date: November 2023
• Source: Rigshospitalet, Denmark
• Contact: Simon Bentsen, MD
• Phone: +4535451793
• Email: simon.bentsen.01[@]regionh.dk
• Is FDA regulated: No
• Study type: Interventional

Clinical Trial Summary

The aim is to examine the expression of αvβ3 integrin using a novel selective radiotracer in patients with chronich ischemic heart disease and investigate if it is a suitable tool for predicting myocardial recovery and thus prognosis after intervention.

Description:

Ischemic heart disease is worldwide the single most frequent cause of death. The number of patients surviving acute myocardial injury is increasing due to improved acute treatment. However, after the initial repair, the tissue undergoes a remodeling phase to compensate for the damaged area. This re-modeling phase can change the structure end geometry of the heart resulting in lower ejection fraction, leading to cardiac dysfunction, which eventually leads to heart failure. Ischemic heart disease is most commently caused by arteriosclerosis of the coronary artery.

If chronic ischemic heart disease is left untreated, it will lead to symptoms to the patient. These symptons occur when the myocardiel oxygen demand exceeds the oxygen provided, due to coronary occlusion.

If the heart suffers from ischemia, the tissue reacts strongly to the hypoxia. The body will as a compensatory mechanism create new vessel to provide the tissue with oxygen. This is known as the biological process of angiogenesis. This complex process involves different angiogenic and pro-fibrotic transcription factors that initiate the restoration of capillaries by sprouting from the existing endothelial cells in response to hypoxia.

Integrin αvβ3 is a transmembrane cell surface receptor that is markedly upregulated in states of angiogenesis. It facilitates migration and proliferation and thereby allowing cells to respond to extracellular environment. Integrin αvβ3 is thus a key player in the angiogenic process. The integrin αvβ3 has a binding site for an RGD peptide (Arg-Gly-Asp motif) and this can be targeted by PET tracers.

RGD-based PET tracers have been shown to accumulate at the site of myocardial necrosis in both human and animal studies. The uptake before interventions may correlate to recovery of cardiac function and thus serve as a prognostic marker after intervention.

Recruitment information / eligibility

• Status: Not yet recruiting
• Enrollment: 42
• Est. completion date: December 1, 2025
• Est. primary completion date: December 1, 2025
• Accepts healthy volunteers: No
• Gender: All
• Age group: 50 Years and older

Eligibility

Inclusion Criteria:

• Age over 50 years

• Patient with known chornic ischemic Heart disease admitted to Rigshospitalet to either PCI og CABG

Exclusion Criteria:

• No prior history of Heart surgery

• Not treated with anti-angiogenic medicine

• Subject with pacemaker, cochlear implant or insulin pump

• Pregnancy

• Lactation

• Severe claustrophobia

• Severe obesity (weight above 140kg)

• Conversion from PCI to CABG

• If a subject is in the fertile age, a pregnancy test will be use prior to injection to the PET_tracer

• If a subject is having a severe allergic reaction to the PET-tracer, the person will be excluded for the rest of the trial

• If the PET-tracer is administered subcutaneous, the person will be excluded for the rest of the trial¨

• Type I or II diabetes

Related Conditions & MeSH terms

• Chronic Ischemic Heart Disease
• Coronary Artery Disease
• Heart Diseases
• Ischemia
• Myocardial Ischemia

Intervention

Drug:
• 68Ga-NODAGA-E[c(RGDyK)]2
200 MBq 68Ga-NODAGA-E[c(RGDyK)]2 administered IV.

Locations

Country	Name	City	State
Denmark	Department of Physiology, Nuclear Medicine and PET	Copenhagen	Region Hovedstaden

Sponsors (1)

Lead Sponsor	Collaborator
Rigshospitalet, Denmark

Country where clinical trial is conducted

Denmark, 

Outcome

Type	Measure	Description	Time frame	Safety issue
Primary	To evaluate myocardial angiogenesis	Analysing change in uptake of 68Ga-NODAGA-E[c(RGDyK)]2 Positron Emission Tomography after intervention	30-35 days
Secondary	Correlation between 68Ga-NODAGA-E[c(RGDyK)]2 and myocardial perfusion	Correlation between uptake of 68Ga-NODAGA-E[c(RGDyK)]2 and change in myocardial perfusion after intervention using Rubidium 82 Positron Emission Tomography	30-35 days
Secondary	Correlation between 68Ga-NODAGA-E[c(RGDyK)]2 and functional recovery	Correlation between uptake of 68Ga-NODAGA-E[c(RGDyK)]2 and functional recovery using Magnetic Resonance after intervention	30-35 days
Secondary	Correlatino between 68Ga-NODAGA-E[c(RGDyK)]2 and viability	Correlation between uptake of 68Ga-NODAGA-E[c(RGDyK)]2 and viability using Flour-Deoxy-Glucose Positron Emission Tomography after intervention	30-35 days