Synergy Between morpHOlogical and inflammatoRy Evaluation in Predicting Long-term Coronary Plaque Progression (SHORE)

University of Bologna

Status

Active, not recruiting

Conditions

Coronary Artery Disease

Inflammation

Acute Coronary Syndrome

Atherosclerosis

Treatments

Diagnostic Test: coronary OCT

Diagnostic Test: 68GaDOTATATE PET/CTCA

Study type

Interventional

Funder types

Other

Identifiers

NCT05436977

SHORE_Bo_2020

Details and patient eligibility

About

Data from human autopsy studies have showed that thrombosis of a ruptured plaque with a large necrotic core, inflammatory cells and a thin fibrous cap, the so-called thin cap fibroatheroma (TCFA), represents the main mechanism for acute coronary syndrome (ACS). Optical coherence tomography (OCT) is an imaging technique that provides high-resolution, cross-sectional images of tissue in situ. The resolution of OCT (10 um) is appropriate for measuring a cap thickness less than65 μm, and even the plaque macrophage density. 68Ga-DOTA-(Tyr3)-octreotate/NaI3-octreotide(68Ga-DOTA-TATE/NOC) Positron Emission Tomography (PET)/Computed Tomography coronary angiography (CTCA), targeting the somatostatin receptor subtype-2 selectively expressed by M1 macrophages may show coronary inflammation. The SHORE protocol aims at evaluating the synergy between OCT and 68Ga-DOTA-TATE/NOC in predicting coronary plaque progression as assessed by CTCA

Full description

ACS are the leading cause of mortality and morbidity in the western world. Despite recommended therapies, after experiencing an ACS episode patients still have an increased cardiovascular risk during follow up. In the CLIMA study OCT criteria of plaque vulnerability at non-culprit sites such as minimum luminal area <3.5mm2, fibrous cap thickness <75 µm, lipid arc extension >180° and macrophage infiltration was associated with an increased risk of cardiac death and myocardial infarction (HR 7.54, 95%CI 3.1-18.6).

Of the 36 OCT defined vulnerable plaques only 7 were associated with events showing a very low positive predictive value (19%). Yet, among the 577 plaques with macrophages accumulation only the 5.2% was associated with the endpoint. The lack of reliable information on plaque inflammation could represent the miss point to better link high risk plaques to plaque progression and/or rupture. Recent studies showed that inflammation in coronary plaques may be measured by means 68Ga-DOTATATE/PET targeting the somatostatin receptor subtype-2 selectively expressed by M1 macrophages.

Thus the investigators aim to evaluate the in vivo natural history of coronary plaques characterized from both the morphological (OCT) and inflammatory (68Ga-DOTATATE PET/CTCA) point of view in patients with ACS and at least 1 intermediated coronary lesion as assessed by FFR/iFR

Enrollment

40 estimated patients

Sex

All

Ages

50+ years old

Volunteers

No Healthy Volunteers

Inclusion criteria

Male or female participants > 50 years old
Able to give written, informed consent and to lie flat
Presentation of ACS within ~2 weeks
At least 1 intermediate (30-80% diameter stenosis) non-culprit coronary artery lesion on angiography, managed medically as clinically indicated (i.e.: negative FFR/iFR)

Exclusion criteria

Women of child bearing potential not using adequate contraception
Contrast allergy or contrast-nephropathy
Uncontrolled atrial fibrillation
Chronic kidney disease (eGFR <30 l/min/1.73m2)
Uncontrolled chronic inflammatory disorder
History of recent malignancy deemed relevant to the study by the investigator
Current use of systemic corticosteroids
Previous coronary artery bypass grafting surgery (CABG) or percutaneous coronary intervention (PCI) before the index event
Contraindication to coronary angiography
Requires CABG or staged non-culprit artery PCI
Coronary vessels that could not be adequately imaged
Severe valvular heart disease
Any medical condition, in the opinion of the investigator, that prevents the participant from lying flat during scanning, or from participating in the study.