Your doctor should be able to figure out a way to use this information to target your plaque.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=130658&CultureCode=en
Peptide receptor radionuclide therapy (PRRT) with radiolabeled
somatostatin analogs, an established treatment for cancer patients,
could offer a novel therapeutic approach to decrease levels of
inflammation in the atherosclerotic plaques of patients with
cardiovascular disease (CVD), reported an abstract¹ study at the
International Conference on Nuclear Cardiology and Cardiac CT, May 5 to 8
in Berlin, Germany.
“Our results should act as a stimulus for further exploration of
radionuclide based interventions in atherosclerosis. Ultimately such
therapies might be used to lower the degree of inflammation in
atherosclerosis which has the potential to reduce the occurrence of
heart attacks,” said Imke Schatka, the first author of the study from
the Department of Nuclear Medicine at Hannover Medical School, Germany.
PRRT is a technique currently used to treat patients with metastatic
neuroendocrine tumours (NETS), a diverse group of malignancies deriving
from the neuroendocrine cell system (the most frequent locations being
pancreas, small intestine and lung).
The discovery of over expression of somatostatin receptors (SSTR) on
NET tumours first opened the way for development of radiolabelled
somatostatin analogs to image tumours during PET/CT scans. DOTATATE is a
somatostatin receptor (SSTR) ligand targeting SSTR-2, a receptor known
to be expressed on 70% of NET tumours. Once tumours have been
visualized, it is possible to target therapy by attaching the
beta-emitter ¹⁷⁷ Lutetium (¹⁷⁷Lu) to the ligand.
Active inflammation has been widely implicated in the initiation,
progression and disruption of vulnerable plaques, and consequently
offers an emerging target for the imaging and treatment of
atherosclerosis. “Since SSTR-2 receptors are also expressed on
macrophages we speculated that DOTATATE-PET/CT might be used to detect
vulnerable plaques and that a PRRT procedure could reduce inflammation
in the arterial wall,” explained Schatka.
For the current study, 11 patients (from a group of 165 undergoing
PRRT for NET tumours) were retrospectively identified because they met
the criteria of only receiving the beta emitter¹⁷⁷Lu treatment after
undergoing two consecutive scans, with a third scan following treatment.
For each of the three scans, vessel wall uptake of the DOTATATE
ligand was measured in six arterial segments of PET images (carotid,
aortic arch, ascending, descending, abdominal aorta, and iliac arteries)
and then the overall vessel uptake was determined for each individual
patient.
Results showed that for the first scan the overall vessel uptake of
the ligand correlated with the age of the patient (P <0.01), the
number of calcified plaques (P <0.001) and furthermore was higher in
subjects with hypercholesterolemia (p=0.04). No significant differences
in overall vessel uptakes were found between scans 1 and 2, confirming
reproducibility in the absence of treatment.
However, when treatment with the beta-emitter ¹⁷⁷ Lu-DOTATATE was
delivered following scan 2, scan 3 showed significant reductions in the
overall vessel uptake of the ligand when compared with both scan 1
(p=0.001) and scan 2 (p=0.004).
“Uptake of the ligand can be considered to be a measure of the
quantity of SSTR receptors, which in turn is likely to correlate with
the number of activated macrophages and the extent of the inflammatory
process,” explained Schatka. “Our results suggest that treatment has had
a beneficial effect in reducing inflammation.”
The next step, said Schatka, would be to get histological proof that
reductions in inflammation really had been imaged with DOTATATE-PET/CT
by looking at carotid artery samples removed from patients during
routine surgery.
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