OBJECTIVE-Peroxisome proliferator-activated receptor-␥ (PPAR␥) agonists (thiazolidinediones [TZDs]) are used for the treatment of diabetes. Bone marrow-derived endothelial progenitor cells (EPCs) improve vascular function and predict cardiovascular risk. The effect of pioglitazone therapy on EPCs was examined. RESEARCH DESIGN AND METHODS AND RESULTS-Weperformed a prospective, randomized, double-blind study on patients with documented stable coronary artery disease and normal glucose tolerance. Of 54 patients with normal fasting glucose levels, 18 showed impaired glucose tolerance and 36 patients with normal glucose tolerance were randomized to 30-day treatment with pioglitazone (45 mg) or placebo in addition to optimal medical therapy. All patients in the TZD group showed an increase of adiponectin levels as an indicator of compliance (11.4 Ϯ 1.1 to 36.8 Ϯ 2.1 g/ml; P Ͻ 0.001). TZD, but not placebo, decreased mean high-sensitivity C-reactive protein to 43 Ϯ 19% (P Ͻ 0.05). Pioglitazone increased CD34 ϩ /kinase insert domain receptor ϩ EPCs to 142 Ϯ 9% and cultured 1,1Ј-dioctadecyl-3,3,3Ј,3Ј-tetramethylindocarbocyanine-labeled acetylated LDL ϩ / lectin ϩ EPCs to 180 Ϯ 3% (P Ͻ 0.05). EPC numbers were not changed in the placebo group. TZD increased the SDF-1-induced migratory capacity to 146 Ϯ 9% per EPC number (P Ͻ 0.05) and upregulated the clonogenic potential of EPCs, increasing the colony-forming units to 172 Ϯ 12% (P Ͻ 0.001). In cultured human EPCs, TZD increased EPC numbers and migration and reduced NADPH-oxidase activity. The TZD effect was reversed by the PPAR␥ antagonist GW9662 and mimicked by treatment with adiponectin.CONCLUSIONS-The PPAR␥ agonist pioglitazone increases the number and function of EPCs in patients with coronary artery disease. The effect represents a potential regenerative mechanism in atherosclerosis and is observed in normoglycemic individuals with stable coronary artery disease.

Some recent studies evaluated the role of fluorine-18 fluorodeoxyglucose (2-[18F]FDG) as a radiopharmaceutical for positron emission tomography/computed tomography (PET/CT) imaging in patients with Coronavirus Disease (COVID-19). This article aims to perform a systematic review in this setting. A comprehensive computer literature search in PubMed/MEDLINE and Cochrane library databases regarding the role of 2-[18F]FDG PET/CT in patients with COVID-19 was carried out. This combination of key words was used: (A) “PET” OR “positron emission tomography” AND (B) “COVID” OR “SARS”. Only pertinent original articles were selected; case reports and very small case series were excluded. We have selected 11 original studies of 2-[18F]FDG PET/CT in patients with COVID-19. Evidence-based data showed first preliminary applications of this diagnostic tool in this clinical setting, with particular regard to the incidental detection of interstitial pneumonia suspected for COVID-19. To date, according to evidence-based data, 2-[18F]FDG PET/CT cannot substitute or integrate high-resolution CT to diagnose suspicious COVID-19 or for disease monitoring, but it can only be useful to incidentally detect suspicious COVID-19 lesions in patients performing this imaging method for standard oncological and non-oncological indications. Published data about the possible role of 2-[18F]FDG PET/CT in patients with COVID-19 are increasing, but larger studies are warranted.

Background: Tumor-induced or oncogenic osteomalacia (TIO) is a rare paraneoplastic syndrome in which osteomalacia is a consequence of fibroblast growth factor 23 (FGF23) secretion by a mesenchymal tumor. The localization of the culprit lesion in patients with TIO is often challenging. Several studies have evaluated the detection rate (DR) of these tumors using somatostatin receptor positron emission tomography (SSTR-PET/CT). We aimed to summarize literature findings on this topic providing pooled estimates of DR. Methods: A comprehensive literature search by screening PubMed, Embase and Cochrane library electronic databases through August 2019 was performed. The pooled DR of culprit tumors using SSTR-PET/CT in patients with TIO was calculated using a random-effects statistical model. Results: Fourteen studies on the use of SSTR-PET/CT in detecting the culprit tumor in patients with TIO were included in the qualitative analysis. The pooled DR of SSTR-PET/CT on a per-patient-based analysis calculated using eleven studies (166 patients) was 87.6% (95% confidence interval (95% CI) 80.2–95.1%). Statistical heterogeneity among studies was detected (I-square = 63%), likely due to the use of different radiolabeled somatostatin analogues, as demonstrated by a subgroup analysis. Conclusions: Despite limited literature data due to the rarity of the disease, SSTR-PET/CT demonstrated a very high DR of culprit tumors in patients with TIO and it could be used as first-line imaging method for this indication.

Background Integrin alpha-V-beta-3 (αvβ3) pathway is involved in intraplaque angiogenesis and inflammation and represents a promising target for molecular imaging in cardiovascular diseases such as atherosclerosis. The aim of this study was to assess the clinical correlates of arterial wall accumulation of 68Ga-NODAGA-RGD, a specific αvβ3 integrin ligand for PET. Materials and methods The data of 44 patients who underwent 68Ga-NODAGA-RGD PET/CT scans were retrospectively analyzed. Tracer accumulation in the vessel wall of major arteries was analyzed semi-quantitatively by blood-pool-corrected target-to-background ratios. Tracer uptake was compared with clinically documented atherosclerotic cardiovascular disease, cardiovascular risk factors and calcified plaque burden. Data were compared using the Mann–Whitney U test, Pearson correlation and Spearman correlation. Results 68Ga-NODAGA-RGD arterial uptake was significantly higher in patients with previous clinically documented atherosclerotic cardiovascular disease (mean TBR 2.44 [2.03–2.55] vs. 1.81 [1.56–1.96], p = 0.001) and showed a significant correlation with prior cardiovascular or cerebrovascular event (r = 0.33, p = 0.027), BMI (ρ = 0.38, p = 0.01), plaque burden (ρ = 0.31, p = 0.04) and hypercholesterolemia (r = 0.31, p = 0.04). Conclusions 68Ga-NODAGA-RGD holds promise as a non-invasive marker of disease activity in atherosclerosis, providing information about intraplaque angiogenesis.

Daily physical activity at the work place is independently associated with a decrease in PCSK9 levels over time.