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Background Short leukocyte telomere length (TL) is associated with atherosclerotic cardiovascular disease. Endothelial repair plays a key role in the development of atherosclerosis. The objective was to examine associations between TL and proliferative dynamics of endothelial colony‐forming cells (ECFCs), which behave as progenitor cells displaying endothelial repair activity. Methods and Results To isolate ECFCs, we performed a clonogenic assay on blood samples from 116 participants (aged 24–94 years) in the TELARTA (Telomere in Arterial Aging) cohort study. We detected no ECFC clones in 29 (group 1), clones with no replating capacity in other 29 (group 2), and clones with replating capacity in the additional 58 (group 3). Leukocyte TL was measured by Southern blotting and ECFCs (ECFC‐TL). Age‐ and sex‐adjusted leukocyte TL (mean±SEM) was the shortest in group 1 (6.51±0.13 kb), longer in group 2 (6.69±0.13 kb), and the longest in group 3 (6.78±0.09 kb) ( P <0.05). In group 3, ECFC‐TL was associated with the number of detected clones ( P <0.01). ECFC‐TL (7.98±0.13 kb) was longer than leukocyte TL (6.74±0.012 kb) ( P <0.0001) and both parameters were strongly correlated ( r =0.82; P <0.0001). Conclusions Individuals with longer telomeres display a higher number of self‐renewing ECFCs. Our results also indicate that leukocyte TL, as a proxy of TL dynamics in ECFCs, could be used as a surrogate marker of endothelial repair capacity in clinical and laboratory practice because of easy accessibility of leukocytes. Registration URL: https://www.clinicaltrials.gov ; Unique identifier: NCT02176941.

Growth/differentiation factor 15 and resistin are 2 markers that could be helpful in stratifying risk for AF in patients with cardiovascular disease. Yet, more research in terms of proteomics and investigation of possible molecular pathways implicated is required.

Background: Atrial fibrillation (AF) affects quality of life and prognosis of patients with cardiovascular disease. Resistin plays an important role in inflammatory response to internal and external factors. The aim of this study is to evaluate the association between resistin and permanent AF (PAF) in patients with cardiovascular disease. Methods: In our study, we included 146 patients with cardiovascular disease. Plasma resistin concentrations and demographic characteristics of patients were recorded. The patients were divided in two groups: 118 patients without a history of PAF (NonAF group), and 28 patients with a history of PAF (AF group). Association of resistin with PAF and other variables was examined by parametric and non-parametric tests, and multivariable linear and univariable logistic regression analysis. Results: No differences of demographic characteristics (gender, age and body mass index (BMI)) between two groups were observed (P > 0.05). Higher median levels of resistin were observed in group AF than in group NonAF (6.90 ng/mL vs. 5.83 ng/mL, P = 0.03). Multivariate linear regression analysis (adjusted to gender, age, BMI, hypertension, diabetes mellitus, coronary artery disease, and mitral valve disease) showed that resistin was associated with PAF (β = 0.79, 95% confidence interval (CI): 0.08 to 1.51, P = 0.03). Conclusions: Our analysis showed that plasma resistin was associated with PAF, and resistin concentration was higher in patients with AF compared to those without AF.

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