Valentina Parisi1, Laura Petraglia2, Vittoria D'Esposito2, Serena Cabaro2, Giuseppe Rengo2, Aurelio Caruso3, Maria Gabriella Grimaldi3, Francesco Baldascino3, Antonio De Bellis3, Dino Vitale3, Roberto Formisano2, Adele Ferro4, Stefania Paolillo5, Laurent Davin6, Patrizio Lancellotti7, Pietro Formisano2, Pasquale Perrone Filardi8, Nicola Ferrara2, Dario Leosco2. 1. Department of Translational Medical Science, University of Naples Federico II, Italy. Electronic address: valentina.parisi@unina.it. 2. Department of Translational Medical Science, University of Naples Federico II, Italy. 3. Casa di Cura San Michele, Maddaloni, CE, Italy. 4. Institute of Biostructure and Bioimaging, CNR, Naples. 5. Italy SDN Foundation, Institute of Diagnostic and Nuclear Development, Naples, Italy. 6. University of Liège Hospital, GIGA Cardiovascular Sciences, Departments of Cardiology, Heart Valve Clinic, CHU Sart Tilman, Liège, Belgium. 7. University of Liège Hospital, GIGA Cardiovascular Sciences, Departments of Cardiology, Heart Valve Clinic, CHU Sart Tilman, Liège, Belgium; Gruppo Villa Maria Care and Research, Anthea Hospital, Bari, Italy. 8. Department of Advanced Biomedical Science, University Federico II of Naples, Naples, Italy.
Abstract
BACKGROUND: Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation. METHODS: Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies. RESULTS: Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001). CONCLUSIONS: The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.
BACKGROUND: Epicardial adipose tissue (EAT) thickness and pro-inflammatory status has been shown to be associated with several cardiac diseases, including aortic stenosis (AS). Thus, cardiac visceral fat could represent a potential new target for drugs. In the present study we evaluate the effect of statin therapy on EAT accumulation and inflammation. METHODS: Echocardiographic EAT thickness was assessed in 193 AS patients taking (n.87) and not taking (n.106) statins, undergoing cardiac surgery. To explore the association between statin therapy and EAT inflammation, EAT biopsies were obtained for cytokines immunoassay determination in EAT secretomes. An in vitro study was also conducted and the modulation of EAT and subcutaneous adipose tissue (SCAT) secretomes by atorvastatin was assessed in paired biopsies. RESULTS: Statin therapy was significantly associated with lower EAT thickness (p < 0.0001) and with lower levels of EAT-secreted inflammatory mediators (p < 0.0001). Of note, there was a significant correlation between EAT thickness and its pro-inflammatory status. In vitro, atorvastatin showed a direct anti-inflammatory effect on EAT which was significantly higher compared to the SCAT response to statin incubation (p < 0.0001). CONCLUSIONS: The present study indicates a robust association between statin therapy and reduced EAT accumulation in patients with AS. The present data also suggest a direct relationship between EAT thickness and its inflammatory status, both modulated by statin therapy. The in vitro results support the hypothesis of a direct action of statins on EAT secretory profile. Overall our data suggest EAT as a potential new therapeutic target for statin therapy.
Authors: Alexandra Jichitu; Simona Bungau; Ana Maria Alexandra Stanescu; Cosmin Mihai Vesa; Mirela Marioara Toma; Cristiana Bustea; Stela Iurciuc; Marius Rus; Nicolae Bacalbasa; Camelia Cristina Diaconu Journal: Diagnostics (Basel) Date: 2021-04-12
Authors: Paolo Raggi; Varuna Gadiyaram; Chao Zhang; Zhengjia Chen; Gary Lopaschuk; Arthur E Stillman Journal: J Am Heart Assoc Date: 2019-06-13 Impact factor: 5.501