Parisi, Valentina (2015) ROLE OF EPICARDIAL ADIPOSE TISSUE IN THE PATHOGENESIS OF CALCIFIC AORTIC STENOSIS. [Tesi di dottorato]
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| Tipologia del documento: | Tesi di dottorato |
|---|---|
| Lingua: | English |
| Titolo: | ROLE OF EPICARDIAL ADIPOSE TISSUE IN THE PATHOGENESIS OF CALCIFIC AORTIC STENOSIS |
| Autori: | Autore Email Parisi, Valentina valentina.parisi@unina.it |
| Data: | 26 Marzo 2015 |
| Numero di pagine: | 26 |
| Istituzione: | Università degli Studi di Napoli Federico II |
| Dipartimento: | Scienze Mediche Traslazionali |
| Scuola di dottorato: | Medicina clinica e sperimentale |
| Dottorato: | Fisiopatologia clinica e medicina sperimentale |
| Ciclo di dottorato: | 27 |
| Coordinatore del Corso di dottorato: | nome email Marone, Gianni marone@unina.it |
| Tutor: | nome email Leosco, Dario [non definito] |
| Data: | 26 Marzo 2015 |
| Numero di pagine: | 26 |
| Parole chiave: | Epicardial adipose tissue, aortic stenosis, cytokines, inflammation |
| Settori scientifico-disciplinari del MIUR: | Area 06 - Scienze mediche > MED/09 - Medicina interna |
| Aree tematiche (7° programma Quadro): | SALUTE e TUTELA DEL CONSUMATORE > Biotecnologie, strumenti e tecnologie generiche per la salute umana |
| Depositato il: | 07 Apr 2015 12:47 |
| Ultima modifica: | 24 Set 2015 10:20 |
| URI: | http://www.fedoa.unina.it/id/eprint/10113 |
| DOI: | 10.6092/UNINA/FEDOA/10113 |
Abstract
Background. The pathophysiologic mechanisms leading to aortic stenosis (AS) are characterized by early atherosclerosis and inflammation. Epicardial adipose tissue (EAT) represents a source of several pro-atherogenic inflammatory mediators involved in coronary atherogenesis. EAT thickness and inflammatory profile are increased in patients with coronary artery disease (CAD). Since the well recognized similarities between AS and CAD pathogenesis, we aimed to evaluate whether anatomic characteristics and pro-inflammatory profile of EAT are also modified in patients with severe isolated AS. Methods and Results. We measured EAT thickness by echocardiography in 95 patients with isolated AS and 44 controls matched for age, gender and body mass index (BMI). In patients referred to aortic valve replacement, plasma, EAT and subcutaneous adipose tissue (SCAT) were collected and analyzed by human cytokine 27 multiplex immunoassay for the assessment of systemic and local inflammatory status. EAT thickness was significantly increased in patients with AS compared to controls. Overall, EAT showed a markedly increased inflammatory profile respect to SCAT. There was a significant relationship between EAT thickness and levels of EAT secreted inflammatory mediators. Conclusions. Our results provide the first demonstration of EAT increased thickness and inflammatory status in patients with severe AS. Overall, these data raise the hypothesis of a potential role of EAT in AS pathogenesis.
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