Plasma IL-18 and IL-18BP are altered differently in reverse remodeling following aortic valve replacement

Abstract

Objectives. Patients with aortic stenosis (AS) develop left ventricular remodeling characterized by changes in extracellular matrix (ECM) and cardiomyocyte-hypertrophy. Aortic valve replacement (AVR) reverses this process (reverse remodeling). We examined plasma levels of interleukin-18 (IL-18) and its binding protein (IL-18BP) before and after AVR for AS since these mediators have been shown experimentally to exert effects on myocardial remodeling. Design. Plasma levels of IL-18 and IL-18BP were analyzed in 22 patients with AS undergoing AVR, preoperatively, two days, six and 12 months postoperatively. Echocardiography and functional testing were performed. Results. IL-18BP was significantly increased by 28% and 15% at two days and six months after AVR, compared to preoperative values. In contrast, IL-18 showed a later peak (increased by 24% at 12 months postoperatively) when IL-18BP was normalized. IL-18 correlated positively with deceleration time (R = 0.44) at this time-point which might indicate an association with diastolic function. Conclusions. We report for the first time that plasma IL-18 and IL-18BP are differentially regulated after AVR for AS with an early increase in IL-18BP postoperatively followed by a later peak in IL-18 at 12 months. Given the known effects of these mediators on myocardial remodeling and function, they might play a role in the reverse and remodeling process associated with AVR.

Key words::

• Interleukin-18
• remodeling
• aortic valve replacement
• aortic stenosis

Acknowledgements

The authors are grateful to the staff at Department of Cardiothoracic Surgery and Department of Cardiology at Ullevål University Hospital, Oslo, Norway and Clinical Trials and Evaluation Unit, Royal Brompton Hospital, London, UK. The authors of this manuscript have certified that they comply with the Principles of Ethical Publishing in the International Journal of Cardiology (18). The study was supported by research grants from Medtronic, Inc., from Center for Heart Failure Research, University of Oslo and The Ingegerd and Viking Olov Bjørk Scholarship received by Professor Theis Tønnessen.

Declaration of interest: The authors report no conflicts of interest. The authors alone are responsible for the content and writing of the paper.