E-Mail karger@karger.com Review Cardiology 2016;135:68–76 DOI: 10.1159/000445882 Remodelling after an Infarct: Crosstalk between Life and Death Roberto Ferrari   a M. Malagù   b S. Biscaglia   b A. Fucili   b P. Rizzo   b   a  Department of Cardiology and LTTA Centre, University of Ferrara, Ferrara, and b  Maria Cecilia Hospital, GVM Care and Research, E.S. Health Science Foundation, Cotignola, Italy ity of the ventricle, a pathologist, for whom remodelling means hypertrophy, fibrosis or apoptosis, or a molecular biologist, who considers remodelling in terms of up- or down-regulation of various pathways and proteins in my- ocytes and the interstitium with a typical embryonic phe- notype. As is often the case in cardiology, a term may be used in an attempt to encapsulate a highly complex concept with a single, intriguing and occasionally cryptic name. Remodelling seems to be a prototypical example of this phenomenon and is probably the reason why we do not have a universal definition for remodelling, arguing even whether it is more appropriate to consider the term ‘car- diac’ versus ‘myocardial’ remodelling [2]. The truth is that remodelling is an evolving concept, originally ap- plied almost exclusively to changes in cardiac structure occurring to the left ventricle (LV) after myocardial in- farction, but recently also applied to the right ventricle and the atria [3, 4]. It was also quickly recognized that the changes that characterize remodelling after infarction could have other causes, i.e. hypertension, aortic valve stenosis, myocarditis, valvular regurgitation and other forms of myocardial injury. Equally, it has become evi- dent that remodelling occurs also in healthy subjects. Ev- ery heart experiences remodelling during growth from Key Words Apoptosis · Hypertrophy · Myocardial infarction · Notch pathway · Remodeling Introduction In the first part of this review (‘Can we improve myo- cardial protection during ischaemic injury?’), which ap- peared last month in Cardiology [1], we described some aspects of ischaemic and reperfusion damage. We em- phasized the role of early reperfusion to salvage the isch- aemic, but still viable, myocardium. However, we also recognized that timely reperfusion is not always feasible, and late reperfusion, although successful, is not able to prevent myocyte necrosis, enabling a vicious circle of damage. This circle of complex events ultimately de- grades the anatomy and function of remaining viable my- ocytes, causing further ventricular dysfunction. This pro- cess is called ‘remodelling’. Although this term became instantly popular and enduring, it hardly ‘speaks for itself’ in providing a precise and unequivocal definition. Thus, the perception of the term ‘cardiac remodelling’ varies ac- cording to whether one is a cardiologist, assessing the ef- fects of remodelling on the volume and pumping capac- Received: March 29, 2016 Accepted: March 29, 2016 Published online: June 7, 2016 Roberto Ferrari, MD, Chair of Cardiology Ospedale di Cona Azienda Ospedaliero-Universitaria di Ferrara Via Aldo Moro 8, IT–44124 Cona (Italy) E-Mail fri  @  unife.it © 2016 S. Karger AG, Basel 0008–6312/16/1352–0068$39.50/0 www.karger.com/crd For editorial comment see p. 67