ABSTRACT
Over recent years there has been a dramatic improvement in our understanding of the pathophysiology that underlies heart failure. In response to myocardial injury or inflammation, a series of processes are activated in an attempt to restore cardiovascular homeostasis1 (Figure 1). Whilst activation of these processes may be of hemodynamic benefit in the short term, chronic activation contributes to an ongoing and progressive decline in cardiac function. This is manifest as the process of ventricular ‘remodelling’.
