Ischaemic heart disease (IHD) continues to be the most common cause of death globally according to WHO and is the most common cause of heart failure in the developed world. 1–4 Heart failure secondary to IHD has been shown to be independently associated with mortality compared with a non-ischaemic aetiology. 5 6 The increasing incidence has been attributed to the success of thrombolytic and primary percutaneous coronary intervention in acute myocardial infarctions, leading to improved patient survival, however often leading to increased morbidity due to left ventricular (LV) remodelling and chronic myocardial dysfunction. The term ischaemic cardiomyopathy (ICM) has been defined as LV systolic dysfunction with one or more of the following: a history of prior myocardial revascularisation or myocardial infarction, more than 75% stenosis in the left main stem or left anterior descending artery, or two vessels or more with a greater than 75% stenosis. 7 There are multiple mechanisms attributed to the development of ICM including mechanical and neurohormonal factors, 8 however the pathophysiological concept of myocardial hibernation has been of particular interest for several decades. Rahimtoola in the 1980s was one of the first to propose the term myocardial hibernation following the observation that patients with LV dysfunction recovered function following surgical revascularisation. 9 10 Hibernating myocardium is a retrospective definition based upon the evidence of functional recovery following revascularisation. 11 It is thought to be an adaptive process to repetitive ischaemia secondary to chronically reduced myocardial blood flow and reduced coronary flow reserve, whereby a loss in contractile apparatus results in reduced demand, which has been coined the ‘smart heart’. 10 In practice, the term ICM encompasses a spectrum of pathophysiological states, ranging from myocardial stunning, hibernation and scarring. Current evidence-based therapies in ICM are aimed at treating LV remodelling, attenuating the sympathetic nervous system’s impact on the heart and also inhibiting the renin angiotensin aldosterone system through β-adrenergic receptor blockers and ACE inhibitors, as with other causes of systolic LV dysfunction. The role of revascularisation remains unclear in those patients without a clear indication for revascularisation (acute coronary syndrome or significant angina), and has divided the cardiology community. This is predominantly as a result of the Surgical Treatment of Ischaemic Heart Failure (STICH) trial, 12 the results of which contradicted those of a large number of observational studies spanning over many decades. 13 14 The aim of this article therefore is to highlight current concepts in the management of ICM, with a focus on the evidence to date on the role of revascularisation. Through this we will also provide an overview of myocardial hibernation and viability and the imaging modalities that can aid in identifying patients that may have the potential to recover myocardial function following revascularisation.