Ischaemic cardiomyopathy: pathophysiology, assessment and the role of revascularisation

### Learning objectives 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 …