Introduction

Worldwide more than 17 million people die every year from cardiovascular disease (CVD) with this number projected to increase to over 23 million by 2030.1 Within Europe, CVD results in four million deaths annually, accounting for 47% of all-cause mortality. Between them, heart attacks and strokes are responsible for around 80% of this mortality.2 The vast majority of acute ischaemic vascular events occur in relation to an underlying atherosclerotic plaque. Plaque rupture is the dominant initiating event, responsible for 60–70% of acute coronary syndromes (ACS), while plaque erosion is responsible for most of the remainder.3 ,4 Irrespective of the mechanism, the consequence is exposure of a thrombogenic substrate to circulating blood. This in turn triggers platelet aggregation and the coagulation cascade which compromises vascular blood flow resulting in downstream end-organ ischaemia and infarction. These events occur abruptly and often without warning. Despite intensive therapies, they recur in as many as 25% of patients.

Until recently, the high-risk plaque has only been identified by retrospective analysis, predominantly from pathological examination of autopsy specimens. This has limited our ability to appreciate the dynamic nature of plaque vulnerability and rupture, and has placed a heavy reliance on invasive angiography to describe the anatomical luminal stenosis severity rather than plaque biology. Prospective identification of plaque rupture events has suggested that the majority of culprit lesions is non-flow limiting, and often overlooked by angiographic and traditional functional investigations. Novel imaging techniques now have the potential to identify the pathological structures and processes associated with plaque rupture. This in turn has raised hopes for strategies …