Cardiovascular disease remains the leading cause of death globally despite advances in medical therapy and risk stratification; ischaemic heart disease was responsible for an estimated 9.5 million deaths in 2016. To address this ongoing global burden of morbidity and mortality, there is a need for more sophisticated methods of diagnosis and prognostication, above and beyond clinical risk scores alone. The majority of myocardial infarction occurs due to ruptured atherosclerotic plaque, leading to acute thrombosis and coronary occlusion. For decades, the concept of the vulnerable plaque—plaques prone to rupture or thrombotic complications—has been central to our understanding of the pathophysiology of acute coronary syndromes. More recently, there has been a shift towards identifying the vulnerable patient through assessment of total atherosclerotic disease burden, in recognition of the fact that most plaque rupture events do not lead to clinical events. Moreover, demonstrating a strong causal link between vulnerable plaques and clinical events has previously proven difficult due to limitations in available invasive and non-invasive imaging modalities. However, we now have an array of imaging techniques that hold great potential for the advancement of vulnerable plaque imaging. These modalities are the subject of state-of-the-art clinical research, aiming to develop the role of atherosclerotic plaque imaging in modern clinical practice and ultimately to improve patient outcomes.
Precise theranostic nanomedicines for inhibiting vulnerable atherosclerotic plaque progression through regulation of vascular smooth muscle cell phenotype switching
