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Acute myocardial infarction ('heart attack') remains the most common cause of death in Australia and atherosclerotic plaque rupture with blood clotting and artery blockage accounts for most myocardial infarctions. Despite this, assessment of specific characteristics that predispose plaques to rupture is not currently incorporated into standard diagnostic or treatment regimes. Non-invasive, molecular imaging of biological processes known to contribute to plaque rupture is an exciting new way to potentially identify patients at risk of heart attack. We recently discovered that the pro-inflammatory enzyme myeloperoxidase (MPO) contributes to the formation of plaque with features of plaque vulnerable to rupture (Eur Heart J 2018;39:3301). Therefore, it is a potential target for molecular imaging of high-risk plaque. Our laboratory is assessing the utility of molecular imaging of myeloperoxidase activity using molecular magnetic resonance imaging (MRI) and positron emission tomography (PET) to specifically identify vulnerable plaque by their increased MPO activity. In addition to using pre-clinical models of plaque instability and rupture, we are increasingly focusing our attention on human carotid and coronary arteries. This work is a collaboration with Dr Alkystis Phinikaridou and Prof René Botnar (King’s College, London) and Dr Imran Rashid (University Hospitals Cleveland) and A/Prof Andrew Jabbour (St Vincent’s Hospital, Sydney). The validation of such diagnostic tools could have significant impact for the assessment management of heart disease.