Karlheinz Peter is Head of the Cardiometabolic Health Department at the University of Melbourne and Deputy Director and Head of the Atherothrombosis and Vascular Biology Program at the Baker Heart and Diabetes Institute. In addition to his research program, Professor Peter also works as an interventional cardiologist at the Alfred Hospital in Melbourne. Professor Peter holds an Investigator Level 3 NHMRC fellowship. He undertook medical training at the University of Freiburg and Heidelberg Germany, followed by further research and clinical training at the Johns Hopkins Medical School, Scripps Research Institute, and University of North Carolina at Chapel Hill, USA. Prior to moving to the Baker Heart and Diabetes Institute, Professor Peter was Director of the Cardiac Catheter Laboratory at the University of Freiburg.

His research is focused on the role of platelets, coagulation and inflammation in the development of thrombosis, atherosclerosis and myocardial infarction and aims to develop novel therapeutic approaches for the treatment of cardiovascular disease. This work has led to the development and numerous patents of novel biomarker and molecular imaging strategies for thrombosis and unstable plaques as well as innovative biotechnological anti-thrombotic, anti-inflammatory and plaque-stabilising approaches.


Understanding, Detecting and Treating Atherosclerotic Plaque Instability toward Reducing Cardiovascular Morbidity and Mortality

Karlheinz Peter, MD PhD
Atherothrombosis and Vascular Biology, Baker Heart & Diabetes Institute
Department of Cardiometabolic Health, University of Melbourne
Department of Medicine & Immunology, Monash University
Department of Cardiology, The Alfred Hospital
75 Commercial Road, Melbourne Vic 3004 Australia


Myocardial infarction (MI) is the number one individual cause of death worldwide and in addition causes most of the cardiovascular morbidity. The major underlying cause is atherosclerosis and, in most cases, the immediate cause of MI is plaque instability and consequent rupture. Preventing plaque rupture by any intervention (diet, medication, interventional approaches) would make a major difference for morbidity and mortality. However, also identifying the unstable, vulnerable atherosclerotic plaque at risk of rupture, and thus the patient at risk of suffering a MI, via non-invasive or invasive methods is central to ultimately preventing MIs. One of the major hurdles for animal research towards developing diagnostic and therapeutic approaches for plaque stabilisation, is the lack of mouse models that represent plaque instability/rupture. Classical mouse models such as ApoE-/- and LDLR-/- represent more atherogenesis, less so the end stage of plaque development, plaque instability and rupture. We have created a mouse model, the tandem stenosis model, that develops predefined haemodynamically driven unstable, rupture-prone plaques as seen in patients with MI. Using this model, we developed and patented novel imaging technologies for identifying unstable plaques and recently started a biotech company devoted to the clinical translation of this technology. Importantly, we use the TS model also as preclinical tool for identifying drugs (and diets) with plaque-stabilising potential and we use it as proteomic and transcriptomic discovery tool to better understand plaque instability. Ultimately, we hope that with our work in the TS mouse model we can contribute to translation and ultimately the prevention of MIs in humans.


myocardial infarction, unstable atherosclerotic plaque, plaque rupture, inflammation, thrombosis

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