Myocardial infarction is a major cause of mortality and morbidity. Typically, the underlying disease is atherosclerosis. Over time patients develop atherosclerotic plaques that become unstable and ultimately some of these vulnerable plaques rupture and cause a thrombotic occlusion of the coronary arteries and thereby cause a myocardial infarction. Many patients die right away with their first myocardial infarction and many of those patients who survive develop severe heart failure.
To avoid these severe consequences, we have developed several biotechnological approaches:
- We developed a mouse model that reflects unstable, vulnerable, rupture-prone plaques as seen in patients.
- We discovered near-infrared autofluorescence as a characteristic feature of unstable plaques and are currently developing a novel invasive imaging approach to detect the dangerous vulnerable plaques before they rupture.
- We developed drugs that stabilise plaques.
- We designed drugs that prevent thrombosis and thus blockage of coronary arteries as a prophylactic approach towards prevention of myocardial infarction.
- We developed drugs that prevent heart failure, that often develops as ischaemia/ reperfusion injury after successful revascularisation of blocked coronary arteries.
For these approaches we use several imaging modalities such as fluorescence imaging, magnetic resonance imaging (MRI), X-ray computed tomography (CT), positron emission tomography (PET) and ultrasound. For our therapeutic approaches we use recombinant fusion proteins as well as small chemical compounds. We provide in vivo proof in mouse models of unstable atherosclerosis, myocardial infarction and thrombosis as well as with human thrombotic and atherosclerotic material. Most of our data have direct translational importance and have the potential to ultimately reduce mortality and morbidity associated with myocardial infarction.