APOE and familial hypercholesterolemia: Although APOE*3-Leiden mice differ from the human situation, because of the absence of coronary atherosclerosis resulting in coronary plaque formation and the lack of rupture followed by thrombus formation, it does provide an excellent model to study the effects of hypercholesterolemia on the pathophysiological processes in an animal model after surgical interventions [27–30] including induction of MI.