LDLR and coronary atherosclerosis: Given the extensive and lethal myocardial infarctions that occur spontaneously at a young age in SR-B1/ApoE dKO mice [20], and in a high fat/high cholesterol diet-dependent manner in SR-B1−/− mice either lacking LDLR or with a hypomorphic mutation in apoE [21,22], we hypothesized that increased susceptibility of cardiomyocytes lacking SR-B1 to cell death may contribute along with the occlusive coronary artery atherosclerosis that develops in these mice to the development of lethal myocardial infarction.