Cardiac fibrosis and diastolic dysfunction after myocardial infarction in apolipoprotein E knockout mice

Department of Medicine, University of Vermont, Burlington, Vermont, USA Correspondence to Dr Burton E. Sobel, MD, Department of Medicine, University of Vermont, Colchester Research Facility, 208 South Park Drive, Colchester, VT 05446, USA Tel: +1 802 656 8955; fax: +1 802 656 8957; e-mail: [email protected] The Editor's Corner appears periodically in Coronary Artery Disease. The Editor and Associate Editors consider scientific, ethical, social, and philosophical issues relevant to cardiology and medicine. From time-to-time, we publish observations and conjectures by the editor and his colleagues such as the following. During the course of our studies of the impact of disorders such as the metabolic syndrome, insulin resistance, hyperlipidemia, and diabetes on the response of the heart in experimental animals to induced myocardial infarction, we noted that the ApoE-deficient mouse exhibited an anomalous response to coronary occlusion as described below. These observations underscore the need for caution in interpreting results of studies of the evolution of myocardial insults in mice with this and other genotypes predisposing to hypercholesterolemia and the need for elucidation of mechanisms responsible for the anomalous responses. Received 3 August 2009 Accepted 6 August 2009