My research group focuses on imaging and understanding of cellular processes in cardiovascular disease. One major area of interest is the subacute phase after ischemic myocardial injury, the ensuing healing process, and its impact on left ventricular remodeling, since a large fraction of patients after myocardial infarction develop heart failure. Several key players have been identified as imaging targets: enzyme activities, including myeloperoxidase as a measure of inflammation, proteases involved in degradation of extracellular matrix, and transglutaminases with repair functions. These targets were imaged noninvasively in mice with MRI, optical, and nuclear techniques. Furthermore, we study cell trafficking during the initial inflammatory phase, and this work identified a biphasic monocytic recruitment after MI and a splenic reservoir for monocytes. Both of these major basic discoveries have been verified in human patients. We further study crosstalk between organ systems in cardiovascular disease, specifically between the immune, central nervous, endocrine, and cardiovascular systems. We discovered that myocardial infarction accelerates atherosclerosis through activation of hematopoietic stem cells in the bone marrow, which overproduces inflammatory leukocytes that travel to atherosclerotic plaque.