Left ventricular remodeling is a key determinant of the clinical course and outcome of systolic heart failure. The myocardial renin-angiotensin system (RAS) has been closely linked to the major maladaptive cellular and molecular changes that accompany left ventricular remodeling. Direct inhibition of various components of the RAS, such as the angiotensin-converting enzyme, angiotensin II type 1 receptor, and aldosterone, has resulted in favorable clinical responses in heart failure. Many questions, however, remain unanswered regarding the timing of initiation, optimum doses, need for simultaneous use of RAS inhibitors, and proper monitoring of RAS blockade. Additionally, significant variation has been noted in individual responses to RAS blockade as a result of genetic differences. Answering these questions requires direct access to the myocardial component of RAS, which is largely independent of its systemic component. Molecular imaging using radiotracers with high affinities for myocardial angiotensin-converting enzyme and angiotensin II type 1 receptors can provide direct access to tissue RAS and thus provide a better understanding of the pathophysiology of left ventricular remodeling in individual patients. This Article briefly reviews the potential for evaluating the tissue expression of angiotensin in heart failure by targeted RAS imaging.