Cardiac molecular imaging to track left ventricular remodeling in heart failure
Journal of Nuclear Cardiology
Cardiac left ventricular (LV) remodeling is the final common pathway of most primary cardiovascular diseases that manifest clinically as heart failure (HF). The more advanced the systolic HF and LV dysfunction, the worse the prognosis. The knowledge of the molecular, cellular, and neurohormonal mechanisms that lead to myocardial dysfunction and symptomatic HF has expanded rapidly and has allowed sophisticated approaches to understanding and management of the disease. New therapeutic targets for pharmacologic intervention in HF have also been identified through discovery of novel cellular and molecular components of membrane-bound receptor-mediated intracellular signal transduction cascades. Despite all advances, however, the prognosis of systolic HF has remained poor in general. This is, at least in part, related to the (1) relatively late institution of treatment due to reliance on gross functional and structural abnormalities that define the “heart failure phenotype” clinically; (2) remarkable genetic-based interindividual variations in the contribution of each of the many molecular components of cardiac remodeling; and (3) inability to monitor the activity of individual pathways to cardiac remodeling in order to estimate the potential benefits of pharmacologic agents, monitor the need for dose titration, and minimize side effects. Imaging of the recognized ultrastructural components of cardiac remodeling can allow redefinition of heart failure based on its “molecular phenotype,” and provide a guide to implementation of “personalized” and “evidence-based” evaluation, treatment, and longitudinal monitoring of the disease beyond what is currently available through randomized controlled clinical trials.
Shirani, Jamshid; Singh, Amitoj; Agrawal, Sahil; and Dilsizian, Vasken, "Cardiac molecular imaging to track left ventricular remodeling in heart failure" (2017). Department of Cardiovascular Medicine Articles & Publications. 16.