PET Radiopharmaceuticals for Imaging Chemotherapy-Induced Cardiotoxicity

Abstract

Abstract Purpose of Review Currently, cardiotoxicity is monitored through echocardiography or multigated acquisition scanning and is defined as 10% or higher LVEF reduction. The latter stage may represent irreversible myocardium injury and limits modification of therapeutic paradigms at earliest stages. To stratify patients for anthracycline-related heart failure, highly sensitive and molecularly specific probes capable of interrogating cardiac damage at the subcellular levels have been sought. Recent Findings PET tracers may provide noninvasive assessment of earliest changes within myocardium. These tracers are at nascent stages of development and belong primarily to (a) mitochondrial potential-targeted and (b) general ROS (reactive oxygen species)-targeted radiotracers. Given that electrochemical gradient changes at the mitochondrial membrane represent an upstream, and earliest event before triggering the production of the ROS and caspase activity in a biochemical cascade, the former category might offer interrogation of cardiotoxicity at earliest stages exemplified by PET imaging, using 18F-Mitophos and 68Ga-Galmydar in rodent models. Summary Both categories of radiotracers may provide tools for monitoring chemotherapy-induced cardiotoxicity and interrogating therapeutic efficacy of cardio-protectants.