PET Radiopharmaceuticals for Imaging Chemotherapy-Induced Cardiotoxicity
Overview
Affiliations
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 F-Mitophos and Ga-Galmydar in rodent models. Both categories of radiotracers may provide tools for monitoring chemotherapy-induced cardiotoxicity and interrogating therapeutic efficacy of cardio-protectants.
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