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. Both categories of radiotracers may provide tools for monitoring chemotherapy-induced cardiotoxicity and interrogating therapeutic efficacy of cardio-protectants.
Keywords: ABCB1; ABCG2; Anthracycline; Cardiotoxicity; Galmydar; PET radiopharmaceuticals.