Abstract

Cardiac dysfunction and myocellular injury from cancer therapeutics are identified by reductions in left ventricular (LV) ejection fraction (LVEF) or >15% deteriorations in myocardial strain.1 Myocardial strain may deteriorate as a result of increases in LV end-systolic volume (LVESV), reductions in LV end-diastolic volume (LVEDV), or both. Decreases in LVEDV caused by hypovolemia from poor oral intake, emesis, or myocardial loss2 occur during cancer treatment. We sought to determine the frequency with which decrements in myocardial strain were mediated by decreases in LVEDV versus increases in LVESV in patients receiving potentially cardiotoxic chemotherapy. The study was approved by the local institutional review board, and participants provided witnessed, written informed consent. Cardiovascular magnetic resonance examinations were performed on a 1.5-T Siemens Avanto scanner <6 hours before chemotherapy administration both before and 3 months after the initiation of cancer treatment. LV volumes, LVEF, LV mass, relative wall thickness, and midwall eulerian circumferential strain (ECC) were calculated from a series of LV short-axis white-blood cine stacks and a midcavity short-axis grid-tagged image.3 In addition, global longitudinal strain (GLS) was assessed from high-temporal-resolution 2- and 4-chamber cine views …

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