Cardiac MRI for the evaluation of oncologic cardiotoxicity

Abstract

Cancer therapeutics-related cardiac dysfunction (CTRCD) is a well-established adverse effect resulting from a number of cancer therapeutics. Newer immunotherapy has been associated with cardiomyopathy and myocarditis making comprehensive imaging useful for early recognition. Cardiac MRI (CMR) offers a comprehensive evaluation to detect CTRCD. Established guidelines for monitoring left ventricular ejection fraction for potential cardiotoxicity have recently incorporated CMR. We will review the utility of CMR in contemporary evaluation for potential oncologic cardiotoxicity.

Keywords: Cardiac MRI; cardiac toxicity; cardio-oncology.

Fig. 1

Demonstration of the comprehensive myocardial evaluation offered by CMR.

Fig. 2

Basic CMR imaging protocol.

Fig. 3

For LV chamber quantification, endocardial (red) contours are delineated at end-diastole (left) and end-systole (right) in a stack of short axis slices that cover the entire left ventricle. Computer-aided analysis packages are used to calculate LV parameters as shown. This patient has a decrease in EF and increase in end-systolic volume which can be seen in CTRCD.

Fig. 4

Guideline for monitoring LVEF for Class I and Class II agents adapted from Plana JC et. al. J Am Soc Echocardiogr 2014;27:911–39. ** CMR should be considered in high risk patients for cardiotoxicity when echo quality is limited or EF is uncertain. A non-contrast abbreviated protocol for EF assessment can be used at baseline and follow-up at intervals directed above. CMR with gadolinium can be used when there are concerns for myocarditis or scar imaging is necessary.

Fig. 5

The graph on the left shows 2 inversion recovery curves for a septal region of interest (blue) and the blood pool, generated from images, shown in the bottom row, taken at different times after an inversion pulse at time t = 0. Similar inversion recovery curves can be generated for each pixel location if the images are all acquired during a breath-hold and for the same cardiac phase. The T1 for each pixel location can be used to generate a T1 map, as shown in the top-right image. T1 maps represent arguably the most succinct and informative summary of the spatial and temporal changes during an inversion recovery. Borrowed with permission from Taylor et al. JACC: Cardiovascular Imaging. 2016.

Fig. 6

T1 and ECV map images. Representative left ventricular (LV) short-axis native T1 (top row) and extracellular volume (ECV, bottom row) maps are shown in similarly-aged participants. The LV and right ventricular (RV) blood pool cavities are noted. On each image, the color of pixels in the images (color scales on left) identifies the native T1 (milliseconds) and ECV (%). Insets on the ECV maps demonstrate the change in color intensity within the anterolateral wall of each ventricle. As shown, ECV is elevated in the cancer survivor previously treated with anthracycline-based chemotherapy. Borrowed with permission from Jordan et al. Circulation Imaging. 2016.

Fig. 7

Demonstrates CMR findings in a case of acute fulminant myocarditis in a patient with metastatic melanoma shortly after receiving his first cycle of Ipilimumab/Nivolumab. (A–B) Native T1-mapping and T2 mapping respectively demonstrating elevated signals along the inferior wall consistent with myocardial edema. LGE imaging (C–D) demonstrate LGE present in the subepicardial mid inferior wall consistent with acute myocarditis.

Fig. 8

CMR findings in a case of a 54 year old female with history of Hodgkin’s Lymphoma treated with radiation at ages 20, 24, 27 and now with recurrent pericardial effusion and dyspnea. (A–B) Real-time cine imaging demonstrates flattening of the septum during inspiration consistent with ventricular interdependence as well as a small pericardial effusion. (C) Tagged cine gradient imaging used to detect fibrotic adhesion of pericardial layers. (D–E) LGE imaging demonstrates pericardial LGE consistent with pericardial inflammation. The consolidation of these findings is consistent with the diagnosis of pericardial constriction.