Late Gadolinium Enhancement Cardiac Magnetic Resonance Tissue Characterization for Cancer‐Associated Cardiac Masses: Metabolic and Prognostic Manifestations in Relation to Whole‐Body Positron Emission Tomography

Figures

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  Figure 1. Study design, inclusive of cardiac mass assessment via late gadolinium enhancement CMR (LGE‐CMR; for contrast enhancement), 18F‐fluorodeoxyglucose (18F‐FDG)–positron emission tomography (PET; for metabolic activity) and subsequent clinical follow‐up (for all‐cause mortality).

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  Figure 2. Representative examples of neoplasm and thrombus as established by long inversion time (long‐TI) late gadolinium enhancement cardiac magnetic resonance (LGE‐CMR) tissue characterization, including neoplasm subtypes comprising diffuse enhancement (left), mixed (prominent enhancing and avascular components; center), and predominantly avascular enhancement (right; arrows indicate contrast‐enhancing regions, asterisks indicate avascular regions). Corresponding 18F‐fluorodeoxyglucose (18F‐FDG)–positron emission tomography (PET) images shown on bottom row: Note prominent FDG avidity corresponding to regions of contrast enhancement, and lack of FDG avidity in both predominantly avascular neoplasm as well as thrombus (far right).

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  Figure 3. Differential detection of mobile cardiac neoplasm. Mobile neoplasm adherent to the aortic valve in a patient with stage IV sarcoma (lesion denoted within yellow circle). Cine–cardiac magnetic resonance (cine‐CMR; top) demonstrates prominent lesion mobility, as shown by migration between systolic and diastolic frames (Video S1). Long inversion time (long‐TI) late gadolinium enhancement CMR (LGE‐CMR; bottom left) demonstrates a focal aortic lesion with patchy contrast enhancement despite nonvisualization on 18F‐fluorodeoxyglucose–positron emission tomography (18F‐FDG–PET; bottom center). Pathology data (bottom right) obtained at surgical resection confirmed LGE‐CMR diagnosis of neoplasm: note fibrous connective tissue and cellular rich area; high magnification (inset) demonstrates spindle cell morphology, cellular atypia, and nuclear pleomorphism (hematoxylin and eosin stain).

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  Figure 4. Differential detection of intramyocardial cardiac neoplasm. Marked asymmetric thickening of the left ventricular (LV)inferior wall in a patient with stage IV hepatocellular carcinoma. Long inversion time (long‐TI) late gadolinium enhancement CMR (LGE‐CMR) demonstrates contrast enhancement, consistent with NEO, whereas 18F‐fluorodeoxyglucose–positron emission tomography (18F‐FDG–PET) demonstrates low FDG avidity compared with surrounding (nonhypertrophied) LV walls. Biopsy of adjacent mediastinal lymph nodes demonstrated atypical cells (hematoxylin and eosin stain); immunostaining (anti–Hep Par 1 [hepatocyte paraffin 1] antibody) showed Hep Par 1–positive (dark brown) cells consistent with hepatocellular carcinoma. Cine‐CMR indicates cine–cardiac magnetic resonance.

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  Figure 5. Quantitative contrast enhancement in relation to positron emission tomography–evidenced metabolic activity. A, Signal‐to‐noise ratio (SNR; left) and contrast‐enhancement heterogeneity (CEH; right) among cardiac mass subgroups partitioned based on diagnostic test interpretation. Note higher SNR for fluorodeoxyglucose (FDG) avid vs nonavid neoplasm (NEO; P=0.004), paralleling higher SNR and CEH for both NEO subtypes vs thrombus (THR; both P<0.001). Data shown as median plus or minus interquartile range. B, Scatter plots demonstrating correlation between SNR and standardized uptake value (SUV) within NEO. Highly mobile lesions excluded from analyses (due to imprecise colocalization). Note significant correlations between magnitude of contrast‐enhancement and FDG avidity (P<0.05).

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  Figure 6. Quantitative metabolic activity as marker of cardiac neoplasm. A, Quantitative standardized uptake values (SUV) within visually scored cardiac mass subtypes. Note correspondence between visually assigned categories and quantitative results, as shown by 3‐ to 4‐fold increment in maximum (top) and mean (bottom) quantitative SUV for neoplasm (NEO) cases visually identified on positron emission tomography (PET) vs cases in which NEO was not visually discernable (P<0.001), as well as similar SUV between thrombus (THR; all PET negative) and NEO cases for which PET read discordantly with cardiac magnetic resonance (CMR; P=0.87 and P=0.32 for maximum and mean SUVs, respectively). B, Receiver operating characteristic (ROC) curves for maximum and mean SUV cutoffs in relation to late gadolinium enhancement CMR evidenced NEO. Note good overall diagnostic performance for quantitative SUV (area under the curve: 0.78); corresponding diagnostic test parameters as derived from ROC curves shown in Table 4.

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  Figure 7. Mortality status. A, Kaplan–Meier survival curves for cardiac magnetic resonance (CMR)–evidenced neoplasm (NEO; solid line) and cancer‐matched controls (dotted line). Note increased mortality among patients with NEO compared with controls matched for primary cancer type and stage (P=0.02). B, Corresponding Kaplan–Meier curves for fluorodeoxyglucose (FDG)–avid NEO and matched controls demonstrates a similar relationship (P=0.04). PET indicates positron emission tomography.