ontrast-weighted images are commonly acquired in MRI, where one tissue-related parameter usually dominates the contrast, such as T1 or T2 weighting. Relative contrast differences across one image indicate different underlying tissue parameters, but this requires several sequences with different contrast weighting for a final diagnosis. These weighted contrasts provide only qualitative information, which limits the ability of qualitative MRI to depict mostly morphologic abnormalities. Pathologic conditions that alter tissue characteristics on a global or diffuse scale may be missed (1). Instead of indirectly visualizing tissue characteristics by using weighted contrasts, quantitative MRI attempts to directly measure them. Thereby, quantitative MRI could facilitate identification of physiologic changes that do not manifest themselves in morphologic changes or could help detect diffuse tissue changes (eg, in liver [2] and cardiac fibrosis [3]) that remain undetected by using qualitative MRI. It can provide more specific information than does qualitative MRI for characterizing pathologic conditions, such as multiple sclerosis (4) or brain tumors (5). Furthermore, quantitative MRI can be used to assess treatment response (6) or can aid in cases where no side comparison can be performed, such as hippocampal sclerosis (7). With quantitative MRI, diseases can be detected before gross morphologic

Aims Cardiac immune-related adverse events (irAEs) from immune checkpoint inhibition (ICI) targeting programmed death 1 (PD1) are of growing concern. Once cardiac irAEs become clinically manifest, fatality rates are high. Cardio-oncology aims to prevent detrimental effects before manifestation of severe complications by targeting early pathological changes. We therefore aimed to investigate early consequences of PD1 inhibition for cardiac integrity to prevent the development of overt cardiac disease. Methods and results We investigated cardiac-specific consequences from anti-PD1 therapy in a combined biochemical and in vivo phenotyping approach. Mouse hearts showed broad expression of the ligand PDL1 on cardiac endothelial cells as a main mediator of immune-crosstalk. Using a novel melanoma mouse model, we assessed that anti-PD1 therapy promoted myocardial infiltration with CD4+ and CD8+ T cells, the latter being markedly activated. Left ventricular (LV) function was impaired during pharmacological stress, as shown by pressure–volume catheterization. This was associated with a dysregulated myocardial metabolism, including the proteome and the lipidome. Analogous to the experimental approach, in patients with metastatic melanoma (n = 7) receiving anti-PD1 therapy, LV function in response to stress was impaired under therapy. Finally, we identified that blockade of tumour necrosis factor alpha (TNFα) preserved LV function without attenuating the anti-cancer efficacy of anti-PD1 therapy. Conclusions Anti-PD1 therapy induces a disruption of cardiac immune homeostasis leading to early impairment of myocardial functional integrity, with potential prognostic effects on the growing number of treated patients. Blockade of TNFα may serve as an approach to prevent the manifestation of ICI-related cardiotoxicity.

Integrated PET/MRI does not provide diagnostic advantages for local tumor staging of breast cancer patients in comparison to MRI alone. Positron emission tomography/MRI and MRI enable an improved determination of the local tumor extent in comparison to PET/CT, whereas all 3 imaging modalities offer a comparable diagnostic performance for the identification of axillary disease.