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Immune Cells in Cancer · Journal article
JAMA Cardiology · September 9, 2026
Encouraging direction, but not yet definitive.
This prospective cohort study of 55 cancer patients found no significant increase in (18F)FDG-PET/CT–detected arterial inflammation at 24 weeks in patients receiving immune checkpoint inhibitors, vascular endothelial growth factor inhibitors, or both, with only modest systemic inflammatory biomarker changes. The findings argue against macrophage-driven plaque activation as the primary mechanism of ICI-associated cardiovascular risk, redirecting focus toward endothelial and thrombotic pathways.
Prospective longitudinal cohort study. Adults with cancer enrolled at the West of Scotland regional cancer hospital network; mean age 66 years (SD 10), 71% male (39/55), 29% female (16/55).. Intervention: Immune checkpoint inhibitor (ICI) monotherapy (n=20), vascular endothelial growth factor inhibitor (VEGFI) monotherapy (n=15), or combined ICI plus VEGFI therapy (n=20). Compared with: Baseline (18F)FDG-PET/CT imaging and biomarkers; between-group comparisons at 24 weeks. n = 55. West of Scotland regional cancer hospital network.
TBRmax did not exceed baseline at 24 weeks in any group: ICIs 1.67 (SD 0.14) vs baseline 1.71 (SD 0.14); VEGFIs 1.72 (SD 0.17) vs baseline 1.72 (SD 0.22); ICIs + VEGFIs 1.64 (SD 0.15) vs baseline 1.74 (SD 0.18); P = .13 ICI therapy was associated with selectively altered T-cell subsets, an effect attenuated by concurrent VEGFI therapy VEGFI therapy alone showed no significant association with circulating immune cells
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These findings challenge the hypothesis that ICI-associated cardiovascular risk is primarily driven by inflammatory plaque activation detectable by PET/CT imaging. Clinicians and researchers should consider pivoting mechanistic investigations toward endothelial dysfunction and thrombotic pathways when evaluating ICI cardiotoxicity prevention strategies.
Prospective cohort study with multimodal imaging and biomarker endpoints showing no detectable arterial inflammation with ICIs or VEGFIs, directly addressing an important but incompletely resolved mechanistic question; limited by modest sample size and surrogate endpoints rather than hard clinical outcomes.
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Quoted from the source exactly as published.
These findings challenge the hypothesis that ICI-associated cardiovascular risk is primarily driven by inflammatory plaque activation detectable by PET/CT imaging. Clinicians and researchers should consider pivoting mechanistic investigations toward endothelial dysfunction and thrombotic pathways when evaluating ICI cardiotoxicity prevention strategies.
Graded across the dimensions that decide whether you should act, each from what the source actually supports. There is no single score, and where a dimension was not assessed it says so.
Importance Immune checkpoint inhibitors (ICIs) have transformed cancer outcomes but may be associated with an increased risk of myocardial infarction and ischemic stroke. Whether this risk is mediated by inflammatory plaque activation and whether coadministered vascular endothelial growth factor inhibitors (VEGFIs) modify the effect remain unresolved. Objective To prospectively characterize the arterial and systemic inflammatory outcomes associated with ICIs, VEGFIs, and combined ICIs plus VEGFIs in patients with cancer. Design, Setting, and Participants This prospective longitudinal cohort study was conducted between August 2022 and June 2024 at the West of Scotland regional cancer hospital network. Adults with cancer who were planned to receive ICI monotherapy, VEGFI monotherapy, or combined ICI plus VEGFI therapy underwent imaging and venous blood sampling at baseline (before treatment) and at 24 weeks. Data were analyzed from June 2024 to October 2025. Exposure Undergoing ( 18 F)fluorodeoxyglucose positron emission tomography computed tomography ([ 18 F]FDG-PET/CT) imaging. Main Outcomes and Measures Arterial inflammation was quantified by ( 18 F)FDG-PET/CT using imaging protocols optimized for vascular assessment. The primary outcome was the between-group difference in change in maximal tissue to background ratio (TBRmax) over time, evaluated by analysis of covariance adjusted for baseline. Systemic inflammatory biomarkers were measured by enzyme-linked immunosorbent assay and a proteomic panel. Circulating immune cell phenotypes were profiled using spectral flow cytometry. Results Of 55 evaluable patients (mean [SD] age, 66 [10] years; 39 male [71%] and 16 female [29%]), 20 received ICIs, 15 received VEGFIs, and 20 received ICIs plus VEGFIs. At 24 weeks, TBRmax did not exceed baseline in any group (ICIs: mean [SD], 1.71 [0.14] vs 1.67 [0.14]; VEGFIs: mean [SD], 1.72 [0.22] vs 1.72 [0.17]; ICIs + VEGFIs: mean [SD], 1.74 [0.18] vs 1.64 [0.15]; among groups: P =.13). Findings were consistent across artery type, calcification status, prior atherosclerotic disease, and steroid exposure. ICI therapy was associated with selectively altered T-cell subsets, an outcome attenuated by concurrent VEGFI therapy, while VEGFI therapy alone had no significant association with circulating immune cells. Across all 3 regimens, systemic inflammatory biomarkers showed only modest changes. Intracellular adhesion molecule-1 and vascular cell adhesion molecule-1 increased in patients exposed to ICIs. Conclusions and Relevance In this prospective cohort study, ICIs and VEGFIs, alone and in combination, were not associated with ( 18 F)FDG-PET/CT–detectable arterial inflammation, and systemic inflammatory outcomes were limited. These findings argue against macrophage-driven plaque activation as a primary mechanism of ICI-associated atherothrombosis and support prioritization of endothelial and thrombotic pathways in future mechanistic and preventive studies.
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