Key result
ICB plus RT appears safe in high-CV-risk NSCLC, but ROS1/NTRK/MET inhibitors and platinum chemo are linked to cardiotoxicity.
Why the study?
Do different anticancer therapies have distinct cardiovascular toxicity profiles in patients with non-small cell lung cancer?
Cohort (n=5,242)
Do different anticancer therapies have distinct cardiovascular toxicity profiles in patients with non-small cell lung cancer?
Effect estimate: 1.32 (95% CI 1.13-1.53)
p-value: p=<0.001
Distinct cardiovascular toxicity profiles of NSCLC therapies can guide risk stratification, favoring ICB plus radiotherapy in high cardiovascular risk patients while cautioning against specific targeted and chemotherapy regimens.
Baseline CV risk should guide NSCLC therapy selection; extends real-world cardiotoxicity evidence.
BACKGROUND: The cardiovascular toxicity profiles of different treatment regimens for non-small cell lung cancer (NSCLC) remain unclear. AIMS: To investigate the associations between NSCLC therapies and arrhythmias, heart failure, pericardial diseases, cardiomyopathy, and coronary artery diseases. DESIGN: An observational cohort study. METHODS: The cardiovascular toxicity risk of anticancer therapies in NSCLC patients was evaluated in a pharmacovigilance study. Exposures included targeted therapy (TARGET), chemotherapy (CHEMO), radiotherapy (RT), immune checkpoint blockade (ICB), and combination therapies. RESULTS: This observational study (n = 5,242) revealed that ICB-RT combinations had superior cardiovascular safety to other regimens. Targeted therapies showed elevated heart failure risk (TARGET vs ICB: 1.32 (95% CI: 1.13-1.53), P < 0.001). Chemotherapy increased coronary artery disease risk (CHEMO vs ICB: 1.28 (95% CI: 1.03-1.60), P = 0.029). ICB showed higher pericardial disease risks (ICB vs CHEMO: 5.88 (95% CI: 4.00-8.33), P < 0.001). Platinum-taxane combinations had 2.14 times higher coronary risk than antimetabolites. Reactive oxygen species 1 (ROS1)/neurotrophic receptor tyrosine kinase (NTRK)/mesenchymal-epithelial transition (MET) inhibitors showed greater heart failure risk (OR = 2.14, 95% CI: 1.41-3.28, P < 0.001) vs EGFR inhibitors. Anti-PD-L1 (OR = 0.68, 95% CI 0.51-0.91, P = 0.009) and anti-CTLA-4 (OR = 0.57, 95% CI: 0.37-0.86, P = 0.008) demonstrated lower pericardial risk versus anti-PD-1. CONCLUSIONS: These findings support the use of ICB plus RT in patients with high cardiovascular risk, while caution is advised with ROS1/NTRK/MET inhibitors and platinum-taxane chemotherapy. Anti-PD-L1 and anti-CTLA-4 may be preferred over anti-PD-1 in patients at risk for pericardial toxicity.
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Mo et al. (2026) conducted a cohort in Non-small cell lung cancer (NSCLC) (n=5,242). Targeted therapy vs. Immune checkpoint blockade was evaluated on Heart failure (1.32, 95% CI 1.13-1.53, p=<0.001). Targeted therapies were associated with an elevated risk of heart failure compared to immune checkpoint blockade (1.32; 95% CI 1.13-1.53; P<0.001) in patients with non-small cell lung cancer.
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