Key result
Elevated follow-up hs-TnI during ICI therapy is linked to ~82% higher all-cause mortality.
Why the study?
Does abnormal follow-up hs-TnI predict all-cause mortality and cardiovascular immune-related adverse events in patients treated with immune checkpoint inhibitors?
Observational (n=621)
No
Does abnormal follow-up hs-TnI predict all-cause mortality and cardiovascular immune-related adverse events in patients treated with immune checkpoint inhibitors?
Hazard Ratio: 1.816 (95% CI 1.302–2.532)
p-value: p=< 0.001
Abnormal follow-up high-sensitivity troponin I after the first cycle of immune checkpoint inhibitors is a significant independent predictor of all-cause mortality and cardiovascular immune-related adverse events.
Background Immune checkpoint inhibitors (ICIs) have revolutionized cancer treatment but are associated with immune-related adverse events (irAEs), including potentially life-threatening cardiovascular (CV) complications. Despite class IIa guideline recommendations for follow-up troponin monitoring, the predictive value of high-sensitivity troponin I (hs-TnI) remains underexplored. Objective To evaluate the predictive value of follow-up hs-TnI for clinical outcomes in patients treated with ICIs. Methods A retrospective, single-center, observational study including patients treated with ICIs and performing hs-TnI measurements following the 1st ICIs cycle. A hs-TnI level > 50ng/L was considered abnormal, adopted by Siemens recommendations cutoff. The primary endpoint was all-cause mortality, and the secondary endpoint was CV irAEs, defined as the composite of myocarditis, pericarditis, acute coronary syndrome, heart failure, and arrhythmias. Results The cohort included 621 patients, with a mean age of 69±12 years, and was predominantly male (64%). Lung cancer was the most common malignancy (20%), and pembrolizumab (anti-PD-1) was the most frequently used ICIs (65%). Baseline cardiovascular (CV) risk factors were common, including hypertension (48%), diabetes mellitus (24%), and hyperlipidemia (38%), while ischemic heart disease was present in 22% of patients. Sixty-two patients (10%) presented with abnormal follow-up hs-TnI. During follow-up, abnormal hs-TnI was significantly associated with increased all-cause mortality (adjusted HR 1.816 [95% CI = 1.302-2.532], p < 0.001) and increased incidence of CV irAEs (adjusted HR 2.395 [95% CI = 1.277-4.492], p = 0.006). Conclusions Follow-up hs-TnI emerged as a significant independent predictor for all-cause mortality and CV irAEs in patients treated with ICIs. These findings highlight the clinical utility of serial hs-TnI monitoring for early risk stratification. Prospective, multicenter studies are warranted to validate these results and optimize CV monitoring strategies in this population.
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Perelman et al. (2025) conducted an observational in Cancer treated with immune checkpoint inhibitors (n=621). Abnormal follow-up hs-TnI (> 50ng/L) vs. Normal follow-up hs-TnI (≤ 50ng/L) was evaluated on All-cause mortality (adjusted HR 1.816, 95% CI 1.302-2.532, p=< 0.001). Abnormal follow-up hs-TnI (>50 ng/L) in patients treated with immune checkpoint inhibitors was significantly associated with increased all-cause mortality (adjusted HR 1.816; 95% CI 1.302-2.532; p<0.001).
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