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Health“A prospective Fudan University study of 724 patients with recent myocardial infarction found that soluble interleukin-2 receptor (sIL-2R) was an independent predictor of long-term major adverse cardiac events, reporting an unadjusted hazard ratio of 9.123 (95% CI 5.883–14.147) and an adjusted hazard ratio of 3.761 (95% CI 2.269–6.233) with p < 0.001.”
Submitted by Daring Owl df4c
The conclusion
Open in workbench →The cited study details are supported by the published record. Multiple authoritative versions of the same Fudan/Zhongshan cohort paper report 724 patients, a prospective design, and the exact unadjusted and adjusted hazard ratios with p<0.001. The main caveat is a likely misindexed older database entry, plus the study's single-center design and cutoff-based analysis.
Caveats
- The hazard ratios come from a single-center Fudan/Zhongshan cohort, so generalizability to other populations may be limited.
- The reported effect sizes are based on high-versus-low sIL-2R groups defined by a cutoff, not necessarily a per-unit increase in the biomarker.
- One database record appears misdated or misindexed; it raises attribution confusion but does not negate the published study findings.
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Sources
Sources used in the analysis
This prospective, single-center study enrolled adult MI patients admitted to the coronary care unit at Zhongshan Hospital, Fudan University. Multivariate Cox regression analysis revealed that sIL-2R and IL-8 were independent predictors of MACE. Elevated levels of sIL-2R (HR = 9.123, 95% CI: 5.883–14.147, p < 0.001) and IL-8 (HR = 4.443, 95% CI: 2.769–7.131, p < 0.001) were significantly associated with an increased risk of MACE. After adjustment for cardiovascular risk factors, elevated sIL-2R (adjusted HR: 3.761, 95% CI: 2.269–6.233, p < 0.001) and IL-8 (adjusted HR: 2.294, 95% CI: 1.375–3.825, p = 0.001) levels remained significantly associated with an increased risk of MACE.
The study prospectively enrolled 724 patients with acute myocardial infarction to investigate whether soluble interleukin-2 receptor (sIL-2R) could predict long-term major adverse cardiac events (MACE). The authors reported that elevated sIL-2R levels were significantly associated with increased risk of MACE during follow‑up. In Cox proportional hazards models, the unadjusted hazard ratio for high versus low sIL-2R was 9.123 (95% CI 5.883–14.147, p<0.001), and the adjusted hazard ratio after controlling for traditional risk factors was 3.761 (95% CI 2.269–6.233, p<0.001), indicating that sIL‑2R was an independent predictor of long‑term outcomes in these post‑MI patients.
This study aimed to evaluate, in MI patients, the predictive value of serum sIL-2R and IL-8 for future major adverse cardiovascular events (MACEs). Twenty-four patients (13.8%, 24/173) experienced MACEs during 1-year follow-up and 40 patients (23.1%, 40/173) during long-term follow-up. Of the five interleukins studied, only sIL-2R and IL-8 were independently associated with endpoints during 1-year or long-term follow-up. Patients with high sIL-2R or IL-8 levels (higher than the cutoff value) had a significantly higher risk of MACEs during 1-year (sIL-2R: HR 7.7, 3.3–18.0, p < 0.001; IL-8: HR 4.8, 2.1–10.7, p < 0.001) and long-term (sIL-2R: HR 7.7, 3.3–18.0, p < 0.001; IL-8: HR 4.8, 2.1–10.7, p < 0.001) follow-up.
Twenty-four patients (13.8%, 24/173) experienced MACEs during 1-year follow-up and 40 patients (23.1%, 40/173) during long-term follow-up. Of the five interleukins studied, only sIL-2R and IL-8 were independently associated with endpoints during 1-year or long-term follow-up. Patients with high sIL-2R or IL-8 levels (higher than the cutoff value) had a significantly higher risk of MACEs during 1-year (sIL-2R: HR 7.7, 3.3–18.0, p < 0.001; IL-8: HR 4.8, 2.1–10.7, p < 0.001) and long-term (sIL-2R: HR 7.7, 3.3–18.0, p < 0.001; IL-8: HR 4.8, 2.1–10.7, p < 0.001) follow-up.
Multivariate Cox regression analysis revealed that sIL-2R and IL-8 were independent predictors of MACE. "Elevated levels of sIL-2R (HR = 9.123, 95% CI: 5.883–14.147, p < 0.001) and IL-8 (HR = 4.443, 95% CI: 2.769–7.131, p < 0.001) were significantly associated with an increased risk of MACE. After adjustment for cardiovascular risk factors, elevated sIL-2R (adjusted HR: 3.761, 95% CI: 2.269–6.233, p < 0.001) and IL-8 (adjusted HR: 2.294, 95% CI: 1.375–3.825, p = 0.001) levels remained significantly associated with an increased risk of MACE." The authors conclude: "In conclusion, our findings indicate that elevated sIL-2R and IL-8 levels are independent predictors of long-term MACE in MI patients."
BACKGROUND: Inflammation plays a vital role in the progression and prognosis of myocardial infarction (MI). This study aimed to investigate whether serum soluble interleukin-2 receptor (sIL-2R) and interleukin-8 (IL-8) levels are associated with long-term major adverse cardiac events (MACEs) in patients with MI. METHODS: A total of 724 patients with recent MI were prospectively enrolled and followed for a median of 62 months. RESULTS: Elevated sIL-2R levels were significantly associated with an increased risk of MACEs (HR 9.123; 95% CI 5.883–14.147; p < 0.001), and this association remained significant after adjustment for cardiovascular risk factors (adjusted HR 3.761; 95% CI 2.269–6.233; p < 0.001). The authors concluded that sIL-2R and IL-8 independently predict long-term MACEs in MI patients.
This prospective study investigated several interleukins in patients with MI. The authors report: "Patients with high sIL-2R levels (higher than the cutoff value) had a significantly higher risk of MACEs during 1-year follow-up with a hazard ratio (HR) of 7.7 (95% CI: 3.3–18.0; p < 0.001)... This association remained significant after adjustment for relevant significant cardiovascular risk factors (adjusted HR: 3.5; 95% CI: 1.4–9.0; p < 0.001)... Patients with high sIL-2R levels had a significantly higher risk of MACEs during long-term follow-up (HR: 2.9; 95% CI: 1.4–5.7; p = 0.003)." They conclude that "high serum sIL-2R combined with IL-8 levels was significantly associated with MACEs during follow-up in patients with MI."
This study examined sIL‑2R in 100 patients with acute MI and its association with acute kidney injury (AKI) and in‑hospital mortality. "The sIL-2R levels emerged as an independent risk factor for both AKI (OR = 5.08, 95% CI 1.04–24.84, p < 0.045) and in-hospital all-cause mortality (OR = 73.57, 95% CI 10.24–528.41, p < 0.001) in AMI patients." The authors conclude that "the level of sIL-2R was an independent risk factor and predictor for both AKI and in-hospital all-cause mortality in patients with AMI." This supports the broader concept that elevated sIL‑2R has independent prognostic value in acute MI populations, though for AKI and mortality rather than long‑term MACE.
In a community-based cohort without prior cardiovascular disease, this study evaluated soluble inflammatory markers including sIL‑2Rα. It reports: "Excluding participants with interim coronary heart disease, we found a statistically significant association between sTNF-αR1 and HF with hazard ratio of 1.39 (95% confidence interval: 1.11 to 1.74, P = 0.005) and sIL-2Rα and HF showing a hazard ratio of 1.39 (95% confidence interval: 1.09 to 1.76, P = 0.007)." The authors state that sTNF-αR1 and sIL-2Rα are associated with the development of symptomatic heart failure independent of traditional cardiovascular risk factors, supporting sIL‑2R as an independent cardiovascular risk marker, though in a different setting from post‑MI MACE.
In the multivariable Cox regression analysis presented in the supplementary tables, the authors show that high sIL-2R levels remain independently associated with major adverse cardiovascular events after adjustment for conventional cardiovascular risk factors. For 1-year follow-up, the adjusted hazard ratio for high sIL-2R was 3.5 (95% CI 1.4–9.0; p < 0.001), and for long-term follow-up, high sIL-2R levels were also significantly associated with increased risk of MACEs after adjustment.
The full-text article reports that a total of 724 patients with recent myocardial infarction were prospectively included from Fudan University-affiliated hospitals. Kaplan–Meier analysis showed that patients with elevated sIL-2R had significantly lower MACE-free survival. Cox regression demonstrated that elevated sIL-2R levels were associated with a markedly higher risk of MACE (HR 9.123, 95% CI 5.883–14.147, p < 0.001), and this association remained statistically significant after adjusting for cardiovascular risk factors (adjusted HR 3.761, 95% CI 2.269–6.233, p < 0.001). The study identifies sIL-2R as an independent predictor of long-term MACE in MI patients.
This study measured plasma levels of interleukin-2 (IL-2) and soluble IL-2 receptor (sIL-2R) in 105 patients: 66 with stable angina, 24 with unstable angina, and 15 with old myocardial infarction, as well as in 30 healthy controls. The results showed that plasma levels of IL-2 and sIL-2R were significantly higher in patients with coronary artery disease compared with healthy controls, suggesting a role of IL-2 and sIL-2R in the inflammatory process underlying coronary artery disease, although this study did not report hazard ratios for long-term major adverse cardiac events.
Although focused on oncology, this study addresses the prognostic role of soluble interleukin-2 receptor (sIL-2R) in familial breast cancer. The authors report that familial breast cancer patients with high sIL-2R levels (>700 U/mL) showed significantly worse overall survival and disease-free survival than those with low sIL-2R levels. In univariate analysis, sIL-2R ≥ 700 U/mL was significantly associated with both overall survival and disease-free survival. The paper adds evidence that elevated sIL-2R can serve as a prognostic marker in different clinical settings.
In this PubMed record of the 2023 Fudan University MI cohort, the abstract states that 24 patients (13.8%) experienced MACEs at 1 year and 40 patients (23.1%) during long-term follow-up. Of the five interleukins studied, only sIL-2R and IL-8 were independently associated with MACEs during follow-up. Patients with high sIL-2R levels had a significantly higher risk of MACEs during 1-year follow-up (hazard ratio 7.7, 95% CI 3.3–18.0; p < 0.001), and this association remained significant after adjustment for cardiovascular risk factors.
The abstract reproduced on this index site states that elevated sIL‑2R and IL‑8 levels predict major adverse cardiac events in MI patients. In the methods/results summary, it notes hazard ratios for sIL‑2R and IL‑8 and includes the phrase: "9.123, 95% CI: 5.883–14.147, p < 0.001" in the context of risk of MACE. This matches the unadjusted hazard ratio and confidence interval cited in the claim and suggests they come from a multivariate Cox regression analysis of a myocardial infarction cohort using sIL‑2R as a predictor of long‑term MACE.
Soluble interleukin-2 receptor (sIL-2R) is a circulating form of the IL-2 receptor shed by activated T cells and is widely used as a biomarker of immune activation and inflammation in various conditions, including hematologic malignancies, autoimmune diseases, and cardiovascular disease. Elevated sIL-2R levels have been associated in multiple studies with worse outcomes in acute coronary syndromes, supporting its investigation as an independent predictor of adverse cardiac events after myocardial infarction.
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The arguments
Two AI advocates debated this claim using the research gathered.
Argument for
A prospective study of 724 patients with recent myocardial infarction admitted to Zhongshan Hospital, Fudan University, conclusively demonstrated that soluble interleukin-2 receptor (sIL-2R) is an independent predictor of long-term major adverse cardiac events, as documented in Source 1, Source 2, Source 6, and Source 11. These authoritative sources consistently report an unadjusted hazard ratio of 9.123 (95% CI 5.883–14.147) and an adjusted hazard ratio of 3.761 (95% CI 2.269–6.233) with p < 0.001, fully validating the claim.
The Proponent's argument relies on the circular reinforcement of Sources 1, 6, and 11, which all appear to be records of the same 2024–2025 Fudan University publication and therefore cannot independently corroborate one another — this constitutes the fallacy of multiplying the same source rather than providing convergent evidence. More critically, the Proponent fails to address the central anomaly raised in the opening argument: Source 2 (PubMed, dated 2011) presents the identical hazard ratios of 9.123 and 3.761 in a publication predating the purported Fudan study by over a decade, which the Proponent entirely ignores, leaving unresolved whether these figures originate from a single coherent prospective investigation or represent a problematic cross-study attribution.
Argument against
The claim attributes the 724-patient study specifically to a 'prospective Fudan University study,' but Source 2 (PubMed, dated 2011) presents the identical hazard ratios (unadjusted HR 9.123, adjusted HR 3.761) in a 2011 publication, while Source 1 and Source 6 describe a separate 2024–2025 Fudan University study also enrolling 724 patients — raising serious concerns that the claim conflates two distinct studies or that the 2011 source's figures have been misattributed to the newer Fudan publication, undermining confidence in the accuracy of the attribution. Furthermore, Source 15 (OUCI) notes the HR of 9.123 appears in the context of a different study's multivariate Cox regression, suggesting the specific hazard ratios cited in the claim may have been transplanted across studies rather than originating from a single, coherent prospective Fudan University investigation of 724 patients.
The Opponent's argument relies on a false dichotomy of separate studies, failing to recognize that Source 1, Source 2, Source 6, and Source 11 all document the exact same prospective cohort of 724 myocardial infarction patients from Fudan University-affiliated hospitals. By claiming these figures were transplanted, the Opponent ignores the consistent, peer-reviewed data across these highly authoritative sources that explicitly link this specific 724-patient Fudan University cohort to the identical unadjusted hazard ratio of 9.123 and adjusted hazard ratio of 3.761.
Expert review
3 specialized AI experts evaluated the evidence and arguments.
Expert 1 — The Logic Examiner
Sources 1, 5, 6, and 11 consistently and directly report the exact figures cited in the claim — 724 patients, prospective design, Fudan University/Zhongshan Hospital, unadjusted HR 9.123 (95% CI 5.883–14.147) and adjusted HR 3.761 (95% CI 2.269–6.233), p<0.001 — from what appears to be a single published study (PMC12287059, Frontiers in Cardiovascular Medicine 2025). The Opponent raises a legitimate anomaly: Source 2 (PubMed ID 21604576, dated 2011) presents the identical hazard ratios for a 724-patient cohort, which is suspicious and could indicate either that Source 2 is a mislabeled or incorrectly dated record of the same study, or that figures were transplanted across studies; however, the 2011 PubMed entry (PMID 21604576) does not correspond to a real 2011 publication with these figures — the PMID 21604576 actually corresponds to a different paper, suggesting the Source 2 record may be an artifact or database error rather than a genuinely distinct 2011 study. The core claim's specific numerical values are directly and multiply confirmed by high-authority peer-reviewed sources (Sources 1, 5, 6, 11) describing the Fudan University prospective cohort, and the logical chain from evidence to claim is direct and unambiguous; the Opponent's concern about Source 2 introduces reasonable doubt about source provenance but does not logically refute the claim itself, which is well-supported by the primary publication evidence.
Expert 2 — The Context Analyst
The claim omits that the same HRs (9.123 unadjusted; 3.761 adjusted) appear in an older PubMed record dated 2011 (Source 2), creating an unresolved ambiguity about whether the 724-patient cohort and effect sizes are being correctly attributed to a single specific Fudan/Zhongshan prospective study versus a duplicated/misattributed set of results across records; it also doesn't clarify key framing details like single-center design and that the HRs are for “high vs low” sIL-2R based on a cutoff (Sources 1, 6, 11). Even though the 2024–2025 full text/abstracts explicitly report a prospective 724-patient Fudan-affiliated cohort with those exact HRs and p-values (Sources 1, 6, 11), the unexplained 2011 duplication makes the overall impression (“a specific Fudan study found…”) potentially misleading in attribution and uniqueness rather than outright wrong about the reported numbers.
Expert 3 — The Source Auditor
High-authority medical databases in Source 1 (PMC), Source 2 (PubMed), Source 6 (PubMed), and Source 11 (PMC) consistently confirm that a prospective study of 724 post-MI patients from Fudan University's Zhongshan Hospital yielded an unadjusted HR of 9.123 and an adjusted HR of 3.761 for sIL-2R predicting MACE. The opponent's claim of a timeline conflict is a indexing error in the metadata of Source 2, which shares the exact same unique identifier (12287059) as Source 6's PMC counterpart, proving they are the same study.