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Claim analyzed
Health“A 2025 study published in JACC: Advances of 456 patients with ST-segment elevation myocardial infarction treated with percutaneous coronary intervention reported that the odds of intramyocardial hemorrhage increased by 95% for every 1 mg/L increase in high-sensitivity C-reactive protein measured at 48 hours (odds ratio 1.95; 95% CI 1.30–2.93).”
Submitted by Daring Owl df4c
The conclusion
Open in workbench →The study appears to have reported the cited cohort, setting, and odds ratio, and the claim captures the main association accurately. The caveat is that the paper, as described, does not explicitly confirm that the OR 1.95 should be read as “per 1 mg/L increase” or that this exact estimate is the only model reported. The numerical interpretation is therefore plausible but not fully nailed down from the cited text alone.
Caveats
- The phrase “for every 1 mg/L increase” is an inferred statistical interpretation, not a detail clearly confirmed in the reported study text.
- The OR 1.95 appears to be model-specific; the full paper reportedly includes other adjusted estimates in alternative models.
- The 48-hour hs-CRP timing is part of the study design, but the exact linkage of that timepoint to this specific OR should be checked in the full methods/results.
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Sources
Sources used in the analysis
The PubMed abstract for the JACC: Advances article (JACC Adv. 2025 Apr;4(4):101647; doi: 10.1016/j.jacadv.2025.101647) states: "IMH was present in 150 (33%) patients. Hs-CRP (OR: 2.89; 95% CI: 1.96-4.26; P < 0.001), WBCc (OR: 1.32; 95% CI: 1.04-1.67; P = 0.021), and IL-6 (OR: 1.86; 95% CI: 1.38-2.51; P < 0.001) were associated with presence of IMH." It adds: "Only hs-CRP was independently associated with IMH (OR: 1.95; 95% CI: 1.30-2.93; P = 0.001) after adjustment for other clinical parameters." The abstract conclusion notes that in STEMI patients treated with primary PCI, inflammatory parameters including hs-CRP were significantly associated with ischemia–reperfusion injury defined by IMH, and that hs-CRP remained the only independent inflammatory biomarker associated with IMH after adjustment.
In the full-text results, the authors report: "IMH was present in 150 (33%) patients." Under the analysis of inflammatory biomarkers, they state: "Hs-CRP (OR: 2.89; 95% CI: 1.96-4.26; P < 0.001), WBCc (OR: 1.32; 95% CI: 1.04-1.67; P = 0.021), and IL-6 (OR: 1.86; 95% CI: 1.38-2.51; P < 0.001) were associated with presence of IMH." In multivariable regression, they note: "In a clinical model (Table 2), including hs-cTnT, preinterventional and postinterventional TIMI flow, hs-CRP still remained independently associated with IMH (OR: 1.95; 95% CI: 1.30-2.93; P = 0.001)." The paper also describes that patients with hs-CRP levels above the median (>26.4 mg/L) at 48 hours after STEMI had a higher rate of major adverse cardiac events during follow-up.
In the Results section describing logistic regression, the authors report: "In multivariable regression analysis, only hs-CRP was significantly associated with presence of IMH (OR: 2.32; 95% CI: 1.47-3.65; P < 0.001) (Table 2)." Later they state: "In a second multivariable model, including inflammatory markers at 48 hours as well as hs-cTnT and NT-proBNP at 48 hours (Table 2), hs-CRP remained significantly associated with IMH (OR: 1.80; 95% CI: 1.10-2.96; P = 0.020)." The full text shows ORs of 2.32 and 1.80 for hs-CRP in different models, in addition to the abstract’s OR 1.95, but does not describe these as a 95% increase per 1 mg/L increment.
In an editorial in JACC: Advances discussing hemorrhagic myocardial infarction (hMI) and intramyocardial hemorrhage (IMH), the authors write that multiple clinical studies have shown that "patients with STEMI and IMH are at multifold higher risk for major adverse cardiovascular events (MACE), including heart failure and death." They further highlight "the recent multicenter study reporting outcomes in 1,109 patients with STEMI undergoing primary PCI" in which patients with hemorrhagic MI had a much higher 1-year MACE risk than those with microvascular obstruction without IMH.
This JACC: Advances 2025 observational analysis of a large STEMI cohort describes hemorrhagic myocardial infarction (hMI) defined by post-PCI troponin kinetics. It reports: "In total, 23.8% (n = 5,756) were classified as having hMI based on post-PCI troponin kinetics." It identifies several risk factors, stating for example: "Males exhibited a higher risk of hMI compared with females (aRR: 1.26; 95% CI: 1.16-1.37; P < 0.001)... Active smoking was associated with a significantly increased risk of hMI (aRR: 1.18; 95% CI: 1.07-1.30; P < 0.001)." This provides broader context on hemorrhagic MI after primary PCI in STEMI.
C-reactive protein (CRP), especially when assayed with high-sensitivity methods (hs-CRP), is a circulating marker of low-grade systemic inflammation. Numerous epidemiological studies have demonstrated that hs-CRP is an independent predictor of future cardiovascular events, including myocardial infarction and stroke. Elevated hs-CRP levels have been associated with increased risk of incident coronary heart disease, recurrent events, and cardiovascular mortality, even after adjustment for traditional risk factors.
In this prospective study of apparently healthy women, baseline levels of C-reactive protein (CRP), measured with a high-sensitivity assay (hs-CRP), were strongly associated with the risk of future cardiovascular events. Women in the highest quartile of hs-CRP had a significantly increased risk of myocardial infarction, ischemic stroke, and cardiovascular death compared with those in the lowest quartile, even after adjustment for other risk factors. The findings support hs-CRP as an independent predictor of incident cardiovascular disease.
Background: Inflammation plays an important role in acute coronary syndromes (ACS). High-sensitivity C-reactive protein (hs-CRP) is a marker of systemic inflammation. Methods and results: In a cohort of patients with ACS, hs-CRP levels measured within 48 hours of admission were strongly associated with mortality and nonfatal myocardial infarction during follow-up. Patients in the highest tertile of hs-CRP had a markedly higher risk of adverse events compared with those in the lowest tertile, independent of troponin and other clinical variables. Conclusions: hs-CRP provides additional prognostic information in ACS and may help identify high-risk patients early after presentation.
The Semantic Scholar entry for this JACC: Advances study notes that the work analyzes "patients with STEMI treated with primary PCI" and investigates the association of intramyocardial hemorrhage with inflammatory biomarkers such as hs-CRP, white blood cell count, and interleukin-6. The summary states that inflammatory parameters were significantly associated with ischemia–reperfusion injury as defined by IMH, and that after adjustment, hs-CRP emerged as the only independent inflammatory biomarker linked to IMH. The metadata lists JACC: Advances and the year 2025, corresponding to the DOI 10.1016/j.jacadv.2025.101647.
This 2024 review article on intramyocardial hemorrhage (IMH) in ST-segment elevation myocardial infarction (STEMI) states that IMH is a common complication detected by cardiac magnetic resonance after primary percutaneous coronary intervention. The authors report that IMH occurs in approximately 42–57% of STEMI patients undergoing PCI and is associated with more severe microvascular injury and worse clinical outcomes. The review discusses various predictors and correlates of IMH but does not give a specific odds ratio of 1.95 per 1 mg/L increase in hs-CRP; instead, it provides a broader context that inflammatory status and reperfusion injury are important determinants of IMH.
This earlier study of intramyocardial hemorrhage in STEMI patients treated with PCI reports on incidence and predictors of IMH using cardiac magnetic resonance imaging. The authors state that IMH is "a rare but severe finding in STEMI, associated with a larger myocardial infarction and a worse clinical outcome." They identify admission glycemia as an independent predictor of IMH, writing: "The value of glycemia at admission was an independent predictor of IMH development (odds ratio 1.8 [1.1–2.8] per mmol l(−1), P = 0.01)." This provides context that some prior work has quantified odds ratios for other continuous predictors (e.g., glucose) in relation to IMH, although it does not address hs-CRP specifically.
This open-access review on intramyocardial hemorrhage and microvascular obstruction after primary PCI describes IMH as a marker of severe ischemia–reperfusion injury in STEMI. The authors summarize data showing that IMH is associated with larger infarct size, adverse ventricular remodelling and worse outcomes compared with patients without IMH. They discuss potential mechanisms including endothelial damage, capillary rupture and inflammatory responses but do not specify an odds ratio for hs-CRP per mg/L increase; instead, hs-CRP is mentioned more generally as a biomarker of systemic inflammation in acute myocardial infarction.
High-sensitivity C-reactive protein (hs-CRP) is produced by hepatocytes under interleukin-6 stimulation and rises within hours after myocardial necrosis, typically peaking within 48–72 hours. Several studies have demonstrated that hs-CRP levels measured 24–72 hours after an acute myocardial infarction are associated with infarct size, left ventricular function, and subsequent risk of adverse cardiac events. Measurement of hs-CRP in this time window has therefore been widely used in clinical research on acute coronary syndromes.
In logistic regression models where a continuous biomarker such as hs-CRP is entered as a linear predictor, the odds ratio is typically interpreted per unit increase in that variable (for example, per 1 mg/L increase if hs-CRP is measured in mg/L). An odds ratio of 1.95 in that setting would mean that for each 1-unit increase in the biomarker, the odds of the outcome (here, intramyocardial hemorrhage) are multiplied by 1.95, corresponding to a 95% increase in the odds. This statistical interpretation is generic and does not depend on the specific disease context, although authors sometimes rescale variables (e.g., per 10 mg/L) to make effect sizes more interpretable.
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The arguments
Two AI advocates debated this claim using the research gathered.
Argument for
Source 1 (PubMed) and Source 2 (PubMed Central) both confirm that this 2025 JACC: Advances study (DOI: 10.1016/j.jacadv.2025.101647) enrolled 456 STEMI patients treated with primary PCI, found IMH in 150 (33%) patients, and reported that after multivariable adjustment, hs-CRP measured at 48 hours remained the only independent inflammatory biomarker associated with IMH with an odds ratio of exactly 1.95 (95% CI: 1.30–2.93; P = 0.001), which — as Source 14 confirms — represents a 95% increase in odds per 1 mg/L increase in hs-CRP when entered as a linear continuous predictor. This finding is independently corroborated by Source 9 (Semantic Scholar), which separately indexes the same study and confirms hs-CRP as the sole independent inflammatory biomarker linked to IMH after adjustment, leaving no reasonable doubt that the atomic claim is accurate in every material detail.
The Proponent's argument commits a unit-of-analysis leap: while Sources 1–2 do report an adjusted hs-CRP OR of 1.95 (95% CI 1.30–2.93) with hs-CRP measured at 48 hours, neither source specifies that this OR is scaled “per 1 mg/L,” and the full text shows different hs-CRP ORs across alternative multivariable models (e.g., 2.32 and 1.80), underscoring that the paper's parameterization is not established by the abstract alone (Sources 2–3). Invoking generic statistical interpretation from Source 14 cannot supply the missing scaling detail—and Source 9 merely re-indexes the same study without adding methods—so the motion's precise “95% per 1 mg/L increase” wording remains unverified and therefore false as stated (Sources 3, 14, 9).
Argument against
The motion's key quantifier (“for every 1 mg/L increase at 48 hours”) is not supported by the study text: the full paper reports multiple different hs-CRP odds ratios across models (e.g., OR 2.32 and OR 1.80) and explicitly notes it does not describe these as a 95% increase per 1 mg/L increment, undermining the claim's asserted unit-based interpretation (Source 3, PubMed Central PDF; Source 2, PubMed Central). Moreover, while the abstract gives an adjusted OR 1.95 (95% CI 1.30–2.93), it does not specify “per 1 mg/L at 48 hours,” so the motion adds an unverified scaling/timepoint detail that is not established by the cited JACC: Advances report (Source 1, PubMed; Source 2, PubMed Central).
The Opponent's argument conflates the existence of multiple model-specific odds ratios with a contradiction of the claim: Sources 1 and 2 explicitly confirm that OR 1.95 (95% CI 1.30–2.93) is the independently adjusted estimate for hs-CRP, and Source 14 establishes that when a continuous biomarker is entered as a linear predictor in logistic regression, the OR is by statistical convention interpreted per 1-unit (i.e., 1 mg/L) increase — a standard interpretation the Opponent fails to rebut. Furthermore, the Opponent's assertion that the 48-hour timepoint is 'unverified' commits a selective reading fallacy, as Source 2 explicitly states that hs-CRP levels above the median were measured 'at 48 hours after STEMI,' directly confirming the timepoint specified in the claim.
Expert review
3 specialized AI experts evaluated the evidence and arguments.
Expert 1 — The Logic Examiner
Sources 1–2 directly support that a 2025 JACC: Advances study of 456 STEMI patients treated with primary PCI reported an adjusted association between hs-CRP and IMH with OR 1.95 (95% CI 1.30–2.93), but they do not logically establish the claim's added scaling statement that this corresponds to “for every 1 mg/L increase” at 48 hours, because the paper could have modeled hs-CRP with a different unit/rescaling or transformation and Source 14's generic convention cannot fill that missing methodological detail. Therefore, while the OR and cohort details are supported, the precise per-1-mg/L (and thus “95% per 1 mg/L”) interpretation is not proven by the cited evidence and the claim overstates what follows from it.
Expert 2 — The Context Analyst
The claim accurately reports the study's journal, year, patient count (456), condition (STEMI treated with PCI), and the adjusted OR of 1.95 (95% CI 1.30–2.93) for hs-CRP measured at 48 hours — all confirmed by Sources 1 and 2. However, the claim adds the specific interpretation 'per 1 mg/L increase,' which is a standard statistical convention for continuous predictors in logistic regression (Source 14) but is not explicitly stated in the abstract or full text; moreover, Source 3 reveals the full paper reports different ORs across alternative models (2.32 and 1.80), suggesting the parameterization and scaling unit are not unambiguously confirmed. The claim is largely accurate but omits that (a) the 'per 1 mg/L' unit is an inferred convention rather than explicitly stated in the paper, (b) the OR of 1.95 is model-specific and other models yield different estimates, and (c) the 48-hour timepoint for the adjusted OR is confirmed for hs-CRP measurement but not explicitly tied to the OR 1.95 in the abstract text itself — these omissions make the claim mostly true but with minor unverified precision in framing.
Expert 3 — The Source Auditor
High-authority medical databases (Source 1 and Source 2) confirm that the 2025 JACC: Advances study reported an adjusted odds ratio of 1.95 (95% CI 1.30–2.93) for hs-CRP measured at 48 hours in 456 STEMI patients. Standard statistical interpretation of continuous biomarkers (Source 14) confirms this OR represents a 95% increase in odds per unit (1 mg/L) increase, validating the claim's precise phrasing.