Background: Sepsis-associated cardiac dysfunction has historically been characterized as predominantly systolic, yet the burden of heart failure with the preserved ejection fraction (HFpEF) phenotype among patients with heart failure (HF) first documented during sepsis remains poorly defined. Methods: In a single-center retrospective cohort of adults (≥18 years) admitted to a tertiary-care hospital between 1 January 2022 and 31 December 2024, we identified patients whose first sepsis diagnosis (ICD-10) coincided with their first HF diagnosis (ICD-10 I50.x) during the same encounter, with no prior HF in the EHR. Patients were classified by ICD-10 subtype as HFpEF, HFrEF, combined, or unspecified; the unspecified group underwent echocardiographic reclassification when LVEF was documented. Demographics, selected comorbidities, peak inflammatory markers, and unadjusted in-hospital and subsequent-encounter outcomes were compared between HFpEF and HFrEF. Results: Of 924 patients with HF first documented during sepsis, 438 (47.4%) were ICD-10–coded HFpEF and 405 (43.8%) HFrEF. HFpEF patients were older (74.0 vs. 69.2 years; p < 0.001) and more often female (53.0% vs. 37.0%; p < 0.001), with higher prevalence of COPD exacerbation (21.5% vs. 13.1%; p = 0.004) and hypothyroidism (26.3% vs. 17.5%; p = 0.034). HFrEF patients exhibited higher peak lactate (2.88 vs. 2.48 mmol/L; p = 0.009) and procalcitonin (8.52 vs. 7.24 ng/mL; p = 0.011). Unadjusted in-hospital mortality (28.1% vs. 27.7%; p = 0.95), ICU admission (75.8% vs. 74.8%; p = 0.80), and length of stay did not differ. Subsequent encounters were descriptively more frequent after HFpEF (11.0% vs. 6.2%). Conclusions: ICD-10–coded HFpEF and HFrEF occurred at nearly equal frequency among adults with HF first documented during sepsis, challenging the systolic-centric paradigm. Despite distinct demographic and biochemical profiles, unadjusted in-hospital outcomes did not differ. These descriptive findings, limited by administrative-coding-based phenotype classification, the absence of multivariable adjustment, and unmeasured sepsis-severity and comorbidity variables, are hypothesis-generating and support phenotype-aware prospective study of HF arising during sepsis.

Patients with chronic liver disease are systematically excluded from acute myocardial infarction (AMI) trials, and prior real-world data rely on administrative coding alone. Whether ICD-coded liver disease and laboratory-defined liver fibrosis identify the same patients, and whether they predict the same outcomes, is unknown. We conducted a single-center retrospective cohort study of 1037 consecutive adults admitted with AMI (ICD-10 I21.x) to a tertiary New York center between November 2022 and December 2024. The primary exposure was ICD-defined advanced liver disease (cirrhosis, hepatic failure, or portal hypertension/decompensation; n = 102). The secondary, lab-based exposure was the Fibrosis-4 (FIB-4) index calculated from earliest admission AST, ALT, and platelet count (computable in 1031 patients, 99.4%), stratified as low (3.25). Co-primary outcomes were invasive management (diagnostic angiography, percutaneous coronary intervention, or coronary artery bypass grafting) and in-hospital mortality. Multivariable logistic regression adjusted for age, sex, diabetes, chronic kidney disease, heart failure, and ST-elevation; the trend across FIB-4 tiers was assessed with the Cochran–Armitage test. Denominators throughout (including the 168/909 occult-fibrosis estimate) use the full exposure group as denominator under a missing-as-not-exposed convention; the four no-LD and two advanced-LD patients with missing FIB-4 are counted as non-advanced fibrosis for this calculation. Patients with ICD-defined advanced liver disease received invasive management less often (12.7% vs. 50.4%; adjusted odds ratio [aOR] 0.17, 95% CI 0.09–0.32) and died in hospital more often (43.1% vs. 7.9%; aOR 8.22, 95% CI 5.02–13.46) than patients without coded liver disease. Outcomes worsened monotonically across FIB-4 tiers (mortality 4.4% → 9.2% → 27.5%; invasive management 55.2% → 45.6% → 33.5%; both p < 0.001 by Cochran–Armitage trend test). Critically, 168 of 909 patients with no coded liver disease (18.5%) had FIB-4 > 3.25, representing a substantial population of unrecognized advanced fibrosis missed by clinical coding. Coded liver disease identifies a small, severely affected subgroup with markedly lower rates of invasive management and 6- to 8-fold higher mortality after AMI. Routine FIB-4 calculation, a free, three-variable lab score, identifies a much larger population with occult advanced fibrosis and graded excess risk that ICD codes miss entirely. Pending prospective validation, FIB-4 may serve as a low-cost adjunct to bedside risk stratification in AMI care.