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Predicting events in ferropenic Acute Heart Failure Patients: The B12 paradox
Session:
SESSÃO DE POSTERS 43 - INSUFICIÊNCIA CARDÍACA E COMORBILIDADES
Speaker:
Mauro Moreira
Congress:
CPC 2025
Topic:
D. Heart Failure
Theme:
11. Acute Heart Failure
Subtheme:
11.4 Acute Heart Failure– Treatment
Session Type:
Cartazes
FP Number:
---
Authors:
Mauro Moreira; José Luís Ferraro; Ana Rodrigo Costa; Inês Gomes Campos; Rafaela G. Lopes; Joel Ponte Monteiro; Adriana Pereira; Aurora Andrade
Abstract
<p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="font-size:12.0pt">Introduction: </span></strong>Heart failure (HF) is a prevalent condition associated with poor short- and long-term prognosis. Iron deficiency is linked to a particularly vulnerable and less understood subset of patients, who often benefit from specific, cyclic ferric supplementation.</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="font-size:12.0pt">Methods: </span></strong>This was a single-centre, retrospective study of patients with acute heart failure (AHF) admitted consecutively to a tertiary centre. Patients with normal iron parameters—defined as TSAT > 20% and Ferritin > 100—were excluded. Clinical history, symptoms, biomarkers, electrocardiogram (ECG), and echocardiogram findings were analyzed. A composite endpoint (CE) was defined to include unplanned hospital visits, diuretic up-titration, hospital admission, and all-cause mortality. Backward Wald logistic regression (BWLR) was used to identify independent predictors of the composite endpoint. Follow-up was conducted for up to 22 months.</span></span></p> <p><span style="font-size:12pt"><span style="font-family:"Times New Roman",serif"><strong><span style="font-family:"Calibri",sans-serif">Results</span></strong><span style="font-family:"Calibri",sans-serif">: </span><span style="font-size:11.0pt"><span style="font-family:"Calibri",sans-serif">A total of 199 patients were included (mean age: 70.45 ± 11.8 years). Of these, 93 patients (46.7%) reached the composite endpoint, including 15 deaths (7.5%). </span></span></span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">BWLR identified the following as independent predictors of the composite endpoint: Previous coronary artery disease, Acute decompensation of chronic HF, Discharge with all four pillars of HF therapy, Transferrin and Vitamin B12. The regression model demonstrated excellent predictive ability for the composite endpoint (AUC = 0.815; 95% CI: 0.747–0.882; P < 0.001). </span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">Vitamin B12 showed a direct association with the composite endpoint (mean B12 levels: 344.8 ± 239.6 vs 475.2 ± 397.8; P = 0.007; BWLR 11th iteration: P = 0.028, OR = 1.001). In contrast, ferritin and TSAT were not significantly associated with the composite endpoint or any of its individual components.</span></span></p> <p><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif"><strong><span style="font-size:12.0pt">Conclusion</span></strong><span style="font-size:12.0pt">: </span>Patients with ferropenic HF exhibited a notably high rate of adverse events during long-term follow-up. In this subgroup, additional iron-related variables did not predict long-term outcomes, underscoring the need for improved prognostication methods. Interestingly, Vitamin B12 was an independent direct prediction of poor outcomes, a finding that contrasts with its behavior in non-ferropenic patients. </span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">The paradox we observed—high B12 associating with poor outcomes—could reflect i</span></span><span style="font-size:11pt"><span style="font-family:Calibri,sans-serif">nflammatory states by which chronic inflammation alters B12 metabolism and iron utilization (functional iron deficiency); liver dysfunction, leading to elevated B12 levels in patients with hepatic congestion or dysfunction, often seen in HF. Ultimately, it may be a compensatory mechanism - elevated B12 may signify a maladaptive response to increased cellular turnover or stress.</span></span></p>
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