Beyond Ejection Fraction: Inflammatory Risk and Mortality in Heart Failure.
- 1Department of Emergency Medicine, Medical University of Sofia, 1527 Sofia, Bulgaria.
- 2Clinic of Cardiology, University Hospital "Tsaritsa Yoanna-ISUL", 8 Byalo More Str., 1527 Sofia, Bulgaria.
Abstract
Background: Inflammation is increasingly recognized as an important contributor to the progression of heart failure and may partly explain differences in prognosis beyond conventional clinical characteristics. Simple laboratory-based inflammatory indices may offer additional prognostic information, but their value across different heart failure phenotypes remains uncertain. Objectives: To investigate the association between the systemic immune-inflammation index and recorded all-cause mortality across the spectrum of heart failure and to evaluate its incremental prognostic value beyond conventional clinical and laboratory variables. Patients and Methods: We evaluated the association between the systemic immune-inflammation index (SII) and recorded all-cause mortality in patients with heart failure. Multivariable logistic regression models included age, sex, heart failure phenotype, cardiovascular comorbidities, NT-proBNP, renal function, and hemoglobin. Model discrimination and calibration were assessed, and additional analyses evaluated multicollinearity, interaction with heart failure phenotype, and the functional form of the association. Results: Among 637 patients, mortality status was available for 634, of whom 165 died (26.0%). After multivariable adjustment, each doubling of SII was associated with higher odds of recorded all-cause mortality (OR 1.42, 95% CI 1.19-1.70; p < 0.001). Previous myocardial infarction, atrial fibrillation, and NT-proBNP also remained independently associated with mortality, whereas LVEF phenotype was not. No significant interaction was observed between SII and heart failure phenotype. Adding SII improved overall model fit (likelihood-ratio χ² = 16.17; p < 0.001) and increased the AUC from 0.710 to 0.732, although the difference in discrimination was not statistically significant (DeLong p = 0.076). There was no convincing evidence of marked non-linearity. Conclusions: A higher systemic inflammatory burden was independently associated with recorded all-cause mortality across the heart failure spectrum. This readily available marker may provide complementary prognostic information, but its incremental value appears modest. External validation is needed before it can be considered for routine risk assessment.
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BibTeX
@article{krastev2026beyond,
title = {{Beyond Ejection Fraction: Inflammatory Risk and Mortality in Heart Failure.}},
author = {Bozhidar Krastev and Natalia Spasova and Desislava Somleva and Neli Georgieva and Slavi Yakov and Elena Kinova and Assen Goudev},
journal = {Clinics and practice},
year = {2026},
month = sep,
doi = {10.3390/clinpract16100175},
url = {https://europepmc.org/article/MED/42930361},
note = {CC BY},
}
RIS
TY - JOUR
TI - Beyond Ejection Fraction: Inflammatory Risk and Mortality in Heart Failure.
AU - Bozhidar Krastev
AU - Natalia Spasova
AU - Desislava Somleva
AU - Neli Georgieva
AU - Slavi Yakov
AU - Elena Kinova
AU - Assen Goudev
PY - 2026
DA - 2026/09/22
JO - Clinics and practice
DO - 10.3390/clinpract16100175
UR - https://europepmc.org/article/MED/42930361
AB - Background: Inflammation is increasingly recognized as an important contributor to the progression of heart failure and may partly explain differences in prognosis beyond conventional clinical characteristics. Simple laboratory-based inflammatory indices may offer additional prognostic information, but their value across different heart failure phenotypes remains uncertain. Objectives: To investigate the association between the systemic immune-inflammation index and recorded all-cause mortality across the spectrum of heart failure and to evaluate its incremental prognostic value beyond conventional clinical and laboratory variables. Patients and Methods: We evaluated the association between the systemic immune-inflammation index (SII) and recorded all-cause mortality in patients with heart failure. Multivariable logistic regression models included age, sex, heart failure phenotype, cardiovascular comorbidities, NT-proBNP, renal function, and hemoglobin. Model discrimination and calibration were assessed, and additional analyses evaluated multicollinearity, interaction with heart failure phenotype, and the functional form of the association. Results: Among 637 patients, mortality status was available for 634, of whom 165 died (26.0%). After multivariable adjustment, each doubling of SII was associated with higher odds of recorded all-cause mortality (OR 1.42, 95% CI 1.19-1.70; p < 0.001). Previous myocardial infarction, atrial fibrillation, and NT-proBNP also remained independently associated with mortality, whereas LVEF phenotype was not. No significant interaction was observed between SII and heart failure phenotype. Adding SII improved overall model fit (likelihood-ratio χ² = 16.17; p < 0.001) and increased the AUC from 0.710 to 0.732, although the difference in discrimination was not statistically significant (DeLong p = 0.076). There was no convincing evidence of marked non-linearity. Conclusions: A higher systemic inflammatory burden was independently associated with recorded all-cause mortality across the heart failure spectrum. This readily available marker may provide complementary prognostic information, but its incremental value appears modest. External validation is needed before it can be considered for routine risk assessment.
SN - 2039-7275
SN - 2039-7283
ER -