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Abstract
Background Immune disorders are key heart failure (HF) triggers, but little is known about whether the status of immunity affects the incidence of HF. To explore this, we used blood cell counts and derived ratios to investigate the association between immunity status markers and HF incidence.
Methods The number and proportion of peripheral blood leucocytes in a physiological state are related to the body’s immune status. Neutrophils, monocytes, SII (systemic immune-inflammatory index), NLR (neutrophil-to-lymphocyte ratio), and PLR (platelet-to-lymphocyte ratio) serve as innate immunity status markers, while lymphocytes and LMR (lymphocyte-to-monocyte ratio) serve as specific immunity status markers. 330 362 UK Biobank (UKB) participants were finally examined. Cox proportional hazard models were used to explore the relationship between immunity status markers and HF incidence. Flexible parametric survival models were used to capture time-varying relationships between blood cell ratios and HRs for HF. Subgroup analyses were conducted by age, sex, and body mass index. Finally, sensitivity analyses were performed to validate the results.
Results During a median follow-up of 14.1 years, 9611 (2.9%) participants developed HF. Neutrophils, monocytes, SII, and NLR were positively associated with HF incidence, with fully adjusted per SD increment HR (95% CI) of 1.20 (1.17 to 1.22), 1.09 (1.07 to 1.12), 1.12 (1.10 to 1.14), and 1.16 (1.14 to 1.18), respectively. Platelets, lymphocytes, and LMR were inversely correlated with HF incidence, with fully adjusted per SD increment HR (95% CI) of 0.97 (0.95 to 1.00), 0.97 (0.95 to 0.99), and 0.90 (0.88 to 0.92), respectively.
Conclusions The innate immunity status markers were positively associated with HF incidence, while specific immunity status markers exhibited an inverse association, offering novel insights for HF prediction and intervention.
- Heart Failure
- Cardiovascular Diseases
- Risk Assessment
Data availability statement
Data are available upon reasonable request. The data that support the findings of this study are available from the UK Biobank project site, subject to registration and application process. Further details can be found at https://www.ukbiobank.ac.uk.
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Data availability statement
Data are available upon reasonable request. The data that support the findings of this study are available from the UK Biobank project site, subject to registration and application process. Further details can be found at https://www.ukbiobank.ac.uk.
Footnotes
JW and ZZ are joint first authors.
JW and ZZ contributed equally.
Contributors FX, NW and YL concepted this paper. JW and ZZ wrote the manuscript, researched data and carried out statistical analysis. YS and BY helped make statistical analysis. JY and YW contributed to data acquisition. All authors approved the final manuscript. FX is the guarantor.
Funding This work was supported by grants from the National Natural Science Foundation of China (82070835 and 82470901).
Competing interests None declared.
Patient and public involvement Patients and/or the public were not involved in the design, or conduct, or reporting, or dissemination plans of this research.
Provenance and peer review Not commissioned; externally peer reviewed.
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