Poster

Immunoglobulin Free Light Chain-κ in association with N-terminal Pro Brain Natriuretic Peptide Levels after Smoking Cessation

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Published online:

Correspondence: Maki Komiyama, nikonikomakirin@yahoo.co.jp

Copyright:

© The Author(s). This work is open access and is licensed under CC-BY-NC 4.0. Users may copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

Objectives: Smoking induces inflammation in the heart and intima layer of blood vessels by activating nuclear factor kappa B, which controls the transcription of immunoglobulin free light chain (FLC)-κ. FLC levels are indicative of higher mortality in the overall population and poorer prognoses in cardiovascular diseases. This study aimed to analyse the effect of smoking cessation (SC) on the levels of FLCs and markers of inflammation and heart failure.

Materials and methods: This study enrolled first visit smokers determined to quit smoking at our hospital. Levels of various clinical parameters, including inflammatory markers, such as FLC, were measured on their first clinic visit and after 3 months of successful SC.

Results: Out of 96 patients who participated in this study, 76 patients (55 males and 21 females) succeeded in SC over a period of 3 months. Body mass index (BMI) values significantly increased from baseline to 3 months after SC (n = 76, p = 0.004).

Conversely, the levels of inflammatory markers including FLC-κ, neutrophil-to-lymphocyte-ratio and N-terminal pro brain natriuretic peptide (NT-proBNP) significantly decreased after SC (p=0.042, p=0.024 and p=0.030, respectively).

Proportional changes in FLC-κ levels observed after SC showed a significant correlation with those of C-reactive-protein (r = 0.349, p = 0.002) and NT-proBNP (r =0.332, p = 0.005) levels in the successful SC group.

Conclusion: Levels of FLC-κ, a novel inflammatory and cardiovascular risk biomarker, decreased significantly after SC in association with NT-proBNP, suggesting the SC-induced reduction of cardiac load as well as a decrease in inflammation.