Association between Inflammation and New-Onset Atrial Fibrillation in Acute Coronary Syndromes
Abstract
:1. Introduction
2. Inflammation in the Pathogenesis of ACS
2.1. Adaptive Immunity
2.2. Innate Immunity
3. Atrial Remodeling
3.1. Structural Remodeling
3.2. Electrical Remodeling
4. Inflammatory Biomarkers
4.1. Interleukin-1 (IL-1)
4.2. Interleukin-6 (IL-6)
4.3. Interleukin-8 (IL-8)
4.4. Interleukin-11 (IL-11)
4.5. Interleukin-17A (IL-17A)
4.6. C Reactive Protein (CRP)
4.7. Tumor Necrosis Factor Alpha (TNF-α)
4.8. Galectin-3 (Gal-3)
4.9. Thrombospondin-1 (TSP-1)
4.10. B-Type Natriuretic Peptide (BNP)
5. Echocardiographic Assessment and Predictive Risk Factors for NOAF
6. Gaps in Evidence and Future Perspectives
7. Conclusions and Main Key Findings
Author Contributions
Funding
Conflicts of Interest
References
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Interleukins | Role in Pathogenesis of AF |
---|---|
Interleukin-1 Interleukin-6 Interleukin-11 | Induces atrial remodeling Pressure-overload-induced sustained AF Induces atrial remodeling Atrial myocardium inflammatory status Shortening of atrial refractory period |
Interleukin 17A | Stimulates cardiac fibroblast proliferation and promotes the occurrence of AF |
Age, left atrial diameter, right atrial diameter, and heart failure are independent risk factors of developing NOAF in ACS patients |
LASr is an independent predictive factor of NOAF in STEMI patients |
Patients with high levels of CRP, TNF-α, and complement levels had a significantly higher risk of AF |
IL-6 contributes to atrial remodeling and induces a pro-thrombotic state by increasing platelet production and coagulation factors, predisposing to AF |
The activation of the IL-1β pathway, different from the NLRP3 inflammasome, could help to assess the appearance of NOAF in patients with ACS |
Angiotensin II and reactive oxygen species (ROS) contribute to abnormal Ca2+ handling and the remodeling promotion of atrial tissue |
In patients with AMI, elevated levels of galectin-3 are associated with a 4.4 times higher risk of developing atrial fibrillation |
BNP independently predicts the occurrence of NOAF in STEMI patients treated by primary PCI |
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Băghină, R.-M.; Crișan, S.; Luca, S.; Pătru, O.; Lazăr, M.-A.; Văcărescu, C.; Negru, A.G.; Luca, C.-T.; Gaiță, D. Association between Inflammation and New-Onset Atrial Fibrillation in Acute Coronary Syndromes. J. Clin. Med. 2024, 13, 5088. https://doi.org/10.3390/jcm13175088
Băghină R-M, Crișan S, Luca S, Pătru O, Lazăr M-A, Văcărescu C, Negru AG, Luca C-T, Gaiță D. Association between Inflammation and New-Onset Atrial Fibrillation in Acute Coronary Syndromes. Journal of Clinical Medicine. 2024; 13(17):5088. https://doi.org/10.3390/jcm13175088
Chicago/Turabian StyleBăghină, Ruxandra-Maria, Simina Crișan, Silvia Luca, Oana Pătru, Mihai-Andrei Lazăr, Cristina Văcărescu, Alina Gabriela Negru, Constantin-Tudor Luca, and Dan Gaiță. 2024. "Association between Inflammation and New-Onset Atrial Fibrillation in Acute Coronary Syndromes" Journal of Clinical Medicine 13, no. 17: 5088. https://doi.org/10.3390/jcm13175088