Abstract
Introduction: Recurrent atrial fibrillation (RAF) following ablation therapy occurs in about 50% of patients. The pathogenesis of RAF is unknown, but is believed to be driven by atrial remodeling in the setting of background inflammation. Structural, electrophysiological and mechanical remodeling has been associated with atrial fibrillation (AF). Inflammation and fibrotic remodeling are the major factors perpetuating AF, as mediators released from the atrial tissues and cardiomyocytes due to mechanical and surgical injury could initiate the inflammatory process. In this article, we have critically reviewed the key mediators that may serve as potential biomarkers to predict RAF. Areas covered: Damage associated molecular patterns, heat shock proteins, inflammatory cytokines, non-inflammatory markers, markers of inflammatory cell activity, and markers of collagen deposition and metabolism are evaluated as potential biomarkers with molecular treatment options in RAF. Expert commentary: Establishing biomarkers to predict RAF could be useful in reducing morbidity and mortality. Investigations into the role of DAMPs participating in a sterile immune response may provide greater insight into the pathogenesis of RAF. Markers evaluating immune cell activity, collagen deposition, and levels of heat shock proteins show the greatest promise as potential biomarkers to predict RAF and develop novel therapies.
| Original language | English (US) |
|---|---|
| Pages (from-to) | 193-207 |
| Number of pages | 15 |
| Journal | Expert Review of Cardiovascular Therapy |
| Volume | 17 |
| Issue number | 3 |
| DOIs | |
| State | Published - Mar 4 2019 |
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All Science Journal Classification (ASJC) codes
- Internal Medicine
- Cardiology and Cardiovascular Medicine
Cite this
Immunopathogenesis and biomarkers of recurrent atrial fibrillation following ablation therapy in patients with preexisting atrial fibrillation. / Rosenberg, John H.; Werner, John H.; Plitt, Gilman D.; Noble, Victoria V.; Spring, Jordan T.; Stephens, Brooke A.; Siddique, Aleem; Merritt-Genore, Helenmari L.; Moulton, Michael J.; Agrawal, Devendra K.
In: Expert Review of Cardiovascular Therapy, Vol. 17, No. 3, 04.03.2019, p. 193-207.Research output: Contribution to journal › Review article
}
TY - JOUR
T1 - Immunopathogenesis and biomarkers of recurrent atrial fibrillation following ablation therapy in patients with preexisting atrial fibrillation
AU - Rosenberg, John H.
AU - Werner, John H.
AU - Plitt, Gilman D.
AU - Noble, Victoria V.
AU - Spring, Jordan T.
AU - Stephens, Brooke A.
AU - Siddique, Aleem
AU - Merritt-Genore, Helenmari L.
AU - Moulton, Michael J.
AU - Agrawal, Devendra K.
PY - 2019/3/4
Y1 - 2019/3/4
N2 - Introduction: Recurrent atrial fibrillation (RAF) following ablation therapy occurs in about 50% of patients. The pathogenesis of RAF is unknown, but is believed to be driven by atrial remodeling in the setting of background inflammation. Structural, electrophysiological and mechanical remodeling has been associated with atrial fibrillation (AF). Inflammation and fibrotic remodeling are the major factors perpetuating AF, as mediators released from the atrial tissues and cardiomyocytes due to mechanical and surgical injury could initiate the inflammatory process. In this article, we have critically reviewed the key mediators that may serve as potential biomarkers to predict RAF. Areas covered: Damage associated molecular patterns, heat shock proteins, inflammatory cytokines, non-inflammatory markers, markers of inflammatory cell activity, and markers of collagen deposition and metabolism are evaluated as potential biomarkers with molecular treatment options in RAF. Expert commentary: Establishing biomarkers to predict RAF could be useful in reducing morbidity and mortality. Investigations into the role of DAMPs participating in a sterile immune response may provide greater insight into the pathogenesis of RAF. Markers evaluating immune cell activity, collagen deposition, and levels of heat shock proteins show the greatest promise as potential biomarkers to predict RAF and develop novel therapies.
AB - Introduction: Recurrent atrial fibrillation (RAF) following ablation therapy occurs in about 50% of patients. The pathogenesis of RAF is unknown, but is believed to be driven by atrial remodeling in the setting of background inflammation. Structural, electrophysiological and mechanical remodeling has been associated with atrial fibrillation (AF). Inflammation and fibrotic remodeling are the major factors perpetuating AF, as mediators released from the atrial tissues and cardiomyocytes due to mechanical and surgical injury could initiate the inflammatory process. In this article, we have critically reviewed the key mediators that may serve as potential biomarkers to predict RAF. Areas covered: Damage associated molecular patterns, heat shock proteins, inflammatory cytokines, non-inflammatory markers, markers of inflammatory cell activity, and markers of collagen deposition and metabolism are evaluated as potential biomarkers with molecular treatment options in RAF. Expert commentary: Establishing biomarkers to predict RAF could be useful in reducing morbidity and mortality. Investigations into the role of DAMPs participating in a sterile immune response may provide greater insight into the pathogenesis of RAF. Markers evaluating immune cell activity, collagen deposition, and levels of heat shock proteins show the greatest promise as potential biomarkers to predict RAF and develop novel therapies.
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UR - http://www.scopus.com/inward/citedby.url?scp=85061982544&partnerID=8YFLogxK
U2 - 10.1080/14779072.2019.1562902
DO - 10.1080/14779072.2019.1562902
M3 - Review article
C2 - 30580643
AN - SCOPUS:85061982544
VL - 17
SP - 193
EP - 207
JO - Expert Review of Cardiovascular Therapy
JF - Expert Review of Cardiovascular Therapy
SN - 1477-9072
IS - 3
ER -