Table 2 |.
Clinical studies showing a correlation between mechanism-b ased markers and AF
| Markera | Material | Correlation with AF | Refs |
|---|---|---|---|
| Proteostasis or protein quality control | |||
| HSPB1 (HSP27) | Atrial tissue | Levels inversely correlated with duration of AF and extent of structural damage (myolysis) | 83 |
| Blood | Concentration predicts AF recurrence after PVI ablation | 131 | |
| Concentration correlates with LAD, LAV and fractionated intervals | 328 | ||
| HSPB7 | Blood | Concentration does not correlate with PAF, PeAF or AF recurrence after PVI ablation | 131 |
| HSPA1A (HSP70) | Atrial tissue | Low levels correlate with high incidence of POAF | 329,330 |
| Blood | Concentration does not correlate with PAF, PeAF or AF recurrence after ablation | 131 | |
| No correlation with incidence of POAF | 329 | ||
| HSPD1/E1 (HSP60/10) | Atrial tissue | Reduced levels in AF with spontaneous SR restoration | 331 |
| Increased in PeAF versus SR | 332 | ||
| No correlation AF | 131,333 | ||
| Blood | Levels of anti-H SPD1 antibodies correlate with POAF | 334 | |
| Levels do not correlate with PAF, PeAF or AF recurrence after ablation | 131 | ||
| Autophagy or mitophagy | |||
| mtDNA (ND1, COX3) | Blood | Increase in PAF in men Increase in AF recurrence after PVI ablation and EC |
123 |
| Increase in POAF | 335 | ||
| DNA damage | |||
| mtDNA (ND1, COX3) | Blood | Increase in PAF in men Increase in AF recurrence after PVI ablation and EC |
123 |
| 8-OHdG | Atrial tissue | Increase in AF vs SR | 130 |
| Blood | Gradual increase in PAF, PeAF, LSPeAF Increase in AF recurrence after PVI ablation Increase in POAF |
130 | |
| Cytoskeletal proteins | |||
| cTnT, hsTnT | Atrial tissue | Gradual decrease in PAF and PeAF vs SR | 84 |
| Blood | Increase correlates with AF onset, recurrence, POAF | 336 | |
| Increase correlates with systemic embolic events in AF | 135 | ||
| cTnI | Atrial tissue | Gradual decrease in PAF and PeAF vs SR | 84 |
| Blood | Increase correlates with AF onset, recurrence, POAF | 336 | |
| cTnC | Atrial tissue | Gradual decrease in PAF and PeAF vs SR | 84 |
| Inflammation | |||
| CRP | Blood | Gradual increase in PAF, PeAF | 132,337 |
| Association with new-o nset AF in CAD | 133 | ||
| Increase correlated with successful EC | 132 | ||
| IL-2 | Blood | Increase in AF recurrence after PVI ablation | 338 |
| IL-6 | Blood | Gradual increase in PAF, PeAF | 339 |
| Correlation with AF and new- onset AF in CKD | 134 | ||
| Correlation with POAF | 340 | ||
| IL-17A | Blood | Increased risk for AF | 341 |
| IL-18 | Blood | Gradual increase in PAF, PeAF | 342 |
| TNF | Blood | Increase in AF versus SR | 337,343 |
| MPO | Blood | Increase in AF versus SR, especially left atrial blood | 344 |
| Levels correlate with AF recurrence after PVI ablation | 345 | ||
8-OHdG, 8-hydroxy-2’-d eoxyguanosine; AF, atrial fibrillation; CAD, coronary artery disease; CKD, chronic kidney disease; CRP, C-r eactive protein; cTnC, cardiac troponin C; cTnI, cardiac troponin I; cTnT, cardiac troponin T; EC, electrical cardioversion; HSP, heat shock protein; hsTnT, high-s ensitivity troponin T; LAD, left atrial diameter; LAV, left atrial voltage; LSPeAF, long-standing persistent atrial fibrillation; MPO, myeloperoxidase; mtDNA, mitochondrial DNA; PAF, paroxysmal AF; PeAF, persistent AF; POAF, post-o perative AF; PVI, pulmonary vein isolation; SR, sinus rhythm; TNF, tumour necrosis factor.
Table provides a selection of biomarkers related to derailed proteasome and protein quality control pathways, degradation of the cytoskeletal proteins, and induction of inflammation, all of which are mechanisms found to drive AF.