Patients with paroxysmal atrial fibrillation had significantly higher baseline hs-CRP levels compared to healthy controls (0.145 mg/dL vs 0.035 mg/dL), which remained elevated 2 weeks after cardioversion.
Case-Control (n=26)
No
Are inflammatory biomarkers (hs-CRP, IL-6, TNF-alpha) elevated in patients with paroxysmal atrial fibrillation compared to healthy controls, and do they normalize after pharmacological cardioversion?
Inflammatory markers remain elevated for at least 2 weeks after cardioversion of paroxysmal AF, suggesting inflammation may be a causative factor rather than merely a consequence of the arrhythmia.
Absolute Event Rate: 0.145% vs 0.035%
p-value: p=<0.05
To clarify whether inflammation is a cause or consequence of atrial fibrillation (AF), we measured high-sensitivity C-reactive protein (hs-CRP), interleukin-6 (IL-6), and tumor necrosis factor alpha (TNF-alpha) before and after pharmacological cardioversion in 15 patients with paroxysmal AF. Levels of hs-CRP, IL-6, and TNF-alpha after cardioversion were significantly higher than those in controls (P < 0.05). Furthermore, the levels of these indices did not differ significantly even at 24 hours and 2 weeks after cardioversion. These results suggest that inflammation is a causative agent of paroxymal AF.
Sata et al. (2004) conducted a case-control in Paroxysmal atrial fibrillation (n=26). Paroxysmal atrial fibrillation vs. Healthy controls with normal sinus rhythm was evaluated on Baseline high-sensitivity C-reactive protein (hs-CRP) levels (p=<0.05). Patients with paroxysmal atrial fibrillation had significantly higher baseline hs-CRP levels compared to healthy controls (0.145 mg/dL vs 0.035 mg/dL), which remained elevated 2 weeks after cardioversion.