Previous studies have shown that younger age, smaller left atrial size, and shorter duration of AF are predictors of sinus rhythm maintenance.4
However, no biochemical marker has been shown to correlate with AF recurrence and many of the recurrences are thought to be secondary to electrical remodelling.9,10
The results of this study indicate that increased CRP concentrations are associated with higher rates of AF recurrence after cardioversion in patients with persistent AF taking antiarrhythmic drugs.
Atrial remodelling may result from several factors. These include chronic haemodynamic factors, such as hypertension and valvar heart disease, electrophysiological factors, and inflammation. Inflammation has been shown to play a part in postoperative AF. Bruins et al11
reported that the time of peak incidence of postoperative atrial arrhythmias correlates with a peak in CRP and CRP–complement complexes. In non-postoperative AF, histological studies have shown inflammatory changes and increased fibrosis in the atrial biopsies of patients with lone AF.6
In addition, Chung et al7
found that CRP concentrations are higher in patients with AF than in healthy controls. These authors also found that CRP concentrations were higher in patients with persistent AF than in those who have paroxysmal AF, suggesting that inflammation may promote the persistence of AF.7
Recently studies have shown that the use of anti-inflammatory agents is associated with a decreased incidence of AF. In a recent study by Cheruku et al
the use of the non-steroidal anti-inflammatory drug ketolorac significantly reduced AF after coronary artery bypass grafting. This was attributed to a decrease in inflammation caused by the non-steroidal anti-inflammatory drug.12
Statins, which have been shown to decrease inflammation,13
also decreased the incidence of AF in recent studies in both animal models and humans.14–17
In addition, recent studies have shown that angiotensin converting enzyme inhibitors may decrease the incidence of AF in patients with reduced left ventricular ejection fraction.18
Furthermore, angiotensin converting enzyme inhibitors have recently been shown in to decrease inflammation.19–22
Madrid et al23
reported that adding the angiotensin receptor blocker irbesartan to amiodarone enhanced the probability of remaining in non-sinus rhythm after cardioversion of patients with persistent AF. This effect was attributed to the possible beneficial effects of blockade of the angiotensin receptor on apoptosis, fibrosis, and electrical remodelling.24–26
These results suggest that inflammation may have a causal role in the pathogenesis of AF.
This was an observational study of consecutive patients taking antiarrhythmic drugs who underwent successful cardioversion. The period over which data were collected was arbitrarily selected. As there were no good prior data, sample size could not be estimated. However, CRP is a marker of inflammation and there is evidence to suggest that inflammation may have a causal role in some forms of AF. However, because this was an observational study, determining causation was problematic.
In our dataset, duration of AF was not strongly related to AF recurrence or to CRP concentration. However, it is important to note that duration of AF in this study refers to how long the patient had been in AF at the time of the cardioversion and not to the duration since AF was first detected. We did not have reliable data on when AF was first diagnosed and so could not take this into account with our analysis.
Lastly, as with all observational studies, confounding caused by factors that were not accounted for is possible. We did restrict our study sample to patients taking antiarrhythmic drugs; although this was not a bias, it may affect the generalisability of the study results.
This study shows that CRP concentrations independently predict recurrence of persistent AF after cardioversion. As was the case in previous studies, from our results we cannot conclude that CRP has a causal role or that AF has an inflammatory basis.7
Nevertheless, among this patient population we saw significantly higher CRP concentrations in the recurrence group than in the non-recurrence group. Inflammation may be more pathogenetic in promoting persistence of AF as Chung et al7
Increased CRP concentration may be a marker of more extensive atrial remodelling that may lead to lower effectiveness of antiarrhythmic drugs. Whether treatments that reduce inflammation and CRP are useful in treating patients with AF warrants further study.