Archief Roodbont

Statins and Atrial Fibrillation

Statins -- in addition to their lipid lowering effects -- may reduce inflammation and oxidative stress. Inflammation (documented by higher levels of C-reactive protein) appears to be involved in the early phase of electrical remodeling (even within 24 hours after AF initiation) and promotes persistence of AF. While inflammation may be a pathogenetic component of AF, the clinical role for antiinflammatory drugs still remains unclear.^[4,5]

In clinical studies, new-onset AF was reduced by statin medication in patients with coronary heart disease or reduced left ventricular function. Sparse data, though, exist on secondary prevention of AF by statin medication. A single study documented lower AF recurrences under statins after cardioversion of lone AF patients,^[8] but no study on secondary prevention in patients with structural heart disease is available. The study by Al Chekakie et al.^[7] and another study by Richter et al.^[9] failed to show any effect of statins in the recurrence rates after catheter ablation of mostly long-lasting AF. This "negative" result does not rule out that statins might prevent AF in a very early stage of the disease where electrical remodeling can be manipulated by inhibiting inflammation and oxidative stress.

C-reactive protein (CRP) has been found to be elevated early after initiation of AF and chronic CRP levels have been indicated to be higher in patients with AF and decrease after conversion to sinus rhythm.^[5,6] CRP was not evaluated in the study by Al Chekakie et al.,^[7] but in the study by Richter et al.^[9] no difference in preablation CRP was found in patients already under statin therapy. In both studies, CRP was not used as prospective selection criterion for postinterventional statin medication. Experimental studies, however, support the hypothesis that CRP levels might identify a subgroup of patients who would benefit from adding antioxidative medication after ablation of AF.