Data from different observational trials have shown that treatment with statins significantly reduces the incidence of new-onset AF in the primary and secondary prevention .
The data are insufficient to recommend the use of statins before EC .
Finally , perioperative statin therapy may represent an important non-antiarrhythmic adjunctive therapeutic strategy for the prevention of postoperative AF
The aim of the present systematic review is to present an overview of the evidence linking atrial fibrillation ( AF ) , inflammation and oxidative stress , with emphasis on the potential of statins to decrease the incidence of different types of AF , including new-onset AF , after electrical cardioversion ( EC ) and after cardiac surgery .
Observational and clinical trials have studied the impact of statin therapy on new-onset , post-EC or postoperative AF .
Effects of pravastatin on ventricular
remodeling by activation of myocardial
KATP channels in infarcted rats: role of
70-kDa S6 kinase
Abstract Reactive cardiomyocyte hypertrophy after myocardial infa rct ion is an important risk factor for arrhythmias . Myocardial ATP-sensitive potassium ( KATP ) channels have been implicated in attenuating cardiac hypertrophy by inhibition of 70-kDa S6 kinase . We investigated the effect of pravastatin on ventricular hypertrophy during remodeling after myocardial infa rct ion and whether the attenuated hypertrophic effect was via activation of myocardial KATP channels . Twenty-four hours after ligation of the anterior descending artery , male Wistar rats were r and omized to either vehicle , nicor and il ( an agonist of KATP channels ) , pravastatin , glibenclamide ( an antagonist of KATP channels ) , or a combination of nicor and il and glibenclamide or pravastatin and glibenclamide for 4 weeks . Infa rct size and mortality were similar among the infa rct ed groups . Cardiomyocyte sizes isolated by enzymatic dissociation after infa rct ion significantly increased at the border zone in vehicle-treated infa rct ed rats compared with sham-operated rats . Rats in the nicor and il- and pravastatin-treated groups significantly attenuated cardiomyocyte hypertrophy , as compared with the vehicle-treated group . Arrhythmic scores during programmed stimulation mirrored those of cardiomyocyte hypertrophy . Increased 70-kDa S6 kinase mRNA expression in cardiac remodeling was confirmed by reverse transcription-polymerase chain reaction , consistent with the results of immunohistochemistry and Western blot for the phosphorylation of 70-kDa S6 kinase .  Nicor and il-induced effects were abolished by administering glibenclamide . Similarly , the beneficial effects of pravastatin were abolished by administering glibenclamide , implicating KATP channels as the relevant target . Activation of KATP channels by pravastatin administration can attenuate ventricular remodeling through a S6 kinase-dependent pathway after infa rct ion
Data from different observational trials have shown that treatment with statins significantly reduces the incidence of new-onset AF in the primary and secondary prevention .
The data are insufficient to recommend the use of statins before EC .
Finally , perioperative statin therapy may represent an important non-antiarrhythmic adjunctive therapeutic strategy for the prevention of postoperative AF
The aim of the present systematic review is to present an overview of the evidence linking atrial fibrillation ( AF ) , inflammation and oxidative stress , with emphasis on the potential of statins to decrease the incidence of different types of AF , including new-onset AF , after electrical cardioversion ( EC ) and after cardiac surgery .
Observational and clinical trials have studied the impact of statin therapy on new-onset , post-EC or postoperative AF .