Atorvastatin for prevention of atrial fibrillation recurrence following pulmonary vein isolation: a double-blind, placebo-controlled, randomized trial. Effect of statin dose on incidence of atrial fibrillation: data from the Pravastatin or Atorvastatin Evaluation and Infection Therapy-Thrombolysis in Myocardial Infarction 22 (PROVE IT-TIMI 22) and Aggrastat to Zocor (A to Z) trials. Atorvastatin prevents atrial fibrillation in patients with bradyarrhythmias and implantation of an atrial-based or dual-chamber pacemaker: a prospective randomized trial. Usefulness of statin drugs in protecting against atrial fibrillation in patients with coronary artery disease. Atorvastatin Given prior to Electrical Cardioversion Does Not Affect the Recurrence of Atrial Fibrillation in Patients with Persistent Atrial Fibrillation Who Are on Antiarrhythmic Therapy High-dose atorvastatin and risk of atrial fibrillation in patients with prior stroke or transient ischemic attack: analysis of the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) trial. The effects of statins and renin-angiotensin system blockers on atrial fibrillation recurrence following antral pulmonary vein isolation. Statins improve surgical ablation outcomes for atrial fibrillation in patients undergoing concomitant cardiac surgery. Effects of rosuvastatin on atrial fibrillation occurrence: ancillary results of the GISSI-HF trial. High-sensitivity C-reactive protein, statin therapy, and risks of atrial fibrillation: an exploratory analysis of the JUPITER trial. Effect of lipid lowering on new-onset atrial fibrillation in patients with asymptomatic aortic stenosis: the Simvastatin and Ezetimibe in Aortic Stenosis (SEAS) study. Improved fibrinolysis after 1-year treatment with HMG CoA reductase inhibitors in patients with coronary heart disease. Efficacy and safety of prescription omega-3-acid ethyl esters for the prevention of recurrent symptomatic atrial fibrillation: a prospective study. Analysis of pravastatin to prevent recurrence of atrial fibrillation after electrical cardioversion. Risk of proarrhythmic events in the Atrial Fibrillation Follow-up Investigation of Rhythm Management (AFFIRM) study: a multivariate analysis. Antiarrhythmic drug therapy after radiofrequency catheter ablation in patients with atrial fibrillation. The effect of statin therapy on ventricular late potentials in acute myocardial infarction.
BACKGROUND It is known that statins are effective in preventing atrial fibrillation ( AF ) in patients undergoing cardiac surgery . OBJECTIVE The purpose of this study was to evaluate the efficacy of statins in preventing AF recurrence following left atrial ablation . METHODS One hundred twenty-five patients who had no statin indication undergoing catheter ablation due to drug-refractory paroxysmal ( n = 90 ) or persistent ( n = 35 ) AF were r and omized in a prospect i ve , double-blind , placebo-controlled trial to receive 80 mg atorvastatin ( n = 62 ) or placebo ( n = 63 ) for 3 months . The primary endpoint was freedom from symptomatic AF at 3 months . Secondary endpoints included freedom from any atrial arrhythmia recurrence irrespective of symptoms , quality of life ( QoL ) , and reduction in C-reactive protein ( CRP ) . RESULTS At 3 months , 95 % of patients in the atorvastatin group were free of symptomatic AF compared with 93.5 % in the placebo group ( P = .75 ) . Similarly , 85 % of patients treated in the atorvastatin group remained free of any recurrent atrial arrhythmia vs 88 % of patients in the placebo group ( P = .37 ) . Mean CRP levels decreased in the atorvastatin group ( mean change -0.75 ± 3 , P = .02 ) and increased in the placebo group ( mean change 2.1 ± 19.9 , P = .48 ) . Mean QoL score improved significantly in both groups ( mean change 13.14 ± 18.2 in the atorvastatin group and 11.10 ± 17.7 in the placebo group , P = .53 ) . CONCLUSION In patients with no st and ard indication for statin therapy  , treatment with atorvastatin 80 mg/day following AF ablation does not decrease the risk of AF recurrence in the first 3 months and should not be routinely administered to prevent periprocedural arrhythmias BACKGROUND Inflammation has been suggested as a factor in the initiation and maintenance of  atrial fibrillation ( AF ) . Several observational studies have suggested that statins , presumably through their anti-inflammatory properties , decrease the risk of AF . METHODS We analyzed 2 large , r and omized trials , PROVE IT-TIMI 22 and phase Z of the A to Z trial , which compared lower- versus higher-intensity statin therapy to evaluate whether higher-intensity statin therapy lowered the risk of AF onset during the 2 years of follow-up . We hypothesized that higher-intensity statin therapy would decrease the risk of AF when compared to lower-intensity statin therapy . From each trial , patients experiencing the onset of AF during follow-up were identified from the adverse event reports . RESULTS Neither study showed a decreased AF risk with higher-dose statin . In PROVE IT-TIMI 22 , 2.9 % versus 3.3 % in the high- versus st and ard-dose statin therapy , respectively , experienced the onset of AF over 2 years ( OR 0.86 , 95 % CI 0.61 - 1.23 , P = .41 ) . In A to Z , rates were 1.6 % versus 0.99 % , respectively ( OR 1.58 , 95 % CI 0.92 - 2.70 , P = .096 ) . In both trials , C-reactive protein levels ( plasma or serum ) tended to be higher among patients experiencing the onset of AF . CONCLUSION Our r and omized comparison among 8659 patients found that higher-dose statin therapy did not reduce the short term incidence of AF among patients after acute coronary syndromes when compared with st and ard dose statin treatment BACKGROUND Increasing evidence suggests that atrial fibrillation ( AF ) is an inflammatory disease . Statins is an anti-inflammatory agent . The present study was conducted to test the efficacy of atorvastatin in preventing paroxysmal AF or atrial high rate episodes ( AHEs ) in patients with bradyarrhythmias and implantation of an atrial-based or dual-chamber pacemaker . METHODS The effect of atorvastatin on time to the first attack of AF or AHE ( > or = 180 per minute and > or = 1 or 10 minutes ) , which was accurately detected by pacemaker interrogation , was evaluated in an open-label prospect i ve r and omized design for 1 year of follow-up . RESULTS Fifty-two patients ( 23 males , 70 + /- 13 years old ) were r and omized to the  statin group ( atorvastatin 20 mg/d ) and 54 ( 25 males , 72 + /- 13 years old ) to the  nonstatin group . Event-free survivals from AHE > or = 1 minute were not significantly different between the 2 groups ( log-rank P = .410 ) . However , patients in the nonstatin group were more likely to develop AHE > or = 10 minutes than those in the statin group ( log-rank P = .028 ) . Atrial high rate episode > or = 10 minutes occurred in 3 ( 5.8 % ) of 51 patients in the statin group after 1 year of follow-up , and 10 ( 19.2 % ) of 52 patients ( odds ratio 0.26 , P = .041 ) in the nonstatin group . The mean left atrial volume of the statin group was significantly lower than that of the nonstatin group at the end of follow-up ( 39.7 + /- 1.7 vs 43.7 + /- 1.9 mL , P < .0001 ) . CONCLUSIONS The present study demonstrated the efficacy of atorvastatin in preventing significant AF ( > or = 10 minutes ) and left atrial enlargement in patients with bradyarrhythmias and implantation of a pacemaker Atrial  fibrillation ( AF ) is prevalent in the elderly , in patients with hypertension , and in patients with coronary artery disease ( CAD ) . We hypothesized that statin therapy might be effective in preventing AF in patients with CAD and examined this hypothesis in a sample of patients with chronic stable CAD without AF , followed prospect ively at a large outpatient cardiology practice . The association between statin use and the risk of developing AF was examined univariately and then with adjustment for potential confounding factors . Four hundred forty-nine men and women between the ages of 40 and 87 years were followed for an average of 5 years . Fifty-two patients ( 12 % ) developed AF during follow-up . Statin therapy was used by 59 % of the patients during the study period and was associated with a significantly reduced risk of developing AF ( crude odds ratio , 0.48 , 95 % confidence interval 0.28 to 0.83 ) . This association remained significant after adjustment for potential confounders , including age , hypertension , left ventricular systolic function , occurrence of heart failure or acute ischemic events , and baseline cholesterol and changes in cholesterol levels ( adjusted odds ratio 0.37 , 95 % confidence interval 0.18 to 0.76 ) . Use of  statins in patients with chronic stable CAD appears to be protective against AF . The underlying mechanism for this effect is unknown but appears to be independent of the reduction in serum cholesterol levels Objective : In this study , our aim was to evaluate the effect of a higher dose of atorvastatin on the recurrence rate of atrial fibrillation ( AF ) after electrical cardioversion ( EC ) in addition to antiarrhythmic therapy . Subjects and Methods : 48 patients with persistent AF were included in this study . The patients were r and omized to an atorvastatin 40-mg treatment group and a control group . Atorvastatin was started 3 weeks before EC and was continued for 2 months after EC . EC was performed using biphasic shocks after 3 weeks of treatment with the orally administered anticoagulant warfarin .  Lipid and inflammatory parameters ( high-sensitivity C-reactive protein , white blood cell count and fibrinogen level ) were evaluated at the baseline and before EC . The endpoint of this study was electrocardiographically confirmed recurrence of AF of > 10 min . Results : There were no significant differences in baseline characteristics and lipid and inflammatory marker levels between the treatment and control groups . Total cholesterol and low-density lipoprotein levels were significantly decreased in patients taking atorvastatin for 2 months compared with baseline values ( 174 ± 31 vs. 129 ± 25 mg/dl , p = 0.001 , and 112 ± 23 vs. 62 ± 20 mg/dl , p = 0.001 , respectively ) , while no significant change occurred in control patients ( 168 ± 26 vs. 182 ± 29 mg/dl , p = 0.07 , and 99 ± 18 vs. 108 ± 26 mg/dl , p = 0.1 , respectively ) . At the end of the 2-month follow-up period , 9 patients ( 20.5 % ) experienced AF recurrence , and there was no significant difference in AF recurrence rate between the treatment and control groups ( 26 vs. 13 % ; p = 0.2 ) . Conclusion : Atorvastatin therapy prior to EC does not prevent the recurrence of arrhythmia in patients with persistent AF who are receiving antiarrhythmic therapy BACKGROUND Observational analyses and short-term r and omized trials have suggested that statins reduce occurrence or recurrence of atrial fibrillation ( AF ) . We tested the hypothesis that long-term treatment with high-dose atorvastatin reduces occurrence of AF in patients with prior stroke or transient ischemic attack . METHODS We examined development of new AF in the SPARCL trial that compared atorvastatin 80 mg daily with placebo in 4,731 patients with prior stroke or transient ischemic attack . Patients who had chronic or paroxysmal AF or were taking medications for treatment or prophylaxis of AF at the time of enrollment were excluded .  Atrial fibrillation was identified from electrocardiograms su bmi tted to a blinded central electrocardiographic laboratory and from investigators ' adverse event reports . RESULTS Patients were followed up for a median of 4.8 years , corresponding to > 20,000 patient-years of observation with a median of 5 electrocardiograms per patient . The primary efficacy measure , the time from r and omization to first occurrence of new AF , did not differ between treatment groups . By intention to treat , there were 139 cases of new AF in the atorvastatin group and 122 cases in the placebo group , corresponding to incidence rates of 1.32 and 1.14 cases per 100 patient-years observation ( hazard ratio 1.15 , 95 % CI 0.90 - 1.46 , P = .26 ) . On-treatment analysis yielded similar findings , with incidence rates of 1.26 and 1.01 cases per 100 patient-years observation in the atorvastatin and placebo groups , respectively ( hazard ratio 1.25 , 95 % CI 0.94 - 1.67 , P = .12 ) . CONCLUSION High-dose atorvastatin does not prevent development of AF in patients with prior stroke or transient ischemic attack INTRODUCTION Ablation has emerged as a major treatment option for atrial fibrillation ( AF ) . However , this procedure is limited by a significant rate of AF recurrence . We aim ed to examine the effects of statins , angiotensin-converting enzyme inhibitors ( ACE-I ) , and angiotensin receptor blockers ( ARB ) on the recurrence rate of AF following ablation . METHODS We conducted a retrospective study of 177 consecutive patients ( mean age = 56 + /- 11 yrs , 69 % males ) who underwent ablation for paroxysmal ( n = 132 ) or persistent AF ( n = 45 ) . Patients were treated with ACE-I ( n = 31 ) or ARB ( n = 18 ) or statins ( n = 50 ) prior to ablation and for the duration of follow-up . RESULTS After a mean follow-up of 13.8 + /- 8.6 months , 72 % of patients were free of AF . For patients taking statins , 33 of 50 ( 60 % ) were free of AF . In patients treated with ACE-I , 17 of 31 ( 55 % ) were free from AF , while in the group of patients treated with ARB , 17 of 18 ( 94 % ) were free from AF . Using Cox regression analysis to correct for baseline variables , treatment with statins did not decrease the recurrence rate ( HR = 1.10 [ 95 % CI : 0.55 - 2.27 ] p = 0.79 ) ; nor did treatment with renin angiotensin system ( RAS ) blockers ( HR 0.94 [ 95 % CI : 0.46 - 1.93 ] p = 0.87 ) . However , subgroup analysis showed that treatment with ARB was associated with a trend towards lower AF recurrence [ HR 0.17 , ( 95 % CI : 0.02 - 1.34 ) p = 0.09 ] . CONCLUSIONS Even though statins and RAS blockers possess anti-inflammatory properties , they did not decrease the recurrence of AF following ablation . However , the subset of patients taking ARB exhibited a trend towards lower AF recurrence . Larger , r and omized studies are needed to address this observation Ablation outcomes were investigated in patients with and without statin pretreatment before cardiac surgery with concomitant surgical ablation for atrial fibrillation ( AF ) . A prospect i ve cohort study was performed containing 149 patients ( n=73 statin group vs. n=76 control group ) undergoing on-pump cardiac procedures with surgical ablation for paroxysmal or persistent AF . Measured outcomes were freedom from AF in the intensive care unit , discharge and at three and six months follow-up and perioperative markers of inflammation ( white blood cell count , C-reactive protein ) . Independent predictors for freedom from AF were assessed . Groups did not differ with respect to EuroSCORE , New York Heart Association class , left atrial size , anti-arrhythmic drug therapy or aortic cross-clamp time . Statin therapy had no impact on postoperative inflammatory markers . Freedom from AF was more frequent in the statin group at discharge ( P=0.07 ) and after three and six months ( P<0.05 ) . Subgroup analysis showed that statin pretreatment was associated with higher rates of freedom from AF for paroxysmal AF at three and six months and for persistent AF after six months ( P<0.05 ) . Importantly , statin-pretreatment was independently predictive for freedom from AF at discharge [ odds ratio ( OR ) : 3.21 ; 95 % confidence interval ( CI ) : 1.2 - 8.55 ; P=0.02 ] and at three months ( OR : 2.91 ; 95 % CI : 1.14 - 7.45 ; P=0.026 ) . Statin therapy prior to ablation surgery improves postoperative freedom from AF for paroxysmal and persistent AF in cardiac surgery patients AIMS This ancillary analysis of the GISSI-HF data base aims at assessing the effect of rosuvastatin on the occurrence of  atrial fibrillation ( AF )  in patients with chronic heart failure ( HF ) who were not in AF at study entry . METHODS AND RESULTS GISSI-HF was a double-blind , placebo-controlled trial testing n-3 PUFA and rosuvastatin vs. corresponding placebos in patients with chronic HF .  Atrial fibrillation occurrence was defined as the presence of AF in the electrocardiogram ( ECG ) performed at each visit during the trial or AF as a cause of worsening HF or hospital admission or as an event during hospitalization . Among the 3690 patients ( 80.7 % ) without AF on their baseline ECG , 15.0 % developed AF during a median follow-up period of 3.7 years , 258 r and omized to rosuvastatin ( 13.9 % ) vs. 294 allocated to placebo ( 16.0 % ) . Although the difference was not significant at unadjusted analysis ( P = 0.097 ) and multivariable analysis adjusting for clinical variables ( P = 0.067 ) , it became significant after adjustment for clinical variables and laboratory examinations ( P = 0.039 ) , and for clinical variables , laboratory examinations , and background therapies ( P = 0.038 ) . CONCLUSION This study shows that there is some evidence of a beneficial effect of rosuvastatin in terms of reduction of AF occurrence in patients with HF . Larger population s are needed to provide a definite answer to the question . Clinical Trials.gov Identifier : NCT00336336 AIMS Increasing evidence supports a role for inflammation in promoting  atrial fibrillation ( AF ) and statins have anti-inflammatory effects that may be relevant for the prevention of AF . However , studies of statin therapy and incident AF have yielded mixed results and not focused on individuals with an underlying pro-inflammatory response . We studied whether high-sensitivity C-reactive protein is associated with incident AF and whether treatment with rosuvastatin is associated with a lower incidence of AF compared with placebo . METHODS AND RESULTS We r and omized men and women with LDL cholesterol < 130 mg/dL and high-sensitivity C-reactive protein ≥2 mg/L to receive either rosuvastatin 20 mg daily or placebo .  Atrial fibrillation was determined from treatment-blind adverse event reports . Among 17 120 participants without prior history of arrhythmia , each increasing tertile of baseline high-sensitivity C-reactive protein was associated with a 36 % increase in the risk of developing AF ( 95 % CI : 1.16 - 1.60 ; P-trend < 0.01 ) . Allocation to rosuvastatin when compared with placebo was associated with a 27 % reduction in the relative risk of developing AF during the trial period ; specifically , AF was reported among 138 participants in the placebo group and 100 in the rosuvastatin group ( incidence rate 0.78 vs. 0.56/100 person-years , HR : 0.73 , 95 % CI : 0.56 - 0.94 , P = 0.01 ) . The exclusion of participants who developed a major cardiovascular event prior to the report of AF yielded similar results . CONCLUSION Within the JUPITER trial cohort of individuals selected for underlying inflammation , increasing levels of high-sensitivity C-reactive protein were associated with an increased risk of incident AF and r and om allocation to rosuvastatin significantly reduced that risk BACKGROUND Lipid-lowering drugs , particularly statins , have anti-inflammatory and antioxidant properties that may prevent atrial fibrillation ( AF ) . This effect has not been investigated on new-onset AF in asymptomatic patients with aortic stenosis ( AS ) . METHODS Asymptomatic patients with mild-to-moderate AS ( n = 1,421 ) were r and omized ( 1:1 ) to double-blind  simvastatin 40 mg and ezetimibe 10 mg combination or placebo and followed up for a mean of 4.3 years . The primary end point was the time to new-onset AF adjudicated by 12-lead electrocardiogram  at a core laboratory reading center . Secondary outcomes were the correlates of new-onset AF with nonfatal nonhemorrhagic stroke and a combined end point of AS-related events . RESULTS During the course of the study , new-onset AF was detected in 85 ( 6 % ) patients ( 14.2/1,000 person-years of follow-up ) . At baseline , patients who developed AF were , compared with those remaining in sinus rhythm , older and had a higher left ventricular mass index a smaller aortic valve area index . Treatment with simvastatin and ezetimibe was not associated with less new-onset AF ( odds ratio 0.89 [ 95 % CI 0.57 - 1.97 ] , P = .717 ) . In contrast , age ( hazard ratio [ HR ] 1.07 [ 95 % CI 1.05 - 1.10 ] , P < .001 ) and left ventricular mass index ( HR 1.01 [ 95 % CI 1.01 - 1.02 ] , P < .001 ) were independent predictors of new-onset AF . The occurrence of new-onset AF was independently associated with 2-fold higher risk of AS-related outcomes ( HR 1.65 [ 95 % CI 1.02 - 2.66 ] , P = .04 ) and 4-fold higher risk of nonfatal nonhemorrhagic stroke ( HR 4.04 [ 95 % CI 1.18 - 13.82 ] , P = .03 ) . CONCLUSIONS Simvastatin and ezetimibe were not associated with less new-onset AF . Older age and greater left ventricular mass index were independent predictors of AF development . New-onset AF was associated with a worsening of prognosis The study was aim ed to investigate the effect of two different statins on the levels of haemostatic variables reflecting procoagulant and fibrinolytic activity in patients with coronary heart disease ( CHD ) , with the hypothesis that statins might beneficially modify these levels . Fifty-eight patients were r and omized to treatment with atorvastatin ( n=28 ) or simvastatin  ( n=30 ) for 1 year . The starting dose in both groups was 20 mg/day . Fasting blood sample s were collected before and after 12-month treatment for determinations of fibrinogen , prothrombin fragment 1 + 2 ( F1 + 2 ) , plasma D-dimer , soluble tissue factor , tissue plasminogen activator ( tPA ) antigen , tPA activity , plasminogen activator inhibitor type-1 activity ( PAI-1 activity ) and serum D-dimer as a global test of fibrinolytic activity . In the total population , improved fibrinolytic activity was observed after 1 year with increased levels of serum D-dimer ( P=.001 ) and tPA activity ( P=.024 ) and a reduction in tPA antigen ( P=.048 ) . No statistically significant changes were observed in any of the measured coagulation variables . Separately examined , an improved fibrinolytic profile was seen in the atorvastatin group with a significant increase in serum D-dimer ( P=.005 ) , a borderline increase in tPA activity ( P=.083 ) and a borderline reduction in tPA antigen ( P=.069 ) . Within the simvastatin group , a reduction in prothrombin F1 + 2 was observed ( P=.038 ) . The differences in changes between the groups were statistically significant only for global fibrinolysis ( serum D-dimer , P=.046 ) . In conclusion , an improved fibrinolytic profile was observed after statin treatment , most pronounced with atorvastatin . The results indicate that the drugs promote a profibrinolytic profile , and may in part explain the benefit of statin treatment rendered in the prevention of CHD BACKGROUND Atrial fibrillation ( AF ) continues to be one of the most common cardiac problems , placing an exp and ing burden on the public health system . In several circumstances , AF can increase the risk of stroke and heart failure . Current pharmacologic treatment options are associated with the potential for significant adverse events , which often outweigh the benefits of achieving sinus rhythm . There is evidence to suggest antiarrhythmic benefits of omega-3 polyunsaturated fatty acids ; however , the data are not conclusive . This study is design ed to further assess the effect of prescription omega-3 ethyl esters ( P-OM3 ) in the prevention of recurrent AF in patients with AF without ( significant ) structural heart disease . METHODS This trial is a 6-month r and omized , double-blind , placebo-controlled , parallel- study design . Patients with confirmed symptomatic paroxysmal or persistent AF ( 5:1 ratio ) will be r and omized to receive either 4 g/d P-OM3 ( Lovaza ; GlaxoSmithKline , Research Triangle Park , NC ) or placebo . The primary end point is the first recurrence of symptomatic AF among patients with paroxysmal AF . Secondary end points include the first recurrence of symptomatic AF among all patients . Safety will be assessed regularly . CONCLUSION This is the first r and omized blinded trial to assess the antiarrhythmic effects of 4 g/d P-OM3 in paroxysmal AF To test the hypothesis that a statin could reduce the recurrence rate of atrial fibrillation after electrical cardioversion ( EC ) , we performed an open , controlled multicenter study . Patients ( n = 114 ) who had atrial fibrillation > 48 hours and who were scheduled for EC were r and omized to receive 40 mg of pravastatin once daily for 3 weeks before and 6 weeks after EC or no drug in addition to st and ard therapy . Pravastatin did not reduce the recurrence rate of atrial fibrillation after EC OBJECTIVES This study examined the risk of proarrhythmic events in patients receiving antiarrhythmic drugs for treatment of atrial fibrillation ( AF ) according to present-day safety guidelines . BACKGROUND Advances in underst and ing the proarrhythmic risk of antiarrhythmic drugs has led to development of safety guidelines for these agents . Such guidelines were used in the Atrial Fibrillation Follow-up Investigation of Rhythm Management ( AFFIRM ) study . METHODS This study was an analysis of the risk of arrhythmic events ( arrhythmic death , resuscitated cardiac arrest , sustained ventricular tachycardia ( VT ) , and torsade de pointes VT ) in the antiarrhythmic drug arm of the AFFIRM study . Each time an antiarrhythmic drug was begun , it was counted as an exposure to that drug and the risk of an arrhythmic event was calculated . RESULTS A total of 2,033 patients received 3,030 exposures to antiarrhythmic drugs . Ninety-six arrhythmic events occurred by six years . Patients with a left ventricular ejection fraction < 40 % had more arrhythmic events . Twelve documented cases of torsade de pointes VT were noted . The incidence of torsade de pointes was 0.6 % at five years ( 95 % confidence interval 0.32 to 1.07 ) . CONCLUSIONS The overall risk of adverse arrhythmic events upon exposure to antiarrhythmic drugs in the AFFIRM study was reasonably low . Strict criteria for the safe use of antiarrhythmic drugs were successful in minimizing proarrhythmic events OBJECTIVES The use of antiarrhythmic drugs after ablation is a controversial issue when evaluating the efficacy of atrial fibrillation ( AF ) ablation . This study compares in a prospect i ve and r and omized fashion the impact of an antiarrhythmic drug in preventing AF recurrence after AF ablation . METHODS From February 2004 to May 2005 , 107 consecutive patients ( mean age 57 + /- 10 years , 69 men ) , with paroxysmal ( 60 % ) or persistent ( 40 % ) drug refractory AF , were r and omly assigned to ablation alone ( Group A , 53 patients ) or combined with the best antiarrhythmic therapy , preferably amiodarone ( Group B , 54 patients ) . All patients underwent cavo-tricuspid and left inferior pulmonary vein (PV)-mitral isthmus ablation plus circumferential PV ablation , using a guided electro-anatomical approach . St and ard electrocardiograms ( ECG ) , and ambulatory and transtelephonic ECG monitoring  were used to assess AF recurrences . Recurrences during the first month after ablation were excluded from this analysis . RESULTS At 12 months of follow-up , no significant difference was observed in the rates of AF recurrences between Group A ( 18/53 patients , 34 % ) and Group B ( 16/54 patients , 30 % ) . The percentage of patients with > /= 1 asymptomatic AF episode was higher in Group B than in Group A ( 10/16 patients , 63 % , vs 5/18 patients , 28 % , P = 0.04 ) . CONCLUSIONS Continuing antiarrhythmic drug therapy in patients who undergo catheter ablation for AF did not lower the rate of AF recurrences . Antiarrhythmic drugs increased the proportion of patients with asymptomatic AF episodes AIMS To determine whether early statin therapy in acute myocardial infa rct ion has any effect on ventricular late potentials which are considered as a noninvasive tool for evaluation of arrhythmogenic substrate . METHODS AND RESULTS Study population consisted of prospect ively enrolled 72 patients presenting with acute myocardial infa rct ion ( < 6 h ) . Thirty-four of the patients were r and omized to pravastatin ( 40 mg/day ) on admission irrespective of lipid levels . All patients received thrombolytic therapy .  Signal-averaged ECG recordings were obtained serially prior to thrombolytic therapy , 48 h after and 10 days later . Late potentials were defined as positive if signal-averaged ECG met at least two of Gomes criteria : filtered total QRS duration > 114 ms , root mean square voltage of the last 40 ms of the QRS < 20 mV , or the duration of the terminal low ( < 40 mV ) amplitude signals > 38 ms . Changes observed in signal-averaged ECG recordings after thrombolysis were evaluated statistically with regard to statin usage . There were no significant differences between the clinical characteristics of the two r and omized groups . There was a significant decrease in the rates of late potentials between the first and third signal-averaged ECG recordings after thrombolytic therapy in pravastatin group . Pravastatin group also had lower incidence of ventricular arrhythmias compared with control group ( 26 vs. 63 % , P=0.021 ) . The in-hospital cardiovascular event rates were also lower in statin group . CONCLUSION Early use of pravastatin reduces the incidence of late potentials following thrombolytic therapy in acute myocardial infa rct ion . Statin therapy also seems to be reducing the incidence of in-hospital ventricular arrhythmias . These beneficial effects of statins might be explained through prevention of new myocardial ischemic episodes due to early plaque stabilization or regulation of endothelial and platelet functions
Use of statins was significantly associated with a decreased risk of incidence or recurrence of AF in patients in sinus rhythm with a history of previous AF or undergoing cardiac surgery or after acute coronary syndrome
OBJECTIVES To improve the evaluation of the possible antiarrhythmic effect of statins , we performed a meta- analysis of r and omized trials with statins on the end point of incidence or recurrence of atrial fibrillation ( AF ) .
BACKGROUND The use of statins had been suggested to protect against AF in some clinical observational and experimental studies but has remained inadequately explored .