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The Impact of Suppressing the Renin-Angiotensin System on Atrial Fibrillation

From Wayne State University, Eugene Applebaum College of Pharmacy and Health Sciences, Detroit, Michigan (Dr Kalus); Henry Ford Hospital, Department of Pharmacy Services, Detroit, Michigan (Dr Kalus); University of Connecticut, School of Pharmacy, Storrs (Dr Coleman, Dr White); and Hartford Hospital, Department of Pharmacy, Hartford, Connecticut (Dr Coleman, Dr White).

Address for reprints: James S. Kalus, PharmD, BCPS, Eugene Applebaum College of Pharmacy and Health Sciences, Wayne State University, 259 Mack Avenue, Suite 2190, Detroit, MI 48201.

	ABSTRACT

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Atrial fibrillation is very common in the United States. After a search of Medline, EMBASE, and CINAHL, 4 trials evaluating inhibitors of the renin-angiotensin system were identified for prevention of new-onset atrial fibrillation, facilitation of electrical cardioversion of atrial fibrillation, and prevention of atrial fibrillation recurrence after electrical cardioversion. A meta-analysis was performed using a random-effects model. Use of an angiotensin-converting enzyme (ACE) inhibitor or angiotensin-receptor blocker (ARB) was associated with a reduction in new-onset atrial fibrillation (OR [95% CI] = 0.51 [0.36-0.72]), a lower failure rate of electrical cardioversion of atrial fibrillation (0.47 [0.24-0.92]), and a lower rate of recurrence of atrial fibrillation after electrical cardioversion (0.39 [0.20-0.75]). With the exception of the new-onset atrial fibrillation analysis, these findings were not associated with statistical heterogeneity. These hypothesis-generating data suggest that inhibitors of the renin-angiotensin system may provide benefit across the spectrum of atrial fibrillation.

Key Words: Atrial fibrillation • angiotensin-converting enzyme inhibitor • angiotensin receptor antagonist • systematic review

The renin-angiotensin system may play a role in the pathophysiology of AF. In animal models, pathogenic structural and electrical remodeling of the atria commonly associated with AF is prevented by inhibition of angiotensin II.⁵ Patients with AF have an increase in atrial tissue angiotensin-converting enzyme concentration as well.⁶

Currently, there are few studies exploring whether renin-angiotensin system inhibition can prevent AF or facilitate electrical cardioversion of the arrhythmia.^7-14 All of the prospective studies are small in size and may not be adequately powered to evaluate these end points.^11-14 The purpose of this meta-analysis was to pool the results of published studies evaluating the impact of angiotensin-converting enzyme (ACE) inhibitors or angiotensin-receptor blockers (ARBs) in patients with AF. Specifically, we sought to determine the influence of these drug classes on the occurrence of new-onset AF, rate of successful direct current cardioversion of AF, and rate of AF recurrence.

	METHODS

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
Identification and Selection of Studies
We conducted a search of Medline (January 1966 through June 2005), EMBASE (1980 through June 2005), and CINAHL (1982 through June 2005) to identify all trials published in English involving the use of ACE inhibitors or ARBs for preventing the development or recurrence of AF or for facilitation of direct current cardioversion of AF. We used the medical subject headings (including all subheadings) and text keywords "(ACE inhibitor) AND (angiotensin receptor blocker) AND (atrial fibrillation)" as our search parameters. In addition, we performed a manual search of the literature using the references of original manuscripts and review articles. We also conducted a search of the Cochrane Database of Systematic Reviews.

Studies were included in this meta-analysis if they met both of the following criteria: (1) they evaluated the addition of an ACE inhibitor or ARB versus placebo or routine treatment and (2) they reported data on incidence of new-onset AF, rate of successful direct-current cardioversion (DCC), or recurrence of AF. Studies reporting new-onset AF were excluded if it was not possible to differentiate whether patients with a history of AF were included in the final count of AF cases.^15-17 Studies published only in abstract form were also excluded.¹⁸

Outcomes and Statistical Analysis
Results of each clinical trial and selected characteristics were summarized and tabulated for analysis. Three separate analyses were performed. The first analysis evaluated the rate of new-onset AF among patients treated with an ACE inhibitor, as compared to those treated with either placebo or an active comparator (new-onset AF analysis). New-onset AF was defined as AF occurring in patients with no previous history of AF. The second analysis evaluated the rate of successful DCC following pretreatment with an ACE inhibitor or ARB versus no pretreatment with these agents (DCC facilitation analysis). For this analysis, failure of DCC was defined as the failure to achieve normal sinus rhythm on the day of DCC. The third analysis evaluated the rate of AF recurrence when an ACE inhibitor or ARB was added to standard of care in patients undergoing DCC (AF recurrence analysis). AF recurrence was defined as AF documented by electrocardiogram or Holter monitor at the specified study follow-up period (range, 6 weeks to 12 months).

The end points of AF occurrence or recurrence and DCC success rate were treated as a dichotomous variable and reported as odds ratios (ORs) with 95% confidence intervals (CIs). Pooled ORs were calculated using Review Manager 4.2.7 software (freely available from the Cochrane Web page¹⁹) using a random-effects model (DerSimonian and Laird methodology). Statistical heterogeneity scores were assessed with a ² test. A P value of <.1 defined significant heterogeneity. Funnel plots of included studies were analyzed to assess the potential for publication bias.

To establish the effect of clinical heterogeneity of the included studies on the results of the meta-analysis, a subgroup analysis was performed. For all 3 analyses, subgroup analysis was used to assess the effect of the class of angiotensin-inhibiting drug used (ACE inhibitor vs ARB). Another subgroup analysis examined the use of concomitant amiodarone for the DCC facilitation and AF recurrence analyses.

	RESULTS

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Studies and Patients
Four studies met inclusion criteria for the new-onset AF analysis (Table I).^7-10 The 4 included studies were all post hoc analyses of large clinical trials, and all included patients with some degree of left ventricular dysfunction. However, the degree of left ventricular dysfunction varied between studies. Two of the studies evaluated ACE inhibitors, while the other 2 evaluated ARBs.

For the DCC facilitation analysis, 4 studies meeting the inclusion criteria were identified (Table II).^11-14 All of these identified studies were included in the AF recurrence analysis as well. All included studies for these analyses were randomized trials, but only 1 study was double blind and placebo controlled.¹¹ The others compared the addition of either an ACE or an ARB to amiodarone versus amiodarone alone. The baseline characteristics of the patients analyzed in the DCC facilitation and AF recurrence analyses are presented in Table II. Of the 370 patients included, 71 were treated with an ACE inhibitor and 133 were treated with an ARB.

Quantitative Data Analysis
New-Onset AF Analysis
Upon meta-analysis, there was a reduction in the occurrence of new-onset AF among patients treated with either an ACE inhibitor or ARB (OR [95% CI] = 0.51 [0.36-0.72], P < .001; Figure 1a). The absolute risk reduction (ARR) with ACE inhibitors or ARBs was 2.6% (95% CI = 1.9-3.3). This finding was associated with significant statistical heterogeneity (P = .008). When evaluated separately, new-onset AF was prevented regardless of whether ACE inhibitors (0.31 [0.11-0.86]) or ARBs (0.64 [0.54-0.75]) were evaluated.

View larger version (31K): [in this window] [in a new window]   Figure 1. (a) New-onset atrial fibrillation. (b) Facilitation of direct current cardioversion. (c) Maintenance of normal sinus rhythm.

When evaluated separately, there was a trend for a benefit in the ACE inhibitor (0.63 [0.18-2.19]) and ARB (0.37 [0.13-1.04]) subgroups, and statistical heterogeneity was not present in either subgroup analysis (P = .21 and P = .44, respectively).

AF Recurrence Analysis
There was also a reduction in the rate of recurrence of AF after direct current cardioversion with concomitant use of ACE inhibitors or ARBs (0.39 [0.20-0.75], P = .005; Figure 1c). The ARR was 19% (9.7-28.0) for this analysis. Statistical heterogeneity was not significant (P = .18). In a subgroup analysis of the 3 studies in which ACE inhibitors or ARBs were added to amiodarone, angiotensin II–inhibiting medications continued to provide benefit (0.41 [0.19-0.89]).

When evaluated separately, there was a nonsignificant trend for an effect on rate of AF recurrence in the ACE-inhibitor-treated patients (OR [95% CI] = 0.49 [0.22-1.05]) or ARB (0.36 [0.10-1.23]). Statistical heterogeneity was significant in the ARB subgroup analysis (P = .06) but not in the ACE inhibitor subgroup analysis (P = .44).

	DISCUSSION

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
This meta-analysis was designed to evaluate the impact of ACE inhibitors and ARBs across the AF spectrum, including prevention of new-onset AF, facilitation of cardioversion to sinus rhythm, and prevention of AF recurrence. All of these outcomes were positively influenced by renin-angiotensin system–inhibiting medications, suggesting that the renin-angiotensin-aldosterone system plays a significant role in the pathophysiology of AF.

Among patients with left ventricular dysfunction who have no history of AF, the use of ACE inhibitors or ARBs can prevent AF from occurring. Based on the results from this analysis, 38 patients would need to be treated with an ACE inhibitor or ARB to prevent new-onset AF in 1 patient. This result is in basic agreement with 2 other meta-analyses evaluating this end point.^20,21 Pharmacologic studies have demonstrated that the renin-angiotensin-aldosterone system is activated during AF in both humans and animals.^5,6 Theoretically, elevated angiotensin II concentrations that contribute to left ventricular remodeling and dysfunction could also lead to atrial remodeling. Remodeling of the atria could serve as the anatomical substrate necessary for the development of AF.²² This theory is supported by the observation that the risk for developing new-onset AF increases with increasing heart failure severity.²³

To the authors' knowledge, this is the first meta-analysis to evaluate the impact of ACE inhibitors or ARBs on DCC success rate. Among patients actively experiencing AF, the use of an ACE inhibitor or ARB can enhance the success of DCC and then prevent the subsequent recurrence of AF. It would be necessary to pretreat 13 patients with ACE inhibitors or ARBs to prevent 1 failed electrical cardioversion. Only 5 patients would need to be treated with ACE inhibitors or ARBs to prevent AF recurrence in 1 patient after DCC. The size of the effect of ACE inhibitors and ARBs on maintenance of sinus rhythm in this meta-analysis is similar to that observed in 2 other recent meta-analyses.^20,21 Facilitation of DCC by ACE inhibitors or ARBs could be explained by attenuation of changes in atrial structure and electrophysiologic function by these agents. It is clear that the presence of AF leads to the development of atrial fibrosis, a structural change that is instrumental in the perpetuation of AF.²² This fibrosis is likely responsible for electrophysiologic changes associated with AF, including reduced atrial effective refractory period or atrial conduction delay.^24,25 Animal studies have demonstrated that treatment with ACE inhibitors or ARBs produces a reduction in atrial fibrosis.^5,26,27 In addition, it has been demonstrated that shortening of the atrial effective refractory period is prevented in dogs treated with an ACE inhibitor prior to rapid atrial pacing.²⁴ This is important because reduced atrial refractoriness occurs after an episode of AF. Therefore, ACE inhibitors may protect against the development of the electrophysiologic changes associated with AF. Finally, administration of angiotensin II reduces atrial conduction velocity, and inhibition of angiotensin II enhances conduction velocity after AF.²⁴ Therefore, the likely pharmacological mechanism by which ACE inhibitors or ARBs facilitate DCC is through attenuation of the atrial structural changes that form the substrate for AF perpetuation. ACE inhibitors and ARBs appeared to prove beneficial by preventing immediate recurrence of AF (within 5 minutes of cardioversion) or early recurrence of AF (within the first 4 weeks following cardioversion).^12-14 This is important because AF recurrence frequently occurs during the first few weeks after cardioversion.

An important subanalysis of our trial was to determine whether ACE inhibitors or ARBs provided benefit when used adjunctively with the antiarrhythmic agent amiodarone. Class III antiarrhythmic drugs can facilitate DCC²⁸ and prevent recurrence after DCC. As such, providing additional benefits with an ACE inhibitor or ARB is clinically relevant.

Given the association between AF and hypertension, another explanation for our meta-analyses results is that patients treated with ACE inhibitors or ARBs experienced a reduction in blood pressure that contributed to a reduction in new-onset AF, improved AF cardioversion rates, or a reduction in AF recurrence. However, in the studies included in the DCC facilitation and AF recurrence analyses, blood pressure data was not reported in 1 study,¹¹ was lower with ARB use in 1 study,¹³ and was not different when an ACE inhibitor or ARB was used in the other 2 studies.^12,14

This meta-analysis suggests a substantial clinical benefit (at least 50% relative improvement in all 3 end points). However, this benefit must be weighed against potential safety issues associated with adding an ACE inhibitor or ARB to therapy. Although safety and tolerability data were not able to be pooled for this meta-analysis, ACE inhibitors or ARBs were generally well tolerated in the studies included. One of the studies included in the new-onset AF analysis reported that potassium concentrations were similar between the ACE inhibitor and placebo groups.⁷ Adverse events were reported in 3 of the 4 studies included in the other 2 analyses.^12-14 Notably, all of these studies evaluated ACE inhibitors or ARBs in combination with amiodarone, and most adverse events were related to amiodarone use (ie, thyroid dysfunction, pulmonary fibrosis, cutaneous reactions, heart block, or bradycardia). However, 1 of the studies noted that 10% of patients discontinued an ACE inhibitor due to cough, hyperkalemia, or elevations in serum creatinine concentrations.¹⁴ The higher incidence of typical ACE inhibitor–induced adverse events in this study may have been due to the inclusion of patients with more comorbidities (more diabetes mellitus, lower ejection fraction) than in the other 2 studies.^12,13

It should be noted that meta-analyses are prone to publication bias. One study assessed the effect of publication bias on meta-analysis in the Cochrane Database.²⁹ Although publication bias was present in approximately 50% of meta-analyses evaluated, this bias altered the conclusion of the analysis in few of the studies. Therefore, publication bias likely has a small effect on meta-analysis results. However, it should not be assumed that a meta-analysis is a substitute for a well-designed, randomized, controlled trial. The use of post hoc data in the new-onset AF analysis and the very small number of studies available for inclusion in all 3 analyses are also limitations. Despite these limitations, the findings of this meta-analysis highlight the need for further research in this area.

Future Directions
These meta-analyses provide hypothesis-generating data and stimulate additional questions about the future role of ACE inhibitors or ARBs for the treatment or prevention of AF. As was mentioned previously, it is not clear whether AF stimulates the renin-angiotensin-aldosterone system, whether increased renin-angiotensin-aldosterone system activity causes AF, or whether both situations occur. With regard to the adoption of these therapies into practice, the optimal dose and duration of ACE inhibitor or ARB therapy is still unknown. In addition, most of the studies evaluated recurrence of AF or facilitation of cardioversion with ACE inhibitors or ARBs in combination with amiodarone; therefore, it remains unclear whether these agents would have the same positive impact in the absence of amiodarone. This may be of particular importance when considering safety and tolerability since amiodarone accounted for most adverse effects in the studies evaluated. Finally, it is unknown whether more complete suppression of the renin-angiotensin-aldosterone system, through inhibition of aldosterone or dual-inhibition of angiotensin II with an ACE inhibitor plus ARB, would have different effects than an ACE inhibitor or ARB alone.

	CONCLUSION

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 
In conclusion, this meta-analysis suggests that ACE inhibitors and ARBs prevent the development of new-onset AF in individuals at risk, improve the likelihood of successful DCC, and prevent recurrence of AF after DCC. These are hypothesis-generating data. Further work is needed to elucidate the pharmacologic mechanisms responsible for these potential beneficial effects and to define the appropriate patient populations that would benefit most from implementation of these therapies.

	REFERENCES

TOP ABSTRACT METHODS RESULTS DISCUSSION CONCLUSION REFERENCES

 

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