Abstract: Surgical aortic valve replacement (SAVR) and, more recently, transcatheter aortic valve implantation (TAVI) have been shown to be the only treatments that can improve the natural cause of severe aortic valve stenosis. However, after SAVR and TAVI, the incidence of new-onset atrial fibrillation (NOAF) is 31%-64% and 4%-32%, respectively. NOAF is independently associated with adverse events such as stroke, death, and increased length of hospital stay. Increasing the knowledge of predisposing factors, optimal postprocedural monitoring, and prophylactic antiarrhythmic and antithrombotic therapy may reduce the risk of complications secondary to NOAF.
J INVASIVE CARDIOL 2015;27(1):41-47
Key words: atrial fibrillation, NOAF, aortic valve stenosis, valvular heart disease
Aortic valve stenosis (AS) is the most frequent valvular heart disease in western countries,1 occurring in 2% of the population above 65 years of age, and the prevalence increases with age.2 Untreated patients with severe AS have a remaining life expectancy of approximately 3 years when presenting with angina or syncope and only 1-2 years when presenting with congestive heart failure.3 Aortic valve implantation by either surgical aortic valve replacement (SAVR) or transcatheter aortic valve implantation (TAVI) changes the natural course of the disease, relieving symptoms and improving prognosis.4-6 Traditionally, aortic valve implantation is performed as SAVR. However, one-third of patients with severe and symptomatic AS are denied SAVR because of unacceptable risk due to older age and comorbidities.7 In 2002, TAVI was introduced as a minimally invasive transcatheter technique; in recent years, TAVI has advanced as an alternative treatment for patients with high or extreme surgical risk.1,4,5 The self-expanding Medtronic CoreValve (MCV) prosthesis system and the balloon-expandable Edwards Sapien valve (ESV) prosthesis (Edwards Lifesciences) are currently the two dominating prosthetic valves used for TAVI. Both SAVR and TAVI improve symptoms and increase life expectancy compared with medical treatment.4-6 A trial including high-risk patients randomized to either TAVI or SAVR reported no difference in mortality between surgical or transcatheter aortic valve implantation.5
SAVR and TAVI are associated with a number of different complications including bleeding, vascular injury, and thromboembolism — particularly stroke and arrhythmia.4,5,8-10 Arrhythmias associated with these interventions are primarily new-onset atrial fibrillation (NOAF) and conduction disturbances, which may require antiarrhythmic medication, anticoagulant therapy, and/or a need for permanent pacemaker,10 as well as increasing the length of hospital stay.8,9 This review discusses NOAF in association with SAVR and TAVI in patients with AS.
Atrial fibrillation (AF) is an uncoordinated contraction of the atria with electrocardiographic (ECG) characteristics including irregular R-R intervals, absence of distinct P-waves, and irregular atrial activity. AF is classified as paroxysmal when it converts to sinus rhythm spontaneously or with intervention within 7 days of onset, persistent if an episode lasts more than 7 days, and permanent if further attempts to restore sinus rhythm have ceased.11 The definition of NOAF lacks standardization as it is often defined as detection of AF in a patient with no previous known AF, but the set-point for minimum episode duration varies.8,12-15 In an effort to standardize different endpoints after TAVI, the Valve Academic Research Consortium proposed that NOAF should be diagnosed as AF detected during hospitalization and lasting long enough to be recorded on a 12-lead ECG or at least 30 seconds on a rhythm strip.16
AF is frequently seen in the elderly population; it is found in 1% of patients between 55-59 years, increasing to 18% in patients >85 years,17 and is reported to be asymptomatic in 12%.18 AF is independently associated with increased mortality as well as risk of stroke and heart failure.19-21 Furthermore, stroke is more likely to be fatal or cause more severe functional impairment and have larger infarct size if the patient concurrently has AF compared with stroke patients without AF.22,23
AF shares several predisposing factors with AS, such as hypertension and advanced age. Additionally, the presence of valvular heart disease is associated with increased risk of AF.2,17,20 Thus, AF is seen preprocedurally in a considerable proportion of patients undergoing SAVR and TAVI. In a range of clinical studies, the prevalence of AF was reported to be 7%-43% before SAVR and 22%-41% before TAVI,4,5,13,15,24-26 and a similar prevalence was described in a meta-analysis that found preprocedural AF in 18% and 31% of patients, respectively.27
Pathogenesis and Incidence of NOAF After Aortic Valve Implantation
New-onset atrial fibrillation frequently develops after SAVR and TAVI procedures (Figure 1).4,5,8,9,12-15,24-26,28 After SAVR, inflammation due to surgical trauma, including incision in the right atrium for venous cannulation, may cause a similar inflammatory response that predisposes patients to NOAF after coronary artery bypass graft (CABG) surgery.29,30 Independent predictive risk factors for NOAF after SAVR are: preoperative age ≥70 years; low body mass index; maximum transvalvular gradient ≥85 mm Hg; history of heart failure; end-systolic interventricular septum thickness ≥1.8 cm; and preoperative and early postoperative left ventricular ejection fraction ≤50%.28 Almassi et al31 reported a tendency for an increased incidence of NOAF after SAVR with concomitant CABG when compared with isolated SAVR, but the study does not state whether the difference was significant or not.
The pathogenesis for arrhythmias during the less invasive TAVI procedure is not well described, but preprocedural enlarged left atrium and transapical approach are associated with increased risk of NOAF.8,13 Rodés-Cabau et al32 reported that transapical TAVI resulted in higher increase of serum markers for myocardial injury compared with transfemoral TAVI. These results could suggest that the increased risk of NOAF after transapical TAVI is related to a more extensive myocardial injury compared with the transfemoral approach.
The incidence of NOAF was reported to be 4%-32% after TAVI in general,8,13-15,24-26 whereas it was reported in 6%-38% and 0%-16% of patients after transapical and transfemoreal TAVI with the ESV, respectively.8,13 Likewise, NOAF was reported in 15% of patients when performing transfemoral and subclavian TAVI with the MCV.14 After SAVR the incidence of NOAF was reported to be 31%-64%.9,12,13,15,24,28,31 In the PARTNER trial by Smith et al,5 patients were randomized to either TAVI with the ESV or SAVR. Not excluding patients with a baseline history of AF, they found a significant difference in the development of NOAF after TAVI and SAVR (9% vs 16% of patients, respectively). Adams et al33 reported that NOAF or worsening preprocedural AF were significantly more common after SAVR when compared with MCV-TAVI (31% vs 12% of randomized patients, respectively). Unfortunately, there are currently no randomized studies comparing the MCV with the ESV that report the incidence of NOAF. In addition, the methods and criteria to determine the incidence of NOAF differ between observational studies, which makes comparisons difficult. NOAF detection is often done by continuous monitoring with varying duration ranging between the first 3-7 days after the procedure or limited to the length of hospital stay,8,13-15 with NOAF defined as a recorded AF episode lasting >30 seconds8,14,15 or 10 minutes.12,13 Furthermore, there is the risk of overestimating the incidence of NOAF. The exclusion of patients with preprocedural AF is often based on a history of previous known AF or short preprocedural screening. As the prevalence of preprocedural AF is high in patients undergoing SAVR and TAVI,4,5,13,15,24-27 and AF can be asymptomatic,18 there is a risk that detected NOAF in some patients is actually the unmasking of preprocedurally unknown AF.
Amat-Santos et al8 reported that 41% of NOAF occurred within 24 hours, 22% between 24-48 hours, 18% between 48-72 hours, and 18% occurred >72 hours after TAVI with the ESV. NOAF was reported from the first postprocedural day after SAVR and with the highest incidence after 3 days; however, the study was limited by a postprocedural monitoring period of only 3 days.13
Impact of NOAF After Aortic Valve Implantation
In a study by Ruel et al,34 patients underwent SAVR with mechanical or bioprosthetic valves with or without concomitant CABG. Thromboembolic stroke occurred in 6.7% of patients within an average of 5.7 years after SAVR, and AF was an independent predictor of stroke. Also, mortality during 10-year follow-up was found to increase by 48% in patients with NOAF versus patients without NOAF after SAVR with or without concomitant CABG.12 Saxena et al9 was unable to confirm an association between NOAF and increased risk of stroke within 30 days or increased mortality within 7 years after isolated SAVR. Instead, patients with NOAF had an increased risk of new-onset renal failure and gastrointestinal complications (Table 1).9
As with SAVR, an association exists between NOAF and the increased risk of complications post TAVI. Stortecky et al26 described a 1-year post-TAVI all-cause mortality rate of 14% in patients with no AF and 31% in patients with preprocedural or NOAF. The mortality rate increased significantly and independently of whether AF was paroxysmal, persistent, or permanent. In a large observational study by Nombela-Franco et al,25 almost 50% of cerebrovascular events (defined as transient ischemic attack or stroke) occurred >24 hours after TAVI. This demonstrates that cerebrovascular events are not exclusively periprocedural complications, but are also related to clinical factors, such as NOAF. Further demonstrating this fact, the study reported that patients who developed NOAF after TAVI had a significantly increased risk of cerebrovascular events during the subacute period of days 1-30. A history of chronic AF increased the risk of cerebrovascular events occurring later than 30 days until a median follow-up of 12 months. Likewise, Amat-Santos et al8 reported that stroke occurred in 14% of patients with NOAF and 3% without NOAF with a significant difference, and all events of stroke with onset >24 hours after TAVI had one or more episodes of NOAF.
However, the inconsistent association between NOAF and complications after SAVR is also found among TAVI studies.8,26 As mentioned earlier, this disparity might be explained by differences in study size, non-matching patient groups, or various methods for detecting NOAF.
Besides the potential reduction in adverse events, there is also an economic benefit to minimizing the occurrence of NOAF. The length of hospital stay has been shown to be significantly extended from a mean of 6-9 days after TAVI8 and from 9-11 days after SAVR9 in patients with NOAF. Furthermore, the length of stay in the intensive care unit and the risk of readmission within 30 days for any reason is increased in patients with NOAF after SAVR.9,28
Charitos et al35 reported that the sensitivity of AF detection with intermittent rhythm monitoring was lower when compared to continuous monitoring. They evaluated the sensitivity of AF detection by reconstructing rhythm histories from 647 patients with known recurrent AF recorded from their implanted continuous monitoring devices and computationally simulating different intermittent rhythm monitoring strategies. The sensitivity of AF detection was significantly inferior for all comparisons of various intermittent monitoring strategies when compared with continuous monitoring, eg, a single monitoring of 30 days or 24-hour monitoring repeated 7 times over the course of a year would only reach a sensitivity of 65% (Figure 2).35 Furthermore, Motloch et al13 monitored the first 3 days after aortic valve implantation and reported that the average duration of the longest NOAF episode was 21 hours after SAVR and 10 hours after TAVI.13 Amat-Santos et al8 reported that one-third of NOAF episodes after TAVI lasted <1 hour.8 Thus, the intermittent, potential asymptomatic and above-mentioned delayed nature of NOAF development justifies a frequent or continuous monitoring strategy for NOAF detection, eg, by telemetry during the first postprocedural days. However, the optimal duration for intense rhythm monitoring is unknown due to the lack of knowledge of the development of NOAF over longer duration after TAVI and SAVR.
Continuous long-term monitoring with implantable loop recorders (ILR) could be a new helpful clinical tool in detecting and describing NOAF and assessing therapeutic response to NOAF treatment.35-37 Pecha et al37 described the use of ILR for detecting recurrent AF in cardiac surgical patients who had concomitant AF ablation. The patients with ILR were more frequently seen by a cardiologist and more often had cardioversions, additional catheter-based ablations, and optimized antiarrhythmic drug management compared with non-ILR patients. This resulted in a tendency toward more patients with an ILR to have sinus rhythm at 1-year follow-up, despite a higher probability of detecting recurrent AF in patients with an ILR.37
Prevention and Treatment of NOAF
Recent guidelines from the American Heart Association/American College of Cardiology/Heart Rhythm Society recommend achieving rate control with beta-blockers or non-dihydropyridine calcium-channel blockers if AF develops after cardiac surgery, and amiodarone and sotalol can be considered as prophylaxis for NOAF development.11 The latter was confirmed in a meta-analysis by Crystal et al,38 who described that amiodarone, sotalol, and beta-blockers could reduce the incidence of NOAF after coronary artery bypass graft surgery with or without concomitant valvular surgery. Additionally, in a systematic review by Marik and Fromm,39 the periprocedural administration of corticosteroids in moderate to high dose was reported to reduce the development of NOAF by more than 50% after cardiac surgery. This result supports the suggestion that inflammation is proarrhythmic, since an adequate pharmacological down-regulation of systemic inflammation seems to inhibit the development of NOAF. A similar pharmacological response has not been investigated after TAVI. Closer monitoring of the heart rhythm after SAVR and TAVI may lead to identification of predictive factors for NOAF, which could help classify patients at high risk of developing NOAF and thus where prophylactic antiarrhythmic therapy could be indicated.8,13,28
During SAVR, simultaneous surgical ablation or Maze procedure can be performed in patients with known AF.1 Budera et al40 compared cardiac surgery patients and found that significantly more patients with concomitant AF ablation (either cryofrequency or radiofrequency ablation) remained in sinus rhythm 1 year after the procedure when compared to non-ablated patients. However, surgical ablation did not cause an increase in periprocedural complications, but no difference in all-cause mortality or stroke rates between ablated and non-ablated patients was observed after 1 year.40 Additionally, a meta-analysis by Reston et al41 reported weak evidence for a reduced stroke rate and increased rate of permanent pacemaker treatment after different types of the Cox-maze III procedure in patients undergoing mitral valve surgery. The analysis reported a need for large randomized trials to conclude the effect on clinical outcomes after antiarrhythmic procedures associated with cardiac surgery.41
Antithrombotic Treatment of NOAF
Currently, TAVI is indicated for patients with high or extreme surgical risk,1 typically having numerous comorbidities and a high thromboembolic risk if NOAF develops. In a study by Amat-Santos et al,8 patients had a median CHADS2 score of 3. Although representing a small subpopulation of the study, 4 out of 10 patients (40%) with postprocedural NOAF who did not receive anticoagulant therapy developed complications related to thromboembolism within 30 days after TAVI. Similar complications were significantly decreased to 1 out of 34 patients (3%) with NOAF who did receive anticoagulant therapy. Reasons for not starting anticoagulation therapy in patients with NOAF included an expected excessive risk of bleeding or short NOAF duration (<12 hours).8 This emphasizes the need for clear guidelines following short durations of NOAF in a group of patients where the risk of both bleeding and thromboembolism is high. The 2012 focused updated European Society of Cardiology guidelines for the management of AF42 state that percutaneous left atrial appendage occlusion may be considered in patients with high risk of stroke and contraindications for anticoagulant therapy. This recommendation is based on expert consensus due to a lack of randomized trials.42
The incidence of cerebrovascular events is highest during the initial 2 months after TAVI.43 Currently, there is no standard recommendation for antithrombotic treatment after TAVI during this early phase. However, the general approach is dual-antiplatelet therapy (usually aspirin combined with up to 6 months of clopidogrel).1,5 If NOAF develops, it is recommended to combine warfarin and 1 antiplatelet drug.1 In a randomized trial by Dewilde et al,44 patients who underwent percutaneous coronary intervention (PCI) and received anticoagulant therapy were assigned to either postprocedural double- or triple-antithrombotic therapy by further adding clopidogrel or clopidogrel plus aspirin, respectively. Patients had different relevant indications, such as AF or mechanical valves, for anticoagulant therapy. The study reported that triple-antithrombotic therapy significantly increased the risk of bleeding and achieved no risk reduction of thrombotic or thromboembolic events during 1-year follow-up. Applying these results to TAVI patients with AF might indicate that triple-antithrombotic therapy is too aggressive considering the high risk of bleeding following TAVI;4,5 however, it should be noted that the PCI patients included in the previous study were generally younger than TAVI patients and had a potentially different thromboembolic risk.
After SAVR with a bioprosthetic valve, it is recommended to give aspirin for the first 3 months and consider anticoagulant therapy during the same period. If AF is present after SAVR, then lifelong anticoagulant therapy is indicated.1 Patients undergoing SAVR with a bioprosthetic valve with or without concomitant coronary artery bypass graft surgery have reduced mortality and risk of readmission due to thromboembolic events, but increased risk of bleeding when warfarin is combined with aspirin compared with aspirin alone.45 Similar results have been described in a Cochrane meta-analysis by Massel and Little46 concerning patients with mechanical valves or bioprosthetic valves and indicators of risk such as AF. The study concluded that combining aspirin or dipyridamol with anticoagulant therapy reduced the mortality and risk of systemic embolism, but increased the risk of major bleeding. Furthermore, in patients with unknown AF status after SAVR with bioprosthetic valves, the risk of stroke and cardiovascular events was increased if anticoagulant therapy was discontinued within the first 3 and 6 months, respectively.47 Applying a similar anticoagulant strategy after TAVI could potentially reduce the excessive risk of cerebrovascular events in the early phase, but more evidence is needed to recommend this strategy.
Both rivaroxaban and dabigatran inhibiting factor Xa and thrombin, respectively, have been shown to result in a non-inferior risk reduction for stroke, systemic thromboembolism, and major hemorrhage in patients with AF and absence of valve disease, when compared with warfarin therapy.48,49 Furthermore, patients treated with dabigatran had reduced risk of major hemorrhage or stroke and systemic thromboembolism depending on the dosage used,48 and rivaroxaban showed reduced risk of intracranial and fatal bleeding.49 These newer anticoagulant agents have yet to be tested in the setting of AF after SAVR using a bioprosthesis or TAVI. In the recent RE-ALIGN trial,50 patients had undergone aortic or mitral valve replacement with a mechanical prosthesis and were randomized to dabigatran or warfarin. The trial had to be prematurely terminated due to excess events of thromboembolism and pericardial bleeding complications in the dabigatran group, with no difference in the preoperative prevalence of AF between the two groups. A possible explanation for the increased risk given by the authors was an excess activation of the coagulation contact pathway. The artificial surface of the valve leaflets and sewing ring may result in overwhelming levels of thrombin, allowing thrombus formation. Factor IX of the contact pathway, among other factors, is inhibited by warfarin, potentially leading to greater inhibition of thrombin formation.50 Considering the lower level of recommendation for anticoagulant therapy using bioprosthetic valves compared with mechanical valves,1 it still seems legitimate to investigate the role of rivaroxaban and dabigatran in patients undergoing TAVI and SAVR with bioprosthetic valves. These newer anticoagulant agents could potentially prevent thromboembolism related to NOAF after TAVI and SAVR with bioprosthetic valves, given their promising results in patients with non-valvular AF.48,49
TAVI and SAVR are the only definitive treatments for severe AS; both interventions improve prognosis and symptoms. TAVI, and to a greater degree SAVR, carries a risk of developing NOAF. This arrhythmia has significant health, economic, and clinical implications, because the length of hospital stay and the risk of stroke and mortality are increased.
Future studies identifying predictive factors for postprocedural NOAF will help in selecting high-risk patients who might benefit from prophylactic antiarrhythmic therapy or surgery. Improving timing of electrocardiographic monitoring will likely reduce the incidence of undiagnosed and untreated NOAF. Furthermore, there is a lack of studies that evaluate optimal antithrombotic therapy after both interventions.
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From the Departments of 1Cardiology and 2Cardiothoracic Surgery, Copenhagen University Hospital, Copenhagen, Denmark; and 3the Department of Clinical Medicine, University of Copenhagen, Copenhagen, Denmark.
Disclosure: The authors have completed and returned the ICMJE Form for Disclosure of Potential Conflicts of Interest. Dr Svendsen reports a research grant, speaker’s bureau, and advisory board fees from Medtronic; research grant from Biotronik. Dr Søndergaard is a consultant for Medtronic. The remaining authors report no conflicts of interest.
Manuscript submitted March 18, 2014, provisional acceptance given April 25, 2014, final version accepted June 2, 2014.
Address for correspondence: Troels Højsgaard Jørgensen, Copenhagen University Hospital, Department of Cardiology, Blegdamsvej 9, 2100 Copenhagen, Denmark. Email: Troels.firstname.lastname@example.org