Cardiac Rhythm Management
Articles Articles 2015 July

Surgical Suture Ligation of the Left Atrial Appendage: Outcomes from a Single-center Study

DOI: 10.19102/icrm.2015.060703

1ARASH ARYANA, MS, MD, 2SHELDON M. SINGH, MD, 3STEVE K. SINGH, MSc, MD, 1P. GEAROID O’NEILL, MD, 1MARK BOWERS, MD and 4ANDRE D’AVILA, MD, PHD

1Regional Cardiology Associates and Dignity Health Heart & Vascular Institute, Sacramento, CA, USA

2Sunnybrook Health Sciences Centre, University of Toronto, Ontario, Canada

3Department of Cardiothoracic Surgery, CHI Baylor St. Luke's Medical Center, Texas Heart Institute, Houston, TX, USA

4Instituto de Pesquisa em Arritmia Cardiaca, Hospital Cardiologico-Florianopolis, Florianopolis, Santa Catarina, Brazil

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ABSTRACT.Surgical exclusion can frequently yield incomplete closure of the left atrial appendage (iLAA). We evaluated the incidence of iLAA and ischemic stroke/systemic embolization (SSE) following surgical suture ligation. Seventy-five patients with non-rheumatic atrial fibrillation (AF) (CHA2DS2VASc: 4.1 ± 1.9) underwent surgical LAA ligation in conjunction with mitral valve/AF surgery and postoperative LAA evaluation using computed tomography (CT) angiography. iLAA was detected in 26/75 patients (35%). At baseline, 2% with closed LAA (cLAA) and 0% with iLAA had suffered SSE (p=0.470). AF was documented in 52% during 48 ± 19 months of follow-up (p=0.479). SSE occurred in 15% with iLAA versus 2% with cLAA (p=0.028). Overall, 62% with iLAA and 43% with cLAA were receiving oral anticoagulation (OAC) (p=0.127), as compared with 0% with and 73% without SSE (p=0.004). As such, the annualized SSE risk was 1.70% (entire cohort), 3.86% (all iLAA patients), and 9.78% (iLAA patients not receiving OAC) per 100 patient-years of follow-up. In a multivariable analysis, iLAA emerged as a significant predictor of SSE. Those with iLAA not receiving OAC exhibited an annualized SSE risk more than two times that predicted by conventional risk stratification schemes. Hence, OAC therapy should be strongly considered in this high-risk patient cohort.

KEYWORDS.cardiac surgery, incomplete closure, left atrial appendage, ligation, stroke prevention.

The authors report no conflicts of interest for the published content.
Manuscript received March 21, 2015, final version accepted May 12, 2015.
Address correspondence to: Arash Aryana, MS, MD, FHRS, Regional Cardiology Associates and Dignity Health Heart & Vascular Institute, 3941 J Street, Suite #350, Sacramento, CA 95819. E-mail: aaryana@rcamd.com

Introduction

Atrial fibrillation (AF) is the most common cardiac arrhythmia, affecting an estimated 6 million individuals in the United States.1 In patients with non-valvular AF, the risk of ischemic stroke/systemic embolization (SSE) is nearly fivefold greater after adjusting for all other risk factors.1 The left atrial appendage (LAA) has been identified as a common site of thrombus formation in patients with AF.2 As such, this structure has been targeted for surgical closure using a variety of techniques for over six decades, a practice that is nowadays frequently performed in conjunction with mitral valve and Maze surgery.3 However, surgical LAA exclusion can often result in incomplete LAA closure (iLAA),37 which may in turn be associated with increased risk of thromboembolism.4,5 In this study, we evaluated the incidence of iLAA and SSE in a cohort of contemporary patients with AF in the absence of rheumatic heart disease undergoing surgical suture ligation of LAA at the time of mitral valve and/or AF surgery.

Methods

Patients with non-rheumatic AF undergoing a first surgical suture ligation of LAA concurrently with mitral valve or Maze surgery by experienced operators at a single center (Mercy General Hospital, Sacramento, California) between January 1, 2008 and December 31, 2012 were enrolled. The surgical approach to LAA ligation consisted of an oversew technique using a double layer of running Prolene suture. All patients underwent gated cardiac computed tomography (CT) angiography ≥3 months postoperatively on an outpatient basis to evaluate the status of their LAA. Any opacification of a “residual” LAA (partial or complete) was classified as iLAA, whereas closed LAA (cLAA) was defined as the absence of contrast flow into the presumed anatomical location of the LAA (Figure 1). All examinations were carefully reviewed and interpreted by two designated, experienced radiologists. Whenever iLAA was present, the LAA morphologies were examined and further classified as either “cactus”, “chicken wing”, “windsock”, or “cauliflower” (Figure 2), based upon previously reported morphological criteria.8 Recurrence of AF following LAA ligation was assessed using in-office, routine electrocardiograms, and whenever present, using cardiac implantable electronic device interrogations. All patients provided informed written consent for their participation in this study. Approval for this study was granted by our institutional review board (Dignity Health institutional review board #14).

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Figure 1: Computed tomography (CT) illustrations of closed left atrial appendage (cLAA) versus incompletely-closed LAA (iLAA). A left atrial image segmented from a cardiac CT angiogram illustrating a cLAA (a) and an iLAA (b), following prior surgical suture ligation. Abbreviations: LIPV: left inferior pulmonary vein; LSPV: left superior pulmonary vein; RIPV: right inferior pulmonary vein.

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Figure 2: LAA morphologies. Left atrial images segmented from cardiac CT angiograms illustrating iLAA with a cauliflower (a), a windsock (b), a chicken wing (c), and a cactus (d) morphology. Abbreviations: RSPV: right superior pulmonary vein.

Statistical analysis

Baseline patient demographics and procedural and clinical outcomes were compared. Continuous variables were analyzed using the two-sample t test or Mann–Whitney test for parametric and non-parametric variables respectively. The χ2 or Fisher exact test was used for parametric or non-parametric categorical variables respectively. Ascertaining predictors of SSE as the primary outcome was achieved using multivariable logistic regression modeling. We included all non-correlated, univariate variables (determined by Pearson’s coefficients) that differed between the two groups (p<0.05), along with all clinically relevant variables of interest. Stepwise regression was performed, eliminating all variables with p>0.10. The result was a parsimonious, clinically relevant model providing the odds ratio (OR) and 95% confidence intervals (CI) for statistically significant independent predictors of SSE. Time-to-event analysis was performed creating univariate Kaplan–Meier curves. Both the log-rank and the Wilcoxon tests were used to compare differences in the cohorts. A Cox proportional hazards model was used to determine the time-dependent predictors of SSE, resulting in a constant hazards ratio (HR) of event risk at each point in time. Additionally, the annualized risk of SSE was calculated for the entire cohort, as well as those with iLAA with or without long-term oral anticoagulation (OAC) therapy. Late follow-up was complete for 100% of patients at a mean of 48 ± 19 months. For all analyses, p-values were two-sided and a p<0.05 was considered significant. Analyses were conducted with use of SPSS Version 20 (IBM SPSS Statistics, Chicago, IL).

Results

Altogether, 75 patients participated in this study. CT angiography detected cLAA in 49 patients (65%) and iLAA in 26 patients (35%). The incidences of iLAA and cLAA were similar across the operators (p=0.268). Baseline patient demographics were similar (Table 1). This included CHADS2 and CHA2DS2VASc risk scores and also the incidences of SSE and their relevant risk factors, with the exception of coronary artery disease, which was more prevalent among patients with iLAA (58% versus 29%; p=0.021), and congestive heart failure, which was more common in those with cLAA (63% versus 35%; p=0.010). Likewise, operative and postoperative outcomes were similar in patients with iLAA and cLAA (Table 2), with the exception of a significantly higher number of SSE in iLAA patients during long-term follow-up. That is, only 1 out of 49 patients with cLAA (2%) developed SSE, 473 days post-LAA ligation. Of note, the same patient had also suffered an ischemic stroke at baseline (CHA2DS2VASc score of 8), prior to cardiac surgery. On the other hand, 4 of 26 patients with iLAA (15%) developed SSE (CHA2DS2VASc score of 4.0 ± 1.8), 348 ± 177 days post-LAA ligation (p=0.004). Also, patients with iLAA and SSE were younger than iLAA patients without SSE (63 ± 20 years versus 75 ± 7 years; p=0.032). None of the iLAA patients with SSE were receiving long-term OAC therapy, as compared with 73% of iLAA patients without SSE (p=0.004). In addition, those with SSE were all diagnosed with recurrent AF during long-term follow-up. Aside from the above differences, all other operative and postoperative findings were similar in iLAA patients with and without SSE. Moreover, as illustrated in Table 3, there were no differences in iLAA morphologies in patients with and without SSE.

Table 1: Baseline demographics of patients with closed left atrial appendage (cLAA) versus incompletely-closed LAA (iLAA)

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Table 2: Operative and postoperative findings in patients with closed left atrial appendage (cLAA) versus incompletely-closed LAA (iLAA) during 48 ± 19 months of follow-up

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Table 3: Incompletely-closed left atrial appendage (iLAA) morphologies in patients with and without stroke/systemic embolization (SSE)

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A Kaplan–Meier analysis illustrating time-to-event for cLAA and iLAA is shown in Figure 3. The annualized risk of SSE per 100 patient-years of follow-up was calculated to be 1.70% for the entire cohort, 3.86% for patients with iLAA, and 9.78% for iLAA patients not receiving long-term oral anticoagulation therapy. In a multivariate analysis, iLAA emerged as a significant predictor of SSE (OR=21.0, 95% CI: 1.9–232; p=0.01). Furthermore, presence of iLAA was found to be notable in Cox proportional hazards (time-dependent) regression, with a hazards ratio of 8.9 (95% CI: 1.0–81; p=0.04) likelihood of experiencing an SSE, as compared to cLAA.

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Figure 3: Kaplan–Meier analysis. A Kaplan–Meier curve showing the probability of SSE-free survival following surgical left atrial appendage (LAA) ligation (days) in patients with cLAA and iLAA.

Discussion

Stroke constitutes the most common lethal and disabling neurologic disease of adult life, and it also remains the most serious complication of AF.1 It has been proposed that the loss of atrial contraction in the setting of AF leads to reduced flow velocities in the LAA, thereby promoting stasis and thrombus formation within this structure.9 The above notion is consistent with findings from a recent systematic review of the literature, which found that in patients with non-valvular AF, 89% of intracardiac thrombi were localized to the LAA.2 Consequently, over the past six decades, the LAA has been extensively targeted for surgical exclusion.3 To date, a number of surgical techniques have been adopted for this purpose,3 and more recently several percutaneous options have been devised.10 The surgical techniques fall broadly into two categories: 1) surgical exclusion or 2) surgical excision. Within the exclusion domain are running or mattressed sutures with or without felt pledgets placed either on the epicardial or more commonly on the endocardial surface of the LAA.3 The most common techniques within the excision strategies include stapled excision or removal and oversew.3 Yet, despite long-standing clinical experience, the success of surgical LAA closure has yet to be systematically evaluated. Additionally, the criteria for cLAA have not been consistently defined. In various studies, they have ranged from a “lack of an anatomical structure remaining between the mitral valve base and the left superior pulmonary vein”4,5 to a “residual stump measuring <1 cm” or mere absence of “persistent flow into the LAA following surgical exclusion” as seen on transesophageal echocardiography.6 As such, the incidence of iLAA fluctuates widely among reported studies, varying anywhere from 10% to 80%.11 But the highest success rate appears to be commonly achieved with surgical excision.5,6

Principal findings

In this study, we evaluated the incidences of iLAA and SSE following surgical suture ligation performed in conjunction with mitral valve and/or Maze surgery in a contemporary cohort of patients with non-rheumatic AF. Several findings in this study are noteworthy. First, the incidence of iLAA in this study was 35%, which is indeed similar to that previously reported in the literature.47 Katz and colleagues4 evaluated 50 patients who underwent surgical LAA ligation in association with mitral valve surgery and similarly reported an iLAA in 36% of their patients. The incidence of iLAA was also investigated in the Left Atrial Appendage Occlusion Study (LAAOS).6 The authors concluded that cLAA proved challenging and operator-dependent, with postoperative transesophageal echocardiography demonstrating an iLAA in 34% of patients subjected to LAA closure using two different surgical techniques. Likewise, Kanderian and colleagues7 examined patients who underwent LAA closure by direct surgical excision, stapler, and suture ligation, and overall discovered an iLAA in 45% of patients (27% with excision, 77% with suture, and 100% with stapler closure). Several explanations have been proposed for the relatively high incidence of iLAA observed following surgical suture ligation.3 First, shallow suture bites used to avoid the adjacent circumflex coronary artery may be to blame. Second, an iLAA could also result from failure to extend the running sutures to the most distal edge of the LAA orifice. For instance, presence of a mitral annuloplasty ring or prosthesis can sometimes pose technical difficulties in this regard. Lastly, the LAA ostium itself can occasionally exhibit complicated anatomical shapes and configurations thereby creating additional technical challenges in achieving complete LAA closure.

Second, in this study, we observed a significantly higher incidence of SSE in patients with iLAA (15%) than cLAA (2%), despite similar CHADS2/CHA2DS2VASc risk scores in the two groups. That is, the CHADS2 and CHA2DS2VASc scores for iLAA patients with SSE and cLAA patients without SSE were in fact identical (both with a mean CHADS2 score of 2.0 and a CHA2DS2VASc score of 4.0). However, iLAA patients not receiving long-term OAC therapy exhibited an annualized SSE risk approaching ∼10% per 100 patient-years of follow-up. The latter risk was more than twice that predicted by conventional risk stratification schemes, virtually equivalent to a CHADS2 score of 4 or a CHA2DS2VASc score of 6. This suggests that conventional risk stratification schema may not offer accurate risk assessment in this particular setting. Moreover, iLAA was found to be an independent predictor of SSE (OR=21.0, 95% CI: 1.9–232, p=0.01) with a hazards ratio of 8.9 (95% CI: 1.0–81; p=0.04). It should be pointed out that these results are generally consistent with those from prior studies which have similarly suggested that presence of iLAA may predict an increased risk of thromboembolism.5,11 For instance, García-Fernández and colleagues5 evaluated 58 patients who underwent surgical LAA ligation and reported a lower incidence of embolic events at 6 years in those who underwent LAA closure (3% versus 17%; p=0.01). Additionally, a multivariate analysis found that absence of LAA ligation served as an independent predictor of embolic events (OR=6.7), and when identification of iLAA was taken into account together with the absence of cLAA the estimated embolic risk further increased to 11.9-fold.5 Katz and colleagues4 similarly studied patients with iLAA and discovered spontaneous echocardiographic contrast or frank thrombus within the iLAA in 9 of 18 patients not receiving OAC, and reported SSE in 4 of these patients (22%). Additionally, in the study by Kanderian and colleagues,7 the prevalence of thrombus identified within the iLAA with persistent flow was significantly elevated (46% with suture and 67% with stapler occlusion), with a late SSE rate of 15% in this patient cohort. Meanwhile, a number of other studies have reported strikingly elevated SSE rates that have been indirectly attributed to the presence of iLAA. For instance, in LAAOS,6 of the 52 patients who underwent concurrent LAA surgical exclusion and coronary artery bypass surgery, at least 12% developed thromboembolic events post-LAA closure, including 12 strokes and 13 transient ischemic attacks. Though the overall incidence of iLAA in this study was 34%, a clear relationship between embolic event rates and presence or absence of iLAA was not examined. Similarly, Bando and colleagues12 evaluated 812 patients who underwent mitral valve surgery and surgical LAA ligation. They determined that 72 patients (9%) experienced late SSE. Among these, 65% had received LAA ligation. But once again the incidence of iLAA among the stroke patients was not investigated. Collectively, these outcomes together with the findings from the current study support the notion that presence of iLAA may in effect be “worse” than no closure at all.11 Though the reason for this is not entirely clear, it is conceivable that due to its “stenotic” neck, iLAA could be associated with a “low-flow” state and increased stasis in turn promoting a greater risk of thromboembolism. The presence of extensive trabeculation and reduced peak flow have both been proposed to influence LAA stasis and thrombus formation.8,10,13 Since in most iLAA patients the overall LAA structure and trabeculae are still preserved, this may create a reduced flow state, in effect promoting an enhanced thromboembolic milieu within the residual LAA. Indeed, our unpublished transesophageal echocardiographic observations suggest that iLAA is invariably associated with reduced peak flow velocities (<20 cm/s), particularly in the setting of AF (Figure 4). Thus, it is plausible that the conventional SSE risk stratification schemes may not accurately predict the embolic risk in patients with iLAA, given the anatomical and physiological differences that govern the flow dynamics involving such an entity versus a non-ligated LAA. This is not entirely surprising. In fact, similar observations are encountered in patients with other distinct cardiac structural abnormalities as in the case of valvular (rheumatic) AF, which is associated with nearly 17-fold greater SSE risk that also remains independent of CHADS2/CHA2DS2VASc risk stratification scores.2

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Figure 4: Incompletely-closed left atrial appendage (iLAA) peak velocities on transesophageal echocardiography. iLAA in a patient with a post-LAA ligation stroke off oral anticoagulation (OAC), in AF, without (a) and with (b) color Doppler, and the latter illustrated when in sinus rhythm (c). As seen, the peak iLAA velocity is reduced (<20 cm/s) in this patient when in AF (b), but increases to >40 cm/s in sinus rhythm (c). (d) iLAA in another patient without SSE on long-term OAC therapy, in sinus rhythm. As seen, the peak iLAA velocity is markedly reduced in this patient (<10 cm/s) even in the absence of AF.

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Figure 5. Incompletely-closed left atrial appendage (iLAA) versus peri-Watchman device leak. Schematics illustrating the supposed patterns of flow and left atrial communication in patients with iLAA (a) and peri-Watchman leak (b). In the current study, the mean iLAA neck diameter (d) in patients with SSE measured 2.8 ± 1.0 mm. In a multicenter study evaluating the long-term outcomes associated with residual flow following percutaneous LAA closure using the Watchman device, the typical peri-Watchman leak (x) similarly measured 2.9 ± 1.0 mm. Yet, the latter was not shown to be associated with increased SSE risk. For now, the reason for this discrepancy remains unclear.

Other implications

As with surgical techniques, there are also limited data available on the incidence and long-term prognosis of iLAA following percutaneous LAA closure strategies. Yet, manifestation of iLAA following various types of endocardial and epicardial percutaneous LAA closure has been reported.1418 Moreover, in some cases, incomplete percutaneous LAA closure has also been associated with thrombus formation and ischemic stroke.14,15 But another study18 evaluating the long-term outcomes associated with residual flow following percutaneous LAA closure using the Watchman device found that despite presence of incomplete LAA closure in 32% of patients at 1 year, residual peri-device leaks were not associated with increased embolic risk. It is interesting to note that in that study the mean peri-Watchman leak measured 2.9 ± 1.0 mm, which is remarkably similar to the size of iLAA neck diameter (2.8 ± 1.0 mm) in patients who suffered SSE in the current study (Figure 5). For now, it remains unclear whether iLAA following percutaneous closure techniques behaves differently from those following surgical ligation or if these discrepant findings somehow reflect variations in embolic risk in diverse patient cohorts. Nonetheless, one may wonder whether in previous LAA closure trials a potential benefit derived from cLAA could in part have been offset by presence of iLAA in certain patients. LAAOS III, a large, randomized prospective trial designed to compare the efficacy of LAA closure for stroke prevention using excision versus stapled closure, to no closure at all,19 may ultimately address this quandary. For now, the findings from the PRAGUE-12 study20 seem encouraging. This study found that the incidence of stroke among those who underwent LAA surgical excision in conjunction with AF surgery was 2.7% at 1 year as compared with 4.3% in the control arm. Although this difference did not reach statistical significance, this may have been influenced by relatively small sample sizes and short-term follow-up. These results are indeed promising and provide further justification to investigate a clear role for cLAA in reducing the SSE risk in patients with AF.

Lastly, it should be emphasized that all cases of SSE encountered in this study occurred in patients not receiving long-term OAC therapy, suggesting that OAC is likely essential to effectively reduce the embolic risk in patients with iLAA. This also gives credence to the idea that at least certain patients with persistently elevated embolic risk and intolerance to long-term OAC may be considered for closure of iLAA using alternate strategies.21,22

Limitations

This study represents a single-center, non-randomized analysis of patients who underwent surgical LAA ligation with concomitant mitral valve and AF surgery. Additionally, CT angiography has never been validated as the test of choice for detection of iLAA. Although the interpreting radiologists in this study were specifically evaluating the CT examinations for presence/absence of this anatomical entity, it is conceivable that presence of iLAA could have been missed in certain cases thereby influencing the reported incidence of iLAA in this study along with the relevant findings. Finally, presence/absence of postoperative AF in this study was assessed using in-office, routine electrocardiograms and whenever present, using routine cardiac implantable electronic device interrogations. As such, the incidence of recurrent AF during follow-up could have been underestimated.

Conclusions

In this study, iLAA was detected in more than one-third of patients with non-rheumatic AF who underwent surgical suture ligation of LAA in conjunction with mitral valve and/or Maze surgery. Patients with this clinical entity experienced a significantly higher risk of SSE as compared to those with cLAA. Furthermore, in a multivariate analysis, iLAA emerged as a significant predictor of SSE. While no cases of SSE occurred in individuals receiving OAC therapy, patients with iLAA not receiving OAC exhibited an annualized risk of SSE approaching ∼10% per 100 patient-years of follow-up. This was more than twice that predicted using conventional risk stratification schemes. Hence, vigilant screening for iLAA and long-term OAC therapy in this high-risk cohort is strongly encouraged.

Acknowledgment

This study was supported by a St. Jude Medical research grant.

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