Clinical and Electrophysiological Characteristics of Patients Developing Macroreentrant Atrial Tachyarrhythmias Following Cardiac Surgery: A Retrospective Cohort Study

ABSTRACT

Introduction

Macroreentrant atrial tachycardias (MRAT) predominate the atrial arrhythmias in patients with operated heart disease, and advances in interventional electrophysiology and catheter ablation technology have pioneered a shift in their management.

Methods

We retrospectively analyzed clinical, procedural, and outcome data from a cohort of patients who had undergone radiofrequency (RF) ablation for MRAT (utilizing high‐density atrial mapping) following cardiac surgery for congenital or acquired heart disease.

Results

Forty‐one patients underwent ablation for a MRAT from 2016 to 2023. These patients had a mean age of 50.17 ± 11.71 years and had undergone cardiac surgical intervention a median of 18 years prior to first presentation with atrial tachyarrhythmia. The commonest repaired lesion was a surgically corrected atrial septal defect. None of the studied patients had a left‐sided macro reentrant circuit. The patients were followed up for a median duration of 2 years following ablation. Twenty‐five patients (60.9%) had CTI‐dependent atrial flutter (AFl). Using a strategy of high‐density activation and voltage mapping and entrainment mapping to define the tachycardia circuit, an acute success rate of 95.1% was noted. Our population continued to do well on medium‐term follow‐up, with 90.2% of patients tachycardia‐free at 2 years. However, seven patients (17.1%) developed sinus bradycardia requiring pacing, and three patients (7.3%) developed incident atrial fibrillation.

Conclusions

A meticulous approach to MRAT mapping utilizing a combination of newer high‐density mapping catheters with entrainment mapping yields high rates of acute (95.1%) and medium‐term success (90.2%) in patients with antecedent cardiac surgery.

In patients with repaired congenital heart disease and macro reentrant atrial tachycardias, a strategy of high‐density mapping, using a combination of isochronal late activation mapping, activation timing, voltage mapping, and entrainment mapping along with selective ablation targeted to the critical isthmi yields excellent (90%) arrhythmia‐free medium‐term survival.

1. Introduction

As the long‐term survival of patients with operated congenital heart disease improves [1], the challenges faced by physicians managing these patients have grown many manifolds [2]. Particularly in the developing world, where unoperated congenital heart disease and late surgical repairs are rampant and access to adequate healthcare is limited [3], the management of these patients can prove to be especially difficult.

From the perspective of the cardiac electrophysiologist, arrhythmias frequently complicate the natural history of repaired congenital heart disease [4]; the most prevalent of these are atrial tachyarrhythmias with a lifetime risk of nearly 50% [5, 6]. Macroreentrant atrial tachycardias (MRAT) predominate the atrial arrhythmias in this population, and advances in interventional electrophysiology and catheter ablation technology have pioneered a shift in the approach to management for these patients [7]. Historically, outcomes with catheter ablation have demonstrated high acute success rates but significant rates of symptomatic recurrence over long‐term follow‐up [8]. The advent of superior electro‐anatomical mapping technologies, high‐density mapping catheters [9, 10], and a better understanding of tachycardia mechanisms have independently been shown to be helpful in clarifying the arrhythmogenic substrate; hence, simplify the ablation procedure.

Given a paucity of data with current ablation technologies, the magnitude of benefit of these advancements on tachycardia‐free survival in this population remains unclear. We designed this study to assess the clinical outcomes of radiofrequency catheter ablation in patients with MRATs following surgical intervention for congenital or acquired heart disease.

2. Methods

We conducted a retrospective cohort study at a single tertiary care center in Southern India, recruiting all patients who underwent catheter ablation for MRAT following surgical intervention for congenital or acquired heart disease during the study period from January 2016 to July 2023.

The primary objective was to define the predictors of acute procedural success and atrial flutter‐free survival over medium‐term follow‐up in our study population. Secondary objectives were to define the clinical, demographic, electrocardiographic, and echocardiographic characteristics of these patients, to assess the prevalence and clinical impact of comorbid tachy‐ (atrial fibrillation, in particular) and brady‐ (especially sinus node dysfunction) arrhythmias in this population, and to study the anatomical patterns of and techniques for ablation in atypical atrial flutter.

We included for analysis all patients older than 10 years of age who had undergone a MRAT ablation procedure over the study period, had an antecedent history of cardiac surgery and had undergone atrial mapping using a multipolar, high‐density (Advisor HD grid, Abbott Cardiovascular). Patients with an unclear or ambiguous electrophysiological diagnosis, with missing baseline clinical data, and with less than 6 months of follow‐up post‐procedurally were excluded from further analysis. “Typical” flutter (cohort 1) was defined as cavo‐tricuspid isthmus (CTI)‐dependent clockwise or counterclockwise right atrial flutter. All other MRAT were classified as “atypical” atrial flutter (cohort 2), including other CTI‐dependent tachycardias (e.g., dual‐loop reentry; lower loop reentry).

Patient clinical and follow‐up details, as well as details regarding the undergone electrophysiological procedure were obtained from review of electronic medical records, electrophysiology reports, and electrophysiology study data (including three‐dimensional electro‐anatomical maps). The management strategy for patients prior to ablation varied per the decision of the treating electrophysiologist, but included one or more of anti‐arrhythmic drug use, elective cardioversion, or radiofrequency ablation. All patients had been followed up with periodic clinical evaluations and 12‐lead electrocardiograms. The project received institutional ethical clearance as part of an established institutional atrial flutter registry. As the study was a retrospective, anonymized review of records, individual patient consent was not sought.

Although the data has been accrued retrospectively, the laboratory protocol remained uniform over time and across operators. All procedures were performed under three‐dimensional electro‐anatomical impedance‐based mapping using an Ensite Precision (Abbott Cardiovascular, St. Paul, Minnesota) mapping system. High‐density mapping utilizing a multipolar mapping catheter (Advisor HD Grid Mapping Catheter) was performed for all patients. As nearly all patients in the study were in tachycardia at the time of the procedure, an initial activation and voltage map was prepared during tachycardia to define the arrhythmia circuit and delineate scar. Additionally, isochronal late activation maps (ILAM) were created in all patients and used to identify zones of deceleration or conduction block (Figure S1). Finally, entrainment mapping was performed in all patients where it was feasible (barring patients with unstable or excessively rapid tachyarrhythmias and those with atrial non‐capture at candidate sites), initially from the distal coronary sinus electrodes (to exclude a left atrial mechanism) and catheters placed just medial and lateral to the CTI. Then entrainment was performed from potential sites that could represent tachycardia isthmus (in particular, from all points with fragmented signals or split potentials and in regions of isochronal crowding). The default strategy was abolishing the conducting channel along with ablation of the CTI using a 4‐mm tip irrigated ablation catheter (FlexAbility Ablation Catheter, Abbott Cardiovascular, St. Paul, Minnesota) with nominal irrigation flow rates set to 17 mL/min during ablation. Power‐controlled temperature‐limited ablations were performed with power set to 25–30 W and a temperature limit of 43°C. Ablation was performed targeting a rapid impedance drop, and stopped with an impedance drop of at least 10 Ω and a reduction of ~80% in the local high‐resolution electrogram. Scar‐homogenization was only considered for patients where the isthmus could not be exactly defined as entrainment mapping was not possible or inconclusive. In all patients who underwent scar modification, additional ablation lesions connecting the scar to the CTI line were performed. Acute success was defined by the termination of tachycardia during ongoing ablation, the demonstration of conduction block across the predefined isthmus, and non‐inducibility of tachycardia at the end procedure. Following successful ablation, tachycardia induction was attempted in all patients by performing double extra‐stimuli (till atrial effective refractory period) and incremental pacing (down to a pacing cycle length of 200 ms).

Statistical analysis was performed using an SPSS software package [11]. Associations were assessed between the two cohorts and demographic variables using a chi‐square test for categorical independent variables and an unpaired sample t‐test for continuous independent variables. A similar protocol was followed to assess univariate relationships with acute procedural outcomes. The data thus collected was utilized to select variables for a multivariate logistic regression model to predict acute procedural outcomes. Finally, Kaplan–Meier analysis was performed to compare tachycardia‐free survival in patients with typical and those with atypical atrial flutter.

3. Results

Over the study period, 100 patients with MRAT underwent radiofrequency ablation at our center. Of these, record review identified 41 patients who had undergone prior cardiac surgery. Per data gathered during electrophysiology study, 25 of our 41 patients (60.9%) were determined to have typical (CTI‐dependent clockwise or counterclockwise flutter), with the remainder having an atypical right‐atrial flutter.

The demographic and clinical characteristics of the study population are presented in Table 1. Our patients had a mean age of 50.17 ± 11.71 years, with an age range of 22–76 years. The genders were evenly distributed (22 male patients; 53.7%). Coexistent noncardiac comorbid illnesses, including type 2 diabetes, hypertension, obesity, pulmonary disease, and dyslipidemia, conventionally considered risk factors for atrial flutter, were uncommon in our study population. The patients had undergone cardiac surgery a median of 18 years (Interquartile range [IQR] 12–32.25 years) prior to first presentation with atrial tachyarrhythmia. One (2.9%) patient had comorbid atrial fibrillation prior to flutter ablation, and an additional three patients (7.3%) developed atrial fibrillation on follow‐up. 16 (40%) patients had received prior rhythm control interventions (including synchronized direct current cardioversion in 12 [29.3%] and prior radiofrequency ablation in 5 [12.5%] patients) and had developed symptomatic recurrences despite therapy. Prior failed attempts at rhythm control therapy were significantly more common in patients with atypical flutter. Left ventricular function was well preserved in most of these patients (mean left ventricular ejection fraction [LVEF] 58.3% ± 8.8%, six patients (14.6%) had left ventricular systolic dysfunction at baseline assessment (defined as a LVEF ≤ 50%)). Follow‐up echocardiographic data was available for four of the six patients with left ventricular dysfunction; all four of these had a recovered systolic function (LVEF > 50%) following atrial flutter ablation.

TABLE 1.

Clinical and demographic characteristics of the study population.

Variables	All patients	Typical flutter (N = 25)	Atypical flutter (N = 16)	p
Demographic and clinical characteristics
Age (years) (Mean ± SD)	50.17 ± 11.7	51.68 ± 12.0	47.81 ± 11.2	0.808
Male sex number (%)	22 (53.7%)	14 (56%)	8 (50%)	0.707
Comorbid diseases (N (%))
Hypertension	4 (9.8%)	3 (12.0%)	1 (6.3%)	0.545
Diabetes	4 (9.8%)	4 (16.0%)	0	0.092
Dyslipidemia	2 (4.9%)	1 (4%)	1 (6.3%)	0.591
Coronary artery disease	6 (14.6%)	5 (20%)	1 (6.3%)	0.224
Atrial fibrillation	3 (7.5%)	1 (4.3%)	2 (12.5%)	0.455
Prior attempt at rhythm version (cardioversion, drugs, or ablation) (N (%))	16 (40%)	6 (25%)	10 (62.5%)	0.018
Prior cardioversion	12 (29.3%)	5 (20%)	7 (43.8%)	0.170
Prior anti‐arrhythmic drug therapy	15 (37.5%)	6 (25%)	9 (56.3%)	0.046
Prior ablation	5 (12.5%)	1 (4%)	4 (25%)	0.051

Significant P‐values (<0.05) are marked in bold font.

The commonest repaired lesions were atrial septal defects (ASD) (28 patients [68.29%]: 20 patients [48.8%] with ostium secundum defects and 8 patients [19.5%] with sinus venosus defects). In nearly all patients with repaired ASDs (27 patients [96.4%]), surgical access was obtained via a right anterolateral atriotomy. A detailed description of echocardiographic findings and surgical details is provided in Table 2. All these unselected post‐surgical patients had a right atrial origin of macroreentrant atrial tachycardia. The vast majority of these patients had demonstrable right atrial scar on voltage mapping (35 patients [85.3%]; 24 [68.6%] with anterolateral scar and 11 [31.4%] with a posterior or posterolateral scar). CTI‐dependent flutter was the etiological diagnosis in 25 patients (60.9%), with only one of these patients having clockwise right atrial activation during the study. Two patients with a primary diagnosis of CTI‐dependent flutter received concomitant ablation lesions in the region of right atrial posterior wall scar; the remainder received a single lesion set in the CTI region. Acute procedural success was noted in all but one patient with typical flutter. The remainder (16 patients [39.1%]) had atypical right atrial macroreentrant atrial tachycardia with anterolateral wall scar related reentry in eight patients and posterior wall scar‐related reentry in six patients. Nearly all patients with atypical flutter received multiple sets of radiofrequency lesions (detailed in Table 3). In most patients (14 patients, 87.5%) ablation was directed to the protected isthmus (procedural details elaborated below). Additional CTI‐dependent flutter was inducible in 10 patients (62.5%) with programmed stimulation. Consequently, ablation of the CTI region in addition to ablation of the protected isthmus of the primary tachycardia circuit was performed in 11 patients (68.8%) with atypical flutter. Acute procedural failure was noted in two of these patients. No major acute procedural complications were noted in either subgroup.

TABLE 2.

Structural heart abnormalities and echocardiographic findings.

Variables	All patients	Typical flutter (N = 25)	Atypical flutter (N = 16)	p
Nature of structural heart defect (N (%))
Repaired ostium secundum atrial septal defect	20 (48.8%)	10 (40%)	10 (62.5%)
Coronary artery disease with left ventricular dysfunction	6 (14.6%)	4 (16%)	2 (12.5%)
Repaired sinus venous atrial septal defect	8 (19.5%)	7 (28%)	1 (6.25%)
Repaired total anomalous pulmonary venous connection	3 (7.3%)	1 (4%)	2 (12.5%)
Repaired tetralogy of fallot (or TOF physiological variants)	2 (4.9%)	2 (8%)	0
Repaired atrioventricular canal defect	2 (4.9%)	1 (4%)	1 (6.25%)
Elapsed duration since prior cardiac surgery (Median [IQR]) (years)	18 (12–32.25)	16 (11–24)	29 (17–34.5)	0.697
Echocardiographic parameters
Left ventricular systolic dysfunction (N (%))	6 (15%)	4 (16.7%)	2 (12.5%)	0.718
Left ventricular ejection Fraction (%) (Mean ± SD)	58.25 ± 8.8	59.0 ± 8.5	57.1 ± 9.3	0.725
Left atrial size (mm) (Mean ± SD)	38.2 ± 6.5	39.1 ± 6.8	36.8 ± 6.2	0.752
Left ventricular internal diastolic dimension (mm) (Mean ± SD)	44.2 ± 5.8	43.4 ± 5.3	45.2 ± 6.5	0.291
Left ventricular internal systolic dimension (mm) (Mean ± SD)	30.3 ± 6.2	29.3 ± 5.4	31.8 ± 7.1	0.210

TABLE 3.

Characteristics of the ablation procedure and procedural outcomes.

Variables	All patients	Typical flutter (N = 25)	Atypical flutter (N = 16)
Ablation characteristics (N (%))
Inducible tachycardia
CTI‐dependent	35 (85.4%)	25 (100%)	10 (62.5%)
Counterclockwise	34 (75.6%)	24 (96%)	10 (62.5%)
Atypical RA MRAT site
Anterior‐anterolateral wall	8 (19.0%)		8 (50%)
Posterior‐posterolateral wall	6 (14.6%)		6 (37.5%)
Lower loop reentry	2 (12.5%)		2 (12.5%)
Site of RA scar
Anterior‐anterolateral	24 (58.5%)	16 (64%)	8 (50%)
Posterior‐posterolateral	11 (26.2%)	5 (20%)	6 (37.5%)
No scar	6 (14.6%)	4 (16%)	2 (12.5%)
Ablation strategy
Ablation of identifiable protected isthmus	39 (95.1%)	25 (100%)	14 (87.5%)
Substrate modification	3 (7.3%)	1 (4%)	2 (12.5%)
CTI ablation	36 (87.8%)	25 (100%)	11 (68.8%)
> 1 circuit identified and ablated	12 (29.3%)	2 (8%)	10 (62.5%)
> 2 circuits ablated	5 (12.2%)	0	5 (31.3%)
Acute success rate	39 (95.1%)	24 (96%)	15 (93.75%)
Follow‐up
Follow‐up duration (Median (IQR)) (years)	2 (1.75–4)	2.5 (2–3.25)	2 (1–5.5)
Tachycardia‐free survival (N (%))	37 (90.2%)	23 (92%)	14 (87.5%)
Repeat ablation (N (%))	3 (7.3%)	1 (4.3%)	2 (12.5%)
Symptomatic sinus dysfunction (requiring pacing) (N (%))	7 (17.1%)	4 (16.7%)	3 (18.8%)
Incident atrial fibrillation (N (%))	3 (7.3%)	1 (4.3%)	2 (12.5%)

On univariate analysis, none of the tested candidate variables including age at diagnosis, the presence of comorbid structural heart disease, the history of prior cardiac surgery, echocardiographic parameters, the receipt of prior rhythm control therapy, the presence of additional tachycardia, or acute procedural success were significantly associated with tachycardia‐free survival at 2 years. Part of this may be attributed to the low event rate in our population. On survival analysis, tachyarrhythmia‐free survival was not different in patients with typical and those with atypical flutter (Figure 1).

FIGURE 1.

Kaplan–Meier survival curves of our study population demonstrating no significant difference in recurrence free survival in patients undergoing catheter ablation for typical versus atypical flutter (HR: 0.84 [0.63–1.05]).

Over a median follow‐up duration of 2 years (IQR 1.75–4 years), four patients (9.8%) developed symptomatic recurrence of atrial flutter necessitating rhythm control therapy (overall recurrence free survival at 2 years: 90.2%), and seven patients (17.1%) developed symptomatic bradycardia (all with sinus node dysfunction) requiring permanent atrial‐based pacing. Over this period, none of the patients developed cardiac decompensation requiring hospital admission (except for dysrhythmias as described above), no patients required redo surgery, and none succumbed to their illness.

4. Discussion

It is established that nearly 5% of patients surviving to adulthood with unrepaired or repaired congenital heart disease will develop atrial tachyarrhythmias [12]. The risk is higher in patients with complex congenital heart disease [13] and increases with advancing age [6]. Atrial arrhythmias in this population are harbingers of abnormal cardiac hemodynamics and adverse clinical events [6]. It becomes imperative, thus, to discuss the mechanisms of MRAT in these patients.

In contrast to more homogenous data from western studies, our study population was epidemiologically distinct in certain important ways. Firstly, while the estimated Indian prevalence of congenital heart disease at an estimated 9/1000 live births is congruent [3] with available global data [14] (8–12/1000 live births), a large population at risk makes the overall number of cases quite large at an estimated 240 000 incident cases each year in the country [15]. Furthermore, a multitude of factors including a lack of awareness, limited access to healthcare, and financial constraints drive the delay in seeking healthcare for congenital heart disease surgical intervention in the country, with a large proportion of patients undergoing reparative surgeries at older ages and in adulthood [16].

The predilection of this population to CTI‐dependent flutter merits some discussion. Two clinical factors in these patients would explain this conundrum. The first is the presence of a fixed line of block secondary to atriotomy scar formation in nearly all these patients. A fixed or functional inter‐caval line of block has been shown to be important to the mechanism of induction of stable typical atrial flutter [17, 18]. Furthermore, dilatation of the right atrium in these patients would not only promote anisotropic conduction slowing across the CTI but has also been demonstrated to correlate with a longer flutter cycle length [19] (this atrial conduction slowing should enable the sustenance of reentry with even minimal slowing across the CTI). Our ablation protocol yielded favorable results, with 90.2% patients having tachycardia‐free survival at 2 years.

The Achilles' heel of atrial flutter ablation in this population appears to be concomitant sinus node dysfunction [20]. Congruent with predicted rates, seven (17.1%) of our patients had symptomatic bradycardia on follow‐up requiring permanent pacemaker implantation, representing the most frequent adverse patient event on medium‐term follow‐up. Importantly, while the study population was small, the prevalence of symptomatic bradycardia was evenly distributed across groups segregated per type of structural abnormality, with no significant predilection for patients who had undergone repair for sinus venosus defects or anomalous pulmonary venous drainage.

There remains a paucity of data on the ablative management and long‐term follow‐up of patients with MRATs following cardiac surgery. In contrast to conventional data [8, 21], our study demonstrates that with current mapping technologies and a meticulous approach to define the circuit, these patients tend to do quite well on follow‐up. Despite adding thus to current literature, the study does suffer from certain limitations. Firstly, this study population represents retrospective data from a single Indian centre and is hence intrinsically subject to a selection bias based on institution‐specific patient selection processes and to a potential information bias driven by the dependence on the electronic medical record system. Furthermore, in spite of a high population prevalence of operated rheumatic heart disease with atrial tachycardia, this group was underrepresented in this study, reflecting an institutional preference to manage these patients with medical therapy. Finally, being a retrospective study, our sample size was limited by the available patient data over the duration of the study period, and some populations (e.g., patients with left atrial flutter) have too small a representation to support robust statistical analysis.

Ethics Statement

The study has been duly approved by the institutional ethics committee at Sree Chitra Tirunal Institute of Medical Sciences and Technology, Thiruvananthapuram.

Consent

As the study entailed retrospective review of available hospital records, individual patient consent was not sought.

Conflicts of Interest

The authors declare no conflicts of interest.

Supporting information

Figure S1. Representative maps from selected patients (A, B) Case 1: A lady in her early 20s who had undergone surgical closure of an ostium secundum atrial septal defect 11 years prior. (A) Isochronal late activation mapping (ILAM) demonstrates a channel of isochronal crowding in the posterolateral right atrium. Electrograms at this site (*) demonstrated low amplitude multicomponent late diastolic signals and entrainment mapping confirmed this site to be the isthmus. (B) The tachycardia slowed and subsequently terminated within three burns to this narrow isthmus. (C–E): Case 2: A lady in her early 30s having undergone surgical closure of a superior sinus venosus defect 30 years prior (C) ILAM demonstrating a channel in the scar on the posterolateral right atrial wall. Note the isochronal crowding in this region and the local electrograms recorded by the high‐density (HD) mapping catheter. Vector A1‐B1 demonstrates multicomponent low voltage signals starting mid‐to‐late diastole and spanning nearly half of the tachycardia cycle length. Entrainment mapping from the site confirmed this to be the critical isthmus (D) The corresponding voltage map during tachycardia, using a definition of voltage 0.1–1.00 mV to define border‐zone, is notable for the presence of a border‐zone area in the region of this isthmus (E) Ablation at the above site led to slowing of the tachycardia cycle length with a change in the activation pattern. This second flutter was successful entrained and terminated with ablation in the cavo‐tricuspid isthmus (CTI). (F) Case 3: A gentleman in his late 20s with a history of surgical Tetralogy of Fallot repair 12 years prior (Trans‐right atrium dacron patch ventricular septal defect closure and pulmonary valve sparing repair). Note the dense scar in the lateral right atrium. The yellow dots represent areas of fragmented atrial signals. The activation and entrainment maps were, however, consistent with a counterclockwise CTI‐dependent flutter and the tachycardia terminated during CTI ablation with no other inducible atrial arrhythmias. Per institutional protocol, no further right atrial ablation or scar homogenization was attempted.

Makkar N., Abhilash S. P., Mohanan Nair K. K., et al., “Clinical and Electrophysiological Characteristics of Patients Developing Macroreentrant Atrial Tachyarrhythmias Following Cardiac Surgery: A Retrospective Cohort Study,” Journal of Arrhythmia 41, no. 4 (2025): e70146, 10.1002/joa3.70146.

Data Availability Statement

Anonymized patient data can be made available on request.