Acute Takotsubo cardiomyopathy after combined atrial ablation: Expanding the spectrum of postablation myocardial stunning

Key Teaching Points.

• •Takotsubo syndrome (TTS) is a rare but important complication after atrial fibrillation ablation, including pulsed field ablation, and may present with acute chest pain, marked troponin elevation, and ischemic electrocardiographic changes mimicking acute coronary syndrome.
• •Postablation TTS is likely mediated by a multifactorial process, including autonomic nervous system disruption from ganglionated plexi ablation, catecholamine surge, microvascular dysfunction, and procedural stress, even in the absence of immediate procedural complications.
• •Distinguishing TTS from acute coronary injury in the postablation setting is critical, given that management differs significantly; the presence of nonobstructive coronary arteries and characteristic apical ballooning with subsequent recovery supports the diagnosis.
• •Combined ablation strategies (eg, pulmonary vein isolation, cavotricuspid isthmus ablation, and slow pathway modification) may increase susceptibility to TTS by producing broader autonomic perturbation across both atria.
• •Marked troponin elevation does not exclude TTS, and reliance on biomarkers alone may be misleading; integration of imaging findings and coronary angiography is essential for accurate diagnosis.

Introduction

Stress-induced cardiomyopathy, also known as Takotsubo syndrome (TTS) or Takotsubo cardiomyopathy, is a reversible form of acute left ventricular (LV) systolic dysfunction precipitated by sudden emotional or physical stressors in the absence of severe coronary artery occlusion.¹ TTS is associated with elevated cardiac enzymes, ischemic electrocardiographic (ECG) changes, reduced LV ejection fraction (LVEF), and transient regional wall-motion abnormalities.¹ It often prompts urgent coronary angiography to exclude acute coronary syndrome. The exact pathogenesis of TTS remains unclear. The most common postulation is that TTS results from a reversible myocardial toxicity secondary to exceedingly elevated catecholamine levels.¹ Most patients recover cardiac function over the course of a few weeks to months with supportive therapy.

Despite the growing recognition of TTS, its occurrence after catheter ablation is rare, and mechanistic links, particularly with pulsed field ablation (PFA), are poorly defined. We report a case of Takotsubo cardiomyopathy developing within 24 hours of catheter ablation including pulmonary vein isolation (PVI) using pulsed field energy and both cavotricuspid isthmus (CTI) line ablation and slow-pathway modification using radiofrequency energy.

Case report

A 63-year-old woman recently diagnosed as having paroxysmal atrial fibrillation (AF), typical-appearing atrial flutter, and supraventricular tachycardia (SVT) presented for elective catheter ablation. Her AF was discovered by ambulatory ECG monitoring with a 3% AF burden after her left posterior cerebral artery ischemic stroke. She reported palpitations and dyspnea during her episodes of AF. Cardiac event monitoring also demonstrated evidence of a narrow-complex tachycardia consistent with SVT during which she reported dizziness and palpitations. Her baseline transthoracic echocardiogram (TTE) 3 months earlier demonstrated normal biventricular size and function (LVEF 65%–70%) with no significant valvular disease or evidence of intracardiac shunting by saline bubble study.

The procedure was done under general anesthesia. Baseline 12-lead ECG demonstrated sinus bradycardia with intact atrioventricular conduction, septal Q waves, and anterolateral T-wave inversions (Figure 1). Heparin was administered, and activated clotting time was maintained between 325 and 375 seconds. A decapolar deflectable catheter was used to cannulate the coronary sinus. She was in normal sinus rhythm with 1:1 atrioventricular conduction. Using intracardiac echocardiography, her LVEF was estimated at 55% with a trace pericardial effusion. No left atrial appendage thrombus was seen. An electrophysiological study was first performed, which induced an SVT with a cycle length of 400 ms. Using electrophysiological pacing maneuvers, the tachycardia was diagnosed as typical atrioventricular nodal reentrant tachycardia. Ablation including slow-pathway modification and CTI line ablation was deferred until after completion of planned PVI.

Figure 1.

Preablation electrocardiogram.

Transseptal left atrial access was performed using a FARADRIVE sheath system with a CONNECT dilator and a radiofrequency transseptal wire under fluoroscopic and intracardiac echocardiographic guidance. Electroanatomic mapping of the left atrium and all 4 pulmonary veins was performed with an Abbott HD Grid multielectrode mapping catheter and the Abbott EnSite 3-dimensional mapping system. Then, PVI was performed using a Boston Scientific pentaspline FARAPULSE catheter. No ST-segment elevations occurred during the procedure. Afterward, the Abbott EnSite catheter was used for postablative electroanatomic mapping, which confirmed adequate PVI with sparing of the posterior wall. Left atrial dwell time was 37 minutes. The sheath was withdrawn from the left atrium, and the Boston Scientific pentaspline FARAPULSE PFA catheter was exchanged for the Abbott TactiFlex radiofrequency ablation catheter. Slow-pathway modification was performed using radiofrequency energy with a maximum output of 30 watts for approximately 60 seconds resulting in an accelerated junctional rhythm without ventriculoatrial block or conduction delay. Afterward, using radiofrequency energy, ablation was performed in a line along the CTI where bidirectional block was achieved. Postablative electrophysiological study was performed with the addition of isoproterenol, and no SVT could be induced. Postablative intracardiac echocardiogram was performed again, which demonstrated normal LV systolic function and a trace pericardial effusion similar to baseline. The procedure was completed. She was successfully extubated and transferred to the recovery room in stable condition. She denied chest pain, dyspnea, or other acute symptoms before discharge. 12-lead ECG after ablation demonstrated sinus bradycardia with left axis deviation, poor precordial R-wave progression, and nonspecific ST-segment changes. She denied any symptoms and was discharged after 4 hours of bed rest.

Approximately 12 hours after discharge, she presented to our emergency department with acute substernal chest pain and marked troponin elevation to 39,000 ng/L. Her 12-lead ECG demonstrated sinus rhythm with intact atrioventricular conduction, normal axis, possible anteroseptal infarct, and nonspecific T-wave abnormalities (Figure 2). Urgent TTE revealed new severe LV dysfunction with apical and midventricular akinesis and preserved basal contractility (Figure 3A–3D), raising concern for left anterior descending artery infarction vs TTS. No LV thrombus was seen.

Figure 2.

12-hour postablation electrocardiogram.

Figure 3.

Transthoracic echocardiography demonstrating severe left ventricular systolic dysfunction with a stress cardiomyopathy pattern. A: Apical 4-chamber view demonstrating apical and midventricular akinesis with relative basal hyperkinesis. B: Apical 2-chamber view confirming regional wall-motion abnormalities involving the mid and apical segments. C: Alternative apical 4-chamber view demonstrating consistent apical ballooning morphology. D: Contrast-enhanced apical view demonstrating absence of left ventricular thrombus and improved delineation of endocardial borders.

Invasive coronary angiography demonstrated angiographically normal coronary arteries without obstructive disease, dissection, or vasospasm (Figure 4A–4D).

Figure 4.

Invasive coronary angiography demonstrating angiographically normal epicardial coronary arteries. A and B: Right coronary artery in multiple projections without evidence of obstructive disease, dissection, or flow limitation. C and D: Left coronary system demonstrating a patent left anterior descending and left circumflex artery with preserved distal flow and no angiographic evidence of stenosis, thrombus, or vasospasm.

LV end-diastolic pressures were normal. In the absence of coronary pathology, the constellation of acute chest pain, ECG changes, troponin elevation, and apical ballooning pattern was most consistent with Takotsubo cardiomyopathy occurring after catheter ablation. She was started on guideline-directed medical therapy for new heart failure with reduced ejection fraction. Her chest pain resolved during this admission. Repeat TTE almost 3 months later demonstrated significant improvement of her LV systolic function with ejection fraction of 50%–55% and residual hypokinesis of the mid- and distal anterolateral wall segments (Figure 5A–5C).

Figure 5.

3-month follow-up transthoracic echocardiography demonstrating recovery of left ventricular systolic function. A: Apical 4-chamber view demonstrating improved global systolic function with resolution of previous apical ballooning. B: Contrast-enhanced view confirming improved endocardial definition and absence of left ventricular thrombus. C: Alternative apical view demonstrating residual mild hypokinesis of the mid- to distal anterolateral wall segments.

Discussion

TTS after catheter ablation of AF is a rare complication. Postablation chest pain accompanied by diffuse repolarization abnormalities and high troponin levels typically prompt urgent evaluation for coronary injury, pericardial complications, or myocardial infarction. In this context, our case is notable because it demonstrates severe myocardial injury markers and classic apical ballooning after uncomplicated PVI using PFA, slow-pathway modification, and CTI ablation with completely normal epicardial coronary vessels. As AF ablation volumes increase worldwide, distinguishing TTS from life-threatening causes of postablation chest pain is essential.

Although the literature on postablation TTS is limited, important patterns have emerged. A 2024 systematic review by Desai et al¹ identified only 13 published cases with 18 patients total who developed TTS after ablation therapy. The clinical pattern among these cases remarkably showed nearly 78% of affected patients being postmenopausal women, all events occurring within 4 days of ablation, and apical ballooning being present in 86% of cases.¹ Although more than 90% of patients documented in the review were noted to have a full recovery, almost 45% experienced serious complications, including ventricular arrhythmias and cardiogenic collapse.¹ This illustrates the clinical relevance of TTS as a complication of ablative therapies.

A unifying theme across literature is that postablation TTS arises from a multifactorial interaction of autonomic disruption, catecholamine surges, microvascular dysfunction, and procedural stress. A widely supported mechanistic pathway involves autonomic nervous system disruption. Ablation near the pulmonary veins directly affects ganglionated plexi that modulate cardiac parasympathetic tone.² Derntl et al² observed postablation increases in sinus rate and decreases in heart-rate variability, suggesting ablation-induced vagal withdrawal with sympathetic predominance. Liu et al³ added to these findings by documenting measurable reductions in parasympathetic activity after PVI, reinforcing autonomic imbalance as a priming mechanism for TTS. The systematic review by Desai et al¹ further highlighted autonomic disruption as the dominant mechanistic theme across cases.

This autonomic disruption may potentiate catecholamine-mediated myocardial toxicity, another well-established driver of TTS pathophysiology. Catecholamine excess can induce myocardial stunning, coronary microvascular dysfunction, and epicardial vasoconstriction.^1,4 Several reports demonstrated this mechanism in postablation settings. Khan et al⁴ described recurrent TTS precipitated by severe bradycardia followed by epinephrine administration during cryoballoon ablation, illustrating how sudden adrenergic surges can trigger ventricular ballooning. Even in the absence of exogenous catecholamines, some cases demonstrated progressive QT prolongation, diffuse T-wave inversion, and disproportionate troponin elevation, consistent with catecholamine-induced myocardial stunning.^5,6 Our patient’s extreme troponin elevation (∼30,000 ng/L) and dynamic repolarization abnormalities may similarly support a neurohormonal mechanism despite the absence of coronary obstruction.

Coronary microvascular dysfunction and vasospasm also represent additional mechanistic contributors. Lesions resulting from ablation may provoke localized inflammation, endothelial disruption, or an imbalance in autonomic input that alters coronary tone.³ Liu et al³ emphasized coronary spasm and microvascular ischemia as contributors to TTS after ablation, even when angiography is normal. In addition, a unique aspect of our case is TTS after the use of PFA, which is a recognized cause of coronary vasospasm especially with application near the coronary arteries.⁷ Although PFA is often described as tissue selective, emerging data suggest that it may still influence adjacent autonomic ganglionated plexi and coronary vasomotor tone depending on lesion location.⁷ The duration of these autonomic effects remains uncertain and may differ from conventional thermal ablation strategies. However, PFA in our case was restricted to the areas necessary for PVI and no acute ST-segment elevations or LV systolic dysfunction was noted during or immediately after catheter ablation. Delayed coronary vasospasm in cases after PVI with posterior wall isolation has been reported; however, the mechanism is not clear.⁸ In our case, despite normal epicardial coronaries, the combination of severe chest pain, marked troponin release, and apical ballooning could suggest the possibility of remote left anterior descending artery vasospasm with residual myocardial stunning, especially given the marked improvement in LVEF during follow-up. Given the marked troponin elevation, coronary embolization or myocardial infarction without obstructive coronary artery disease was also considered in the differential diagnosis. However, this was felt to be less likely given therapeutic anticoagulation, the absence of intraprocedural ST-segment elevation, normal coronary angiography without focal obstruction or distal flow limitation, and the characteristic apical ballooning pattern extending beyond a single coronary territory. In addition, immediate postprocedural intracardiac echocardiography demonstrated preserved LV systolic function, supporting a delayed rather than immediate ischemic insult. Cardiac magnetic resonance imaging may have further strengthened diagnostic certainty by evaluating for ischemic scar or late gadolinium enhancement and should be considered in similar future cases.⁹

Procedural and physiological stress may further augment susceptibility. Ablation provokes sympathetic activation through thermal injury, rapid atrial pacing, sedation-related hemodynamic changes, and patient anxiety. Psychological or emotional vulnerability may also amplify this adrenergic response.⁶ In addition, the severity spectrum of postablation TTS is broad. 1 case described a fulminant TTS presentation culminating in pulseless electrical activity immediately after ablation, illustrating how closely the TTS can mimic catastrophic procedural complications.¹⁰ Furthermore, Takotsubo cardiomyopathy has been described after administration of isoproterenol,¹¹ which was used during our case. Therefore, although TTS after the use of PFA is not well described, the clinical presentation in our case was likely multifactorial, with potential contributions from PFA, radiofrequency ablation, isoproterenol administration, autonomic perturbation, and procedural stress. Although our patient did not experience intraprocedural instability, her subsequent presentation with significant chest pain, repolarization abnormalities, and marked troponin elevation 24 hours after ablation reinforces that TTS can manifest as a dramatic, high-risk clinical syndrome even in the absence of procedural complications or immediate hemodynamic collapse.

Furthermore, the extent and distribution of ablation lesions may also influence risk. Several cases of patients who underwent additional posterior wall or superior vena cava isolation highlight broader lesion sets among TTS presentations.^1,2,10 Larger ablation burdens likely disrupt wider autonomic networks.² Our case contributes insight by demonstrating that TTS can follow combined PVI and CTI ablation, potentially implicating multiregional ganglionated plexus modulation as an amplifying factor. By engaging both left and right atrial autonomic networks, this combination may create a more profound autonomic shift, potentially lowering the threshold for TTS. Formal autonomic metrics such as heart-rate variability were not collected, limiting further assessment of autonomic imbalance in this case.

An additional consideration in our patient is her previous posterior circulation ischemic stroke, given that cerebrovascular injury has been associated with autonomic dysregulation and sympathetic overactivity.¹² The baseline ECG demonstrated repolarization abnormalities, including precordial T-wave inversions and prominent U waves, which may reflect altered autonomic tone. It is possible that preexisting autonomic vulnerability related to previous stroke, combined with vagal denervation and procedural adrenergic stress during ablation, collectively lowered the threshold for development of TTS in this case.

Despite marked troponin elevation and apical myocardial dysfunction, significant recovery, as seen in our case, is consistent with the >90% normalization rate reported in the literature. Importantly, the magnitude of troponin elevation in TTS can overlap with acute coronary syndromes, making reliance on biomarkers alone insufficient for diagnosis. Instead, the combination of nonobstructive coronaries, characteristic wall-motion patterns, and rapid functional recovery should prompt consideration of TTS in the postablation setting.

Conclusion

Postablation TTS seems to result from a convergence of autonomic denervation, catecholamine excess, microvascular dysfunction, and procedural stress. This case expands current understanding by illustrating TTS after PVI and CTI ablation, demonstrating an unusually high troponin elevation despite unobstructed coronaries. Furthermore, TTS after the use of PFA is not well described and may be an important trigger. As AF ablation volume and lesion complexity continue to expand, electrophysiologists should maintain heightened awareness of TTS as a potential cause of postprocedural chest pain, ECG abnormalities, or biomarker elevation. Early recognition is essential to differentiate TTS from emergent procedural complications and guide appropriate supportive care, enabling the high likelihood of full recovery.

Funding Sources

This research was supported (in whole or in part) by The University of Tennessee Health Science Center (UTHSC) and UTHSC-affiliated entity. The views expressed in this publication represent those of the authors and do not necessarily represent the official views of UTHSC or any of its affiliated entities.

Disclosures

The authors have no conflicts of interest to disclose.