Seizure-induced Takotsubo cardiomyopathy mimicking STEMI: A case report

S. Ajay1, S. Aravindakumar2

1DNB Cardiology resident, Kauvery Heart city, Trichy

2Chief consultant and interventional cardiologist, Kauvery Heart city, Trichy

Abstract

We present the case of a 73-year-old female with no prior history of cardiac or neurological disorders who experienced transient loss of consciousness followed by fluctuating levels of consciousness. Electrocardiography (ECG) revealed significant ST-segment elevation, and echocardiography demonstrated mid-apical hypokinesia with reduced ejection fraction. Coronary angiography showed normal coronary arteries, leading to a diagnosis of Takotsubo cardiomyopathy (TTC), likely precipitated by a neurological event. This case underscores the importance of considering TTC in patients presenting with acute coronary syndrome (ACS) symptoms, especially when triggered by neurological events such as seizures. The diagnostic limitation of not performing an EEG during the altered mental status episodes is also highlighted.

Introduction

Takotsubo cardiomyopathy, also known as stress-induced cardiomyopathy or “broken heart syndrome,” is characterized by transient left ventricular dysfunction, typically presenting with apical ballooning. First described in Japan, the condition often mimics acute myocardial infarction (AMI) but lacks obstructive coronary artery disease. Emotional or physical stressors frequently precede TTC episodes, with seizures identified as potential triggers. Understanding the interplay between neurological events and cardiac manifestations is crucial for accurate diagnosis and management.

This case highlights the diagnostic challenge of distinguishing seizure-induced TTC from true acute coronary syndrome, as well as the difficulty in confirming non-convulsive status epilepticus (NCSE) when EEG is not performed during the periods of altered mental status.

Case Presentation

Patient information

A 73-year-old female with no significant medical history presented with a sudden loss of consciousness lasting approximately 30 minutes. Upon regaining consciousness, she remained drowsy and disoriented for 12 hours. After a brief period of lucidity, she experienced another episode of drowsiness lasting 30 minutes before full recovery.

Investigations

Electrocardiogram (ECG): Performed one-hour post-initial episode, revealed significant ST-segment elevations in leads I, aVL, and V1-V6, with less pronounced reciprocal ST depressions in inferior leads. The ST elevations persisted for three days and reduced by 3 mm after 3 days of symptom onset.

ECG – day 1

ECG – day 2

ECG – day 3

Echocardiography: Demonstrated mild concentric left ventricular hypertrophy (interventricular septal thickness of 1.3 cm) with severe hypokinesia of mid and apical segments, resulting in an ejection fraction of 30%. No significant valvular abnormalities were noted.

Echocardiogram: Apical 4 chamber view and long axis view in systole showing non contractile mid and apical segments

Coronary Angiography: Conducted after the patient regained full consciousness, revealed normal epicardial coronary arteries, effectively ruling out obstructive coronary artery disease.

Laboratory Tests: Complete blood count, renal and liver function tests were within normal limits. Initial serum potassium was 2.6 mmol/L, indicating hypokalemia.

Neurological Assessment: MRI brain, MRA, and MRV showed only age-related changes. EEG, performed after the patient regained full consciousness for the second time, was normal.

Management

Cardiac Care: The patient was managed for suspected acute coronary syndrome with antiplatelets, heparin, and diuretics. Noradrenaline infusion was initiated for cardiogenic shock two hours post-angiography and tapered off after ten hours as the patient’s condition improved. Discharged with anti-failure medications.

Neurological Care: Given the clinical presentation, non-convulsive status epilepticus (NCSE) was suspected, and levetiracetam 500 mg intravenously twice daily was administered, later transitioned to oral dosing.

Supportive Measures: Oxygen therapy at 4-6 L/min via a face mask and diuretics were provided.

Outcome and Follow-Up

The patient was discharged three days post-angiography. ECG still exhibited ST-segment elevations, reduced by 1-2 mm. Echocardiographic findings remained unchanged. A follow-up ECG and echocardiogram were scheduled for two weeks post-discharge to reassess cardiac function.

Discussion

This case highlights the diagnostic challenges of differentiating Takotsubo cardiomyopathy from acute myocardial infarction, particularly when precipitated by neurological events such as seizures. The persistent ST-segment elevations and regional wall motion abnormalities observed in this patient are characteristic of TTC. The normal coronary angiography findings further support this diagnosis.

Pathophysiology of Seizure-Induced TTC

The exact mechanism of TTC remains incompletely understood. However, catecholamine excess due to physical or emotional stress is believed to play a central role. Seizures can induce a surge in catecholamines, leading to myocardial stunning and the characteristic ventricular dysfunction seen in TTC. This catecholamine-mediated myocardial stunning is thought to result from direct myocardial toxicity, coronary microvascular dysfunction, or both.

Challenges in diagnosing NCSE

A significant limitation in this case was the lack of an EEG during the drowsy episodes. NCSE is characterized by prolonged seizure activity without convulsions, often presenting as fluctuating consciousness. Since EEG was performed only after the patient regained full consciousness, it may have missed active epileptiform discharges. The absence of EEG during altered mental status phases makes definitive diagnosis challenging.

Despite this limitation, the clinical course, response to antiseizure medication, and neurologist’s assessment strongly suggest NCSE as a possible trigger for TTC in this patient. Future cases would benefit from continuous EEG monitoring during altered mental status episodes to confirm the diagnosis.

Review of Literature

Seizure-induced Takotsubo cardiomyopathy has been documented in various case reports and series. A review of 36 cases of seizure-associated TTC found that the condition predominantly affects postmenopausal women, with a mean age of 61.5 years. The clinical presentation often mimics acute coronary syndrome, with chest pain and ECG changes, but without obstructive coronary disease. These findings underscore the importance of considering TTC in patients presenting with cardiac symptoms following a seizure.

A study by Wittstein et al. (2005) demonstrated that patients with stress cardiomyopathy exhibit significantly elevated catecholamine levels compared to those with STEMI, supporting the role of sympathetic overactivity in disease pathogenesis. Similarly, a study by Elesber et al. (2007) found that TTC patients generally have favorable long-term outcomes, with left ventricular function normalizing in most cases.

Conclusion

Seizure-induced Takotsubo cardiomyopathy is a critical differential diagnosis in patients presenting with acute coronary syndrome symptoms post-seizure. Early recognition and appropriate management are essential to prevent unnecessary interventions and to provide optimal care. This case emphasizes the need for a multidisciplinary approach, involving both cardiology and neurology specialties, to effectively manage such complex presentations. The importance of timely EEG in diagnosing NCSE is also highlighted, as missing this critical window can delay appropriate neurological management.

Reference

  • Wittstein, I. S., Thiemann, D. R., Lima, J. A., et al. (2005). Neurohumoral features of myocardial stunning due to sudden emotional stress. New England Journal of Medicine, 352(6), 539-548.
  • Elesber, A. A., Prasad, A., Lennon, R. J., et al. (2007). Four-year recurrence rate and prognosis of the apical ballooning syndrome. Journal of the American College of Cardiology, 50(5), 448-452.
  • Bybee, K. A., Kara, T., Prasad, A., et al. (2004). Systematic review: Transient left ventricular apical ballooning—a syndrome that mimics ST-segment elevation myocardial infarction. Annals of Internal Medicine, 141(11), 858-865.

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