Recurrent syncope due to ischemic ventricular tachycardia masquerading as a seizure disorder treated with coronary revascularization: a case report

Abstract

Background

Syncope has many possible causes, and its diagnosis depends on a thorough clinical history supported by targeted investigations. Ventricular tachycardia is an important but often overlooked cause, particularly in patients with ischemic heart disease, where timely diagnosis allows for potentially curative interventions.

Case Presentation

A 52-year-old Black Ethiopian woman had recurrent syncope initially misdiagnosed as a seizure disorder. Ambulatory electrocardiography revealed sustained monomorphic ventricular tachycardia. Coronary angiography demonstrated critical mid–left anterior descending artery stenosis. She underwent percutaneous coronary intervention and commenced long-term oral amiodarone. During over one year of follow-up, she remained free of syncope.

Conclusion

This case highlights ischaemia-associated ventricular tachycardia as a potentially reversible cause of syncope that may mimic seizures. Improvement was observed after revascularization, though the mechanism remains inferred and may have been influenced by concomitant amiodarone. Clinicians should consider cardiac arrhythmias in atypical seizure-like episodes, especially in adults with cardiovascular risk factors.

Introduction

The precise diagnosis of the etiology for recurrent syncope usually relies on an accurate and detailed medical history. The management of syncopal attacks caused by ventricular tachycardia in patients with ischemic heart disease requires a combined approach of revascularization, implantable cardioverter-defibrillator (ICD), catheter ablation, and pharmacologic therapy. The role of coronary revascularization in these patients outside of the acute coronary syndrome period is controversial. Major society guidelines recommend revascularization as one of the primary treatment modalities in patients with coronary ischemia presenting with ventricular fibrillation or polymorphic ventricular tachycardia [1, 2].

The role of coronary intervention in ischemic heart disease-related monomorphic ventricular tachycardia remains uncertain. This reservation is due primarily to the structural reentry circuit-based mechanism of the tachycardia, which is unlikely to be modified by revascularization. This pathophysiological mechanism has not been tested in prospective randomized trials. Few retrospective trials that have evaluated the role of revascularization in the treatment of this patient population have been inconsistent [3, 4].

Here, we report a case of a 52-year-old Black Ethiopian woman with recurrent syncope caused by sustained monomorphic ventricular tachycardia of ischemic origin. The patient was managed with percutaneous coronary revascularization, oral amiodarone, and other standard medical therapies with no recurrence of syncope over a year of follow-up.

Case presentation

This is a 52-year-old Black Ethiopian woman with a history of untreated dyslipidemia and hypertension who presented with recurrent episodes of loss of consciousness and palpitations over a period of one year. The episodes usually lasted less than 1 minute, and the patient immediately regained consciousness with no confusion. Episodes occurred almost exclusively during daytime activities, including home duties and social engagements. There was no report of prodromal symptoms, tongue biting, abnormal body movement, urinary or fecal incontinence, or major injury during the incidents. She also had no chest pain or dyspnea. Her initial visit was to a nearby hospital, and she was misdiagnosed with seizure disorder and started on antiepileptic medication (phenytoin 100 mg twice daily), but the symptoms continued to recur. She later visited Gesund Cardiac and Medical Center in Addis Ababa, Ethiopia, a year after she began to experience the symptoms. A review of her medical history, particularly the brief nature of the symptoms with no subsequent confusion and absence of epileptiform body movements, suggested cardiac syncope rather than a seizure disorder.

Physical examination revealed a blood pressure of 150/90 mmHg. The remaining vital signs, as well as the cardiovascular and neurological examinations, were unremarkable. The clinical timeline of the patient’s presentation, diagnosis, and management is shown in Table 1.

Table 1.

Clinical timeline of patient’s presentation, diagnosis, and management.

Date	Clinical Features	Diagnosis and Management
March 2018	Elevated blood pressure on evaluation for an unrelated problem	Hypertension and dyslipidemia Not on regular follow-up or treatment
Jan 2022	Recurrent transient loss of consciousness	Seizure disorder Started on anti-epileptic agents
Jan 2023	Episodes of loss of consciousness continued to recur despite anti-epileptics	Syncope secondary to recurrent ventricular tachycardia Percutaneous coronary intervention, amiodarone, aspirin, clopidogrel, and atorvastatin
October 2024	No episodes of syncope for over 1 year and 6 months	Aspirin, atorvastatin, metoprolol, and amiodarone

Initial investigations, including complete blood count, fasting blood sugar, and blood chemistry, were normal. The lipid profile revealed a mildly elevated low-density lipoprotein cholesterol level (145 mg/dl). A resting electrocardiogram (ECG) revealed a normal sinus rhythm. Resting transthoracic echocardiography revealed normal cardiac chamber dimensions, normal left ventricular systolic and diastolic function, and no regional wall motion abnormality.

Subsequently, 48-hour Holter-ECG monitoring (Fig. 1) was performed as the patient experienced intermittent symptomatic episodes. It revealed paroxysms of sustained monomorphic ventricular tachycardia (VT), which correlated temporally with episodes of palpitation and presyncope experienced by the patient.

Figure 1.

48-hour Holter-ECG monitoring revealed paroxysms of sustained monomorphic ventricular tachycardia.

She was also admitted for invasive coronary angiography to look for possible underlying ischemic heart disease since she has risk factors for atherosclerosis (hypertension and dyslipidemia). Invasive coronary angiography revealed a 95% stenosis of the mid-left anterior descending artery (LAD), as depicted in Fig. 2A and B.

Figure 2.

Invasive coronary angiography revealed mid-left anterior descending artery 95% stenosis as seen in RAO cranial (red arrow in A) and LAO cranial (blue arrow in B) views, and successful percutaneous coronary intervention (PCI) to LAD was done as shown in LAO cranial view with achievement of TIMI grade III flow (white arrow in C).

Successful percutaneous coronary intervention (PCI) to LAD was done with achievement of TIMI grade III flow (Fig. 2C). Given the patient’s documented sustained VT associated with hemodynamic instability and recurrent syncope, she fulfilled Class I indications for secondary-prevention implantable cardioverter-defibrillator (ICD) implantation, in line with the 2022 European Society of Cardiology (ESC) guidelines for the management of ventricular arrhythmias and the prevention of sudden cardiac death.

ICD implantation was recommended during shared decision-making, but the patient could not access it due to local unavailability and financial limitations for treatment abroad, representing a structural barrier to guideline-recommended care. In the interim, she was started on amiodarone 400 mg orally twice daily, along with aspirin 81 mg, clopidogrel 75 mg, atorvastatin 80 mg, and metoprolol succinate 25 mg once daily, in line with ESC guidelines when device therapy is unavailable. Contingency plans included close rhythm monitoring, continued optimization of medical therapy, and referral to a local charitable cardiac center for potential missionary-supported intervention, such as device implantation, should VT recur or symptoms worsen.

Follow-up and outcomes

The patient was discharged with similar doses of aspirin, clopidogrel, atorvastatin, metoprolol succinate, and amiodarone. She had no recurrence of syncope over a follow-up period of 1 year and 6 months. She also has optimal lipid and blood pressure control.

Discussion

We reported a case of a middle-aged woman with cardiac syncope, who was initially misdiagnosed with seizure disorder. She had recurrent ventricular tachycardia of ischemic origin that was managed successfully with coronary revascularization and long-term amiodarone therapy.

Distinguishing the causes of transient loss of consciousness, particularly differentiating syncope from seizure, can be challenging, as demonstrated in our case. Previous studies have indicated that up to 26% of patients diagnosed with epilepsy may have non-epileptic seizures [5, 6]. Up to 40% of these patients, particularly those not responding to antiepileptic medications, may have an underlying cardiovascular syncope misdiagnosed as a seizure disorder [7]. A similar case from India described a patient with convulsive cardiac syncope initially mistaken for epilepsy [8]. In our patient, the absence of epileptiform movements or post-ictal confusion and the continued recurrence of symptoms despite anti-epileptic treatment are clues suggesting alternate diagnoses. Our approach illustrates the importance of detailed history taking in distinguishing between syncope and seizure as the cause of transient loss of consciousness. The role of ambulatory monitors in patients with paroxysmal symptoms can’t be overstated as well [9].

The use of coronary revascularization and anti-arrhythmic drugs in the management of patients with clinical profiles similar to ours is based on limited evidence. Particularly, the role of revascularization therapy in this patient population has been a topic of debate for several decades. Sustained monomorphic VT is rarely caused by ischemia, and revascularization alone may not prevent VT recurrence. However, the exclusion or treatment of significant CAD is reasonable in these patients, especially before catheter ablation, as per the ESC 2022 VT guidelines [1]. Given our patient has ventricular tachycardia and risk factors for ischemic heart disease, the decision to perform diagnostic cardiac catheterization was appropriate in this patient.

In the largest study that compared PCI with medical therapy for patients with syncope and obstructive coronary artery disease, there was no significant difference in 90-day all-cause readmission risk or long-term risk of readmission for syncope, though there was an increased indication for pacemaker or defibrillator therapy in the medically treated group [3]. In contrast, a large retrospective observational study involving 606 patients with an ICD implanted for ischemic cardiomyopathy revealed the benefit of revascularization in preventing recurrent VT or mortality in patients with ischemic cardiomyopathy who underwent ICD implantation for secondary prevention but not in patients who underwent the implantation for primary prevention [4]. This supports the presumed benefit seen in our patient who underwent revascularization and could have been a candidate for ICD implantation for secondary prevention of VT had the device been available in our setup.

In a case report from a New York hospital, an 81-year-old patient who presented with recurrent syncope was evaluated for ischemic heart disease after echocardiography showed mild LV dysfunction, a Holter ECG revealed NSVT, and an EP study also showed recurrent NSVT. A pharmacologic stress test and SPECT revealed ischemic myocardium, and subsequent coronary angiography revealed significant multivessel disease, including distal left main stenosis. CABG was successfully performed, and the patient has no recurrence of syncope over subsequent visits [10]. The benefits of revascularization have also been reported in patients who presented with syncope and an ECG finding of Wellen’s syndrome. In two such case reports, patients presented with syncope in the absence of chest pain. There was no recurrence of syncope in the follow-up period after successful revascularization [11, 12].

Another small study evaluating the potential benefit of PCI in patients with coronary artery disease and monomorphic VT revealed the failure of revascularization to prevent recurrent VT or mortality a year after treatment [13]. The patients included in this study were elderly (mean age of 73 years), had lower ejection fraction (mean ejection fraction of 37%), and the vast majority presented with acute coronary syndrome. This may not be an ideal representation of our patient, who is relatively young, has preserved ejection fraction, and presented with chronic coronary syndrome.

Some mechanistic studies have shed light on the possible mechanisms of monomorphic VT in patients without myocardial scar. A hibernating myocardium, in the absence of scar, has been shown to act as a substrate for reentry circuit in human and animal studies [14, 15]. On the other hand, a study in patients with ischemia without obstructed coronary arteries has revealed the presence of small myocardial scars in a significant proportion of the patients [16]. These scars detected on cardiac magnetic resonance imaging (MRI) in patients without a history of myocardial infarction can form a reentry circuit for monomorphic VT. These mechanistic studies support the possible role of coronary revascularization in patients with monomorphic ventricular tachycardia associated with a hibernating myocardium or a limited amount of myocardial scar detected only on cardiac MRI [17, 18].

Our patient was started on amiodarone as an alternative to ICD as per the ESC 2022 guidelines on VT, due to unavailability of ICD [1]. Amiodarone has been shown to reduce arrhythmia-related deaths by more than one-third but does not affect overall mortality in postmyocardial infarction patients [19]. Beta-blockers have been shown to reduce the risk of arrhythmic death in post-MI patients [10]. The OPTIC trial assessed the efficacy of beta-blockers alone, beta-blockers and amiodarone, or sotalol alone in preventing ventricular arrhythmias in patients with an ICD [20]. Compared with beta-blockers alone, amiodarone plus beta-blockers significantly reduced the risk of shock, while compared with beta-blockers alone, sotalol tended to reduce shock. Our patient has been receiving metoprolol and amiodarone since her diagnosis, in line with recommendations for preventing recurrent ventricular tachycardia. Advanced therapies, including catheter ablation and ICDs, are indicated for patients with monomorphic VT and ischemic heart disease to prevent syncope as well as sudden cardiac death [1, 2].

Our patient met Class I indications for secondary-prevention ICD implantation, in accordance with the 2022 ESC guidelines for the management of ventricular arrhythmias and prevention of sudden cardiac death [1]. Device implantation was not possible due to local unavailability and financial constraints preventing treatment abroad. Given the subtotal coronary stenosis, absence of prior myocardial infarction, and limited data on VT recurrence, the team opted for coronary revascularization and initiated amiodarone with metoprolol to reduce VT risk.

Although the patient’s VT responded favourably to revascularization, the generalizability of this strategy is limited by two factors. First, the causal link between ischemia and VT remained uncertain due to the absence of functional ischemic testing or cardiac MRI. Second, the apparent benefit of revascularization was confounded by the concomitant use of amiodarone.

Conclusions

This case highlights ischaemia-associated ventricular tachycardia as a potentially reversible cause of syncope that may mimic seizures. Improvement was observed after revascularization, though the mechanism remains inferred and may have been influenced by concomitant amiodarone. Clinicians should consider cardiac arrhythmias in atypical seizure-like episodes, especially in adults with cardiovascular risk factors.

Authors’ contributions

MAG was involved in conceptualization, data curation, validation, and writing—original draft and writing— review and editing. BA was in validation and writing—review and editing. GS was involved in data curation and writing—review and editing. All the authors read and approved the final manuscript.

Conflict of interest

The authors declare no conflict of interest.

Funding

No funding was received for this case report.

Data availability

Data supporting the findings of this case report are available from the corresponding author upon reasonable request.

Ethical approval

Ethical approval was not required.

Informed consent

Written informed consent was obtained from the patient for publication of her case details.