Acute symptomatic seizures and ventricular fibrillation - a multimodality approach to a rare complication of myocardial infarction. Case report

Cardiovascular diseases remain the leading cause of mortality worldwide, and acute myocardial infarction (MI) is one of the most common and life-threatening cardiovascular diseases. Arrhythmias are common during the early hours of MI and are also important prognostic factors. The incidence of ventricular arrhythmias (VA) has declined over recent decades, due to reperfusion strategies and the early use of beta-blockers. However, 6–8% of patients still develop hemodynamically significant ventricular tachycardia or ventricular fibrillation. Ventricular arrhythmias may sometimes be followed by a symptomatic seizure, but clear differentiation between a convulsive syncope and an epileptic seizure is essential for appropriate management. Distinguishing between the two entities may sometimes be difficult, as they share a number of common characteristics.

We report the case of a 44-year-old male patient who presented to our hospital’s emergency room for severe chest pain and diaphoresis that started one hour prior to the presentation, after moderate physical activity. The patient had a history of untreated hyperlipidemia and was a smoker (40 pack-year). He also had significant family medical history, both his father, as well as his grandfather dying from myocardial infarction around the age of 40 and his brother having an ischemic stroke when he was 36-year old.

Upon admission, the patient was hemodynamically stable and had ongoing chest pain, with normal physical examination was normal.

The electrocardiogram (ECG) showed sinus rhythm with ST-segment elevation in the inferior leads and non-sustained ventricular tachycardia (Figure 1). There was no-ST elevation in the posterior or the right leads.

Figure 1

The initial high sensitivity troponin I was extremely elevated at 22827 ng/l and echocardiography at admission showed preserved left ventricle ejection fraction (LVEF) and hypokinesia of the basal segments of the interventricular septum and the inferior wall. Pulmonary radiography showed no pathological findings.

The diagnostic of acute inferior ST-elevation myocardial infarction (STEMI) was established. The patient received loading doses of aspirin and ticagrelor and underwent emergency coronary angiography, which revealed acute near-occlusion of the middle segment of the right coronary artery (RCA). The left anterior descending artery (LAD) and the circumflex artery (LCX) did not present any significant lesions (Figure 2, panel A). Right coronary artery angioplasty was performed, with the insertion of a 3.0x28 mm drug eluting stent (DES) in the second segment of the RCA. The passing of the 0.014” angioplasty guidewire into the distal RCA was complicated by dissection at the site of the culprit lesion. Another 0.014” guidewire was placed in the false lumen and was maintained there in order to seal the dissection (Figure 2, panels B and C). Two iv boluses of eptifibatide glycoprotein IIb/IIIa inhibitor were administered during the procedure. The final result was good, without any residual stenoses and TIMI3 distal flux in all the coronary arteries (Figure 2, panel D).

Figure 2

Upon admission in our coronary intensive care unit the patient was angina-free, but he developed atrial fibrillation, with a heart rate of 148 beats per minute and good hemodynamic tolerance. He received intravenous amiodarone for chemical conversion.

After a short time, the patient developed recurrent ventricular fibrillation and he needed resuscitation by five 200 J electric shocks in approximately 5 minutes. We concomitantly administered intravenous adrenaline, as well as lidocaine. After resuscitation the blood pressure was 120/90 mm Hg, the heart rate 150 beats per minute (sinus tachycardia on the monitor), and the oxygen saturation 95% in ambient air. Persistent tonic-clonic seizures appeared, with alteration of the consciousness. The patient was sedated with diazepam and propofol and intubated.

The cardiac echography performed after the resuscitation showed moderate left ventricle systolic disfunction (LVEF 40%), diffuse kinetics disorder, no mechanical complications and no pericardial effusion. The patient had a good evolution and was retransferred to our clinic the next day.

The follow-up echocardiography showed mild systolic dysfunction (LVEF 50%), inferior and posterior wall hypokinesia, type 1 diastolic dysfunction, no significant valvular disease, no pericardial effusion. The strain pattern was compatible with inferior myocardial infarction, but didn’t show features suggestive of other myocardial pathologies (Figure 3).

Figure 3

Biologically, there were to pathologic findings. The criteria for familial hypercholesterolemia were not met.

Taking into account the tonic-clonic seizure, a neurological examination was performed, without pathological findings. Moreover, both a cerebral CT scan, as well as an MRI were made. No recent vascular changes were identified. A posterior fossa arachnoid cyst of 47/11/46 mm was identified, but without clinical implications (Figure 4). Doppler ultrasound of cervical vessels identified bilateral atheroma plaques in the internal carotid arteries without hemodynamic significance. The electroencephalogram (EEG) was normal (Figure 5).

Figure 4

Figure 5

Suspicion of Fabry disease was raised, but refuted by normal serum alpha galactosidase levels. Direct and indirect Coombs tests were also normal and so were thyroid hormones, blood homocysteine and blood cobalamin.

24-hour ECG Holter monitoring revealed background sinus rhythm, with rare monomorphic atrial and ventricular extrasystoles, without systematization.

The patient was discharged with double antiplatelet therapy (acetylsalicylic acid and ticagrelor), beta blocker, angiotensin converting enzyme inhibitor, statin at maximum dose and proton pump inhibitor. No neurological treatment was recommended so far.

Therefore, the tonic-clonic seizures were interpreted in the context of cerebral hypoxemia secondary to recurrent arrhythmic episodes. The patient will repeat the cerebral imagistic investigations and the EEG at one year after the event.

At 2-month follow-up the patient was neurological and cardiovascular asymptomatic.

Our case describes a patient with an acute symptomatic seizure occurring in the setting of acute myocardial infarction complicated by intraprocedural right coronary artery dissection and followed by ventricular fibrillation. The seizure occurred promptly following a systemic stimulus, differentiating it from an epileptic seizure. Coronary artery dissection implies a tear in the wall of the artery, with the compression of the lumen, which leads to a reduction in blood flow and additional ischemia¹.

Acute seizures represent 1% of all visits to emergency departments in the United States. One-third of acute seizures are not due to epilepsy, but provoked by underlying potentially life-threatening acute conditions². The two entities have many similar clinical features. Both involve transient loss of consciousness (LOC). Syncope is the LOC and loss of muscle tone due to reversible cerebral hypoperfusion. It is characterized by sudden onset, spontaneous and complete recovery. Epileptic seizure is the result of an abnormal, excessive and hypersynchronous neuronal activity in the brain^3,4.

Convulsive syncope (or symptomatic seizure) are terms previously used to describe generalized seizure-like activity attributed to transient cerebral hypoperfusion secondary to cardiac arrhythmia⁵.

Appropriate differentiation between the two pathologies is essential, so that unnecessary medications or procedures may be avoided^6,7. Moreover, anticonvulsant medications have been reported to have cardiotoxicity. Pregabalin has been related to heart failure⁸, oxcarbazepine was reported to induce resistant VF⁹, and carbamazepine can cause atrioventricular (AV) block^10,11, hypotension¹² or hypertension¹³. All those adverse effects, might, in fact, worsen the initial cause of the generalized seizure, if the right diagnosis has not been made.

Cardiac arrhythmias are a rare precipitant factor for acute symptomatic seizures, due to hypotension-induced cerebral hypoxemia. A case published by Cunnington et al. described a patient who developed seizure in the setting of cardiac arrest in Takotsubo cardiomyopathy with ventricular fibrillation¹⁴. Sabu et al. described a patient with ventricular tachycardia presenting with acute symptomatic seizure¹⁵. Yin et al. reported a similar case of acute seizure following polymorphic ventricular tachycardia¹⁶.

Considering the important family history of the patient, we screened him for epilepsy, as well as for the most frequent systemic diseases that could predispose to both cardiac arrhythmias or epileptic seizures. Blood biomarkers, as well as the EEG and the transthoracic echocardiography (including strain imaging) showed no pathological findings compatible with the aforementioned afflictions.

This case emphasizes the importance of the correct differentiation between acute symptomatic seizure (or convulsive syncope) and an epileptic seizure in a patient presenting with seizure-like activity. We illustrate the value of thorough history taking, and multimodal imagistic, electrocardiographic and electroencephalographic screening in identifying the underlying cause of the seizure-like activity, in order to correctly treat it and prevent its recurrence. Moreover, our case highlights the importance of modern imaging techniques in managing rare complications of myocardial infarction.