A rare presentation of ST-elevation, mimicking an acute coronary syndrome, as a manifestation of seizure disorder—a case report

Acute coronary syndrome (ACS) remains a significant contributor to morbidity and mortality, accounting for approximately 15% of New Zealand’s annual deaths, with mortality rates exceeding those of many Western countries.¹

Neurological conditions, including stroke and intracranial haemorrhage (ICH), can mimic the presentation of ACS with ST-elevation on electrocardiogram (ECG), without obstructive coronary disease.^2,3 Seizures presenting with acute ST-elevation is much more rarely described. While the pathophysiology remains unclear, understanding the potential causes of ST-elevation myocardial infarction (STEMI) with non-obstructive coronary arteries is important for making a diagnosis and determining further management.⁴ Here we present a rare case of seizures mimicking an ACS, presenting with ST-elevation with normal coronary arteries.

Case report

A 21-year-old epileptic man with poor medication compliance presented following five successive seizures over a period of hours without full recovery. He was initially unresponsive with a low-grade fever, but haemodynamically stable with normal cardiorespiratory examinations and no rashes. Investigations demonstrated an acute kidney injury (AKI) (creatinine [Cr] 250 micromol/L, N = 60–105 micromol/L), leukocytosis (17.2 x10⁹/L, N = 1.9–7.5 x10⁹/L) with neutrophilia (12.4 x10⁹/L, N = 1.9–7.5 x10⁹/L) and elevated C-reactive protein (22mg/L, N <8mg/L). Elevated lactate levels were observed on admission, which quickly normalised and remained stable. Ceftriaxone and acyclovir were given as empiric cover for meningoencephalitis, levetiracetam and phenytoin as anti-epileptics, as well as ketamine, quetiapine and haloperidol for agitation.

ECG the following day demonstrated sinus rhythm with a newly prolonged corrected QT interval (QTc) and global T-wave inversion, presumed to be medication related (Figure 1 and 2). Over subsequent days he remained agitated, requiring intermittent sedatives and on-going cardiac monitoring. A progressive AKI (Cr 713 micromol/L) was observed. As urinalysis was not performed, the exact trigger remains uncertain, however rhabdomyolysis is considered the most likely cause based on the presentation and associated elevation in creatine kinase (CK 2077 U/L).

View Figure 1–3.

Day-5 ECG demonstrated dynamic inferolateral ST-elevation, with reciprocal ST-depression without haemodynamic compromise (Figure 3). CT head excluded ICH or hydrocephalus. Urgent echocardiogram demonstrated normal biventricular size and systolic function, normal valves, and no features of Takotsubo cardiomyopathy. There was no significant metabolic acidosis or electrolyte derangement noted. High-sensitivity troponin-I, not previously measured, was elevated (498ng/L, N <20ng/L).

Dual anti-platelet therapy was given, and urgent coronary angiogram demonstrated normal coronary arteries with no evidence of coronary vasospasm at the time of contrast injection. Subsequently, agitation gradually improved with persistent QTc prolongation; AKI steadily improved with fluid rehydration (Cr 116 micromol/L), and anti-epileptic medications were re-introduced with no further seizures observed.

Discussion

ACS typically relates to atherosclerotic plaque rupture or erosion, with STEMI resulting from complete culprit artery occlusion. It is well documented that other conditions, including acute neurologic events, can give rise to cardiac abnormalities.^2,3 The so-called neurogenic stunned myocardium can mimic an ACS presentation, with ischaemic ECG changes (including ST-elevation), elevated troponin and occasionally reduced cardiac function, without significant coronary artery obstruction.⁵

Seizure patients demonstrating ST-elevation is more rarely described. One case described a 75-year-old woman with known ischaemic heart disease presenting with severe headaches and hypertensive emergency without ICH, complicated by a seizure with acute ST-elevation and troponin rise.⁶ Coronary angiography demonstrated 80% in-stent restenosis of a prior coronary stent without evidence of thrombus or plaque-rupture on intravascular imaging.⁶ Her final diagnosis was posterior reversible encephalopathy syndrome secondary to malignant hypertension causing seizures.⁶

One proposed mechanism for the neuro-cardiac association involves sympathetic overactivity with a catecholamine surge (potentially triggered by illness-related stress) following damage to areas of the brain controlling the autonomic nervous system.⁷ These excess catecholamines may induce direct cardiotoxicity, or precipitate coronary vasospasm. Similarly, studies report more highly elevated plasma epinephrine and norepinephrine levels being associated with hypertension, ST-segment changes and poorer clinical outcomes.^2,8,9 If coronary vasospasm is suspected, specific provocation testing with acetylcholine can be considered.¹⁰ CT coronary angiogram can serve as an alternative to invasive angiography for ruling out significant obstructive coronary artery disease (CAD), especially in younger patients with a low risk of CAD. However, for cases where the diagnosis is uncertain and there is clinical urgency due to haemodynamic instability or evidence of ongoing ischaemia, invasive angiography remains the preferred approach.¹¹

In summary, this case demonstrates that ST-elevation can occur following seizures without associated coronary plaque. Though the underlying pathophysiology remains unclear, it may be related to increased circulating catecholamines, and while specific guidelines are lacking, neurogenic stunned myocardium and other stress-induced cardiomyopathies are typically reversible and managed medically.^5,12 Clinicians should be alert to this possibility in patients with acute seizure episodes.