Document Type

Conference Proceeding

Publication Date

5-1-2026

Abstract

Acute non-ischemic myocardial injury results from myocardial oxygen supply-demand mismatch in the absence of critical coronary stenosis or atherothrombotic plaque rupture, and may be precipitated by acute physiologic stress, including sustained sympathetic overactivity. Troponin elevation may occur in 6.7-10.9% of post-seizure cases, with higher incidence among the elderly and individuals with cardiovascular risk factors. We present the case of a 55-year-old woman with long-standing epilepsy, dyslipidemia, multiple sclerosis treated with ocrelizumab, and significant cardiovascular risk factors (20 pack-year smoking history, occasional alcohol use, family history of early myocardial infarction) who presented to the emergency room after a witnessed generalized tonic-clonic seizure lasting 5 minutes. Post-ictal, the patient was hemodynamically stable (BP 133/89 mmHg, HR 62 bpm, RR 19, SpO₂ 95%) and denied chest pain, dyspnea, or other cardiac symptoms. Serial 2-hour high-sensitivity troponin measurements demonstrated marked elevation following a characteristic postictal pattern: 528 ng/L (baseline) → 1033 → 1716 → 1652 → 3753 (6 hours post-seizure) → 4102 ng/L (8 hours post-seizure). Additional laboratory findings included mildly elevated creatine kinase (168 U/L), borderline QTc prolongation (467 ms), with normal serum electrolytes. Electrocardiogram demonstrated sinus rhythm at 66 bpm with nonspecific ST-T wave changes, consistent with postictal repolarization abnormalities described in literature. Left heart catheterization was promptly performed via the right radial access that demonstrated normal epicardial coronary arteries without obstructive disease. The left ventricular end diastolic pressure was elevated at 26 mmHg. Transthoracic echocardiogram showed a newly reduced left ventricular systolic function with an ejection fraction of 40-45%. Additionally, hypokinesis of basal to mid anteroseptal and anterolateral wall segments (a variant pattern distinct from classic apical ballooning-takotsubo syndrome), abnormal diastolic dysfunction, and inferior vena cava dilatation were seen. The patient was diagnosed with seizure-induced neurogenic stress cardiomyopathy and acute myocardial injury in the setting of supply-demand mismatch from seizureinduced hyper catecholaminergic-mediated coronary vasospasm. This case demonstrates that even a single, brief generalized tonic-clonic seizure (not exclusively status epilepticus) can cause profound cardiac injury with marked troponin elevation in patients with cardiovascular risk factors. Such presentations may closely mimic acute coronary syndrome and often necessitate invasive evaluation to exclude critical coronary stenosis or plaque rupture. Clinicians should maintain a high index of clinical suspicion for seizure-induced neurogenic stress cardiomyopathy in postictal patients, particularly in older patients with underlying cardiovascular risk factors. Measurement of serum cardiac markers may prove to be an important tool in the diagnosis and prompt treatment.

Comments

American College of Physicians Michigan Chapter and Society of Hospital Medicine Michigan Chapter 2026 Resident and Medical Student Day, May 1, 2026, Troy, MI

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