Iron Infusion-Induced Kounis Syndrome Presenting as Inferior ST-Segment Elevation Myocardial Infarction with Normal Coronaries: A Case Report

Introduction

Kounis syndrome, first described by Kounis and Zavras, represents the concurrence of acute coronary syndromes with hypersensitivity reactions mediated by mast cell activation and release of inflammatory mediators such as histamine, leukotrienes, and platelet-activating factor. 1-3 These mediators can induce coronary vasospasm, endothelial dysfunction, and platelet aggregation, leading to myocardial ischaemia or infarction (Figure 1).

Three variants of Kounis syndrome have been described: Type I, occurring in patients with normal coronary arteries due to vasospasm; Type II, involving plaque rupture or erosion in patients with pre-existing atherosclerosis; and Type III, associated with stent thrombosis.1,2 A wide range of triggers have been implicated, including drugs, foods, insect stings, and environmental exposures, with medications being the most commonly reported cause.4

Intravenous iron preparations, though generally safe, have been associated with rare but potentially severe hypersensitivity reactions, including anaphylaxis. 5 Cardiovascular manifestations during such reactions may be under-recognised and can mimic acute myocardial infarction, posing diagnostic and therapeutic challenges.

We report a case of intravenous iron-induced anaphylaxis complicated by transient inferior ST-segment elevation myocardial infarction (STEMI) with normal coronary arteries, consistent with Type I Kounis syndrome.

Case Report

A 38-year-old woman with iron-deficiency anaemia and no prior cardiovascular history received intravenous iron sucrose (Orofer). Within minutes, she developed acute retrosternal chest pain, palpitations, dizziness, and profound hypotension. Clinical examination revealed features of anaphylaxis with circulatory collapse.

Immediate treatment included intramuscular adrenaline, intravenous corticosteroids, and antihistamines. Persistent hypotension required initiation of noradrenaline infusion.

Electrocardiography (ECG) demonstrated ST-segment elevation in leads II, III, and aVF, with reciprocal changes (Figure 2), suggestive of inferior STEMI. Acute coronary syndrome (ACS) therapy was initiated.

Transthoracic echocardiography revealed regional wall motion abnormalities in the inferior wall, with an ejection fraction of 42%–45%.

Emergency coronary angiography showed smooth, unobstructed coronary arteries (Figure 3).

Cardiac magnetic resonance imaging (MRI) demonstrated diffuse left ventricular hypokinesia without late gadolinium enhancement, thereby excluding myocarditis and supporting a diagnosis of stress cardiomyopathy (Figure 4).

Based on the temporal relationship with anaphylaxis, transient ischaemic ECG changes, and normal coronaries, a diagnosis of Type I Kounis syndrome was established.

Discussion

This case highlights allergic myocardial ischaemia precipitated by drug-induced anaphylaxis. Mast-cell degranulation releases vasoactive mediators that cause coronary vasoconstriction and myocardial ischaemia, even in the absence of coronary artery disease.1-3

Intravenous iron is a recognised but uncommon cause of severe hypersensitivity reactions. 5 The occurrence of concurrent myocardial ischaemia suggests Kounis syndrome, particularly the Type I variant in patients without underlying coronary disease.

Management is complex, as treatment of anaphylaxis and myocardial ischaemia may conflict. Adrenaline remains the cornerstone of anaphylaxis management but may exacerbate ischaemia. Morphine and beta-blockers are generally avoided due to their potential to worsen vasospasm or hypotension. 2,3 Careful haemodynamic monitoring and individualised therapy are essential.

Early recognition is critical, as this condition can mimic acute coronary syndrome and lead to unnecessary invasive interventions. Clinicians should maintain a high index of suspicion when cardiac symptoms occur in the setting of allergic reactions.

Declarations

Patient consent

Written informed consent was obtained from the patient for publication of this case report and accompanying clinical details. All identifying information has been anonymised.

CARE guidelines

This case report is prepared in accordance with the CARE guidelines for reporting of clinical cases.