Kounis syndrome (allergic myocardial infarction)
Definition and clinical frame
Kounis syndrome is an acute coronary syndrome (ACS) that occurs in temporal association with an allergic or hypersensitivity reaction. It is a clinical syndrome rather than a separate disease entity.
Mast‑cell and basophil degranulation releases mediators (histamine, leukotrienes, prostaglandins, platelet‑activating factor, tryptase) that can cause coronary vasospasm, provoke plaque erosion or rupture with thrombosis, or trigger stent thrombosis.
In the emergency department it should be managed by combining established anaphylaxis algorithms (Resuscitation Council UK; NICE CG134) with ACS pathways (NICE NG185; NICE CG95).
Pathophysiology
- Mast‑cell and basophil mediator release causes coronary vasoconstriction, increased vascular permeability and platelet aggregation.
- Resulting cardiac injury may be:
- transient vasospasm with ischaemia,
- plaque disruption with thrombotic myocardial infarction,
- hypersensitivity‑related stent thrombosis.
Practical classification (helps guide escalation)
- Type I: coronary vasospasm in patients with angiographically normal coronary arteries; troponin may be normal or only mildly raised.
- Type II: allergic reaction precipitates plaque rupture/acute MI in patients with pre‑existing atherosclerosis.
- Type III: acute stent thrombosis due to hypersensitivity to stent components.