Allergic Myocardial Infarction: An Unusual Cause of Stent Thrombosis

Key words: allergic angina; allergic myocardial infarction; acute coronary syndrome; stent thrombosis; Kounis syndrome

A 67-year-old man with history of hypertension, type 2 diabetes mellitus, and cigarette smoking was admitted for acute coronary syndrome with ST-segment elevation myocardial infarction (STEMI) in the inferior leads.

Thirty minutes before the onset of chest pain, he was accidentally exposed to multiple wasp stings. The patient rapidly developed diffuse skin rash without anaphylactic shock symptoms. Emergency service recorded STEMI in the inferior leads with an electrocardiogram and the patient was taken to our catheterization laboratory to perform primary percutaneous coronary intervention (PCI).

Also, 3 years prior, he experienced inferior STEMI treated with primary PCI and 2 drug-eluting stents implanted from proximal to mid right coronary artery (RCA). Ticagrelor was withdrawn 12 months after the revascularization, while aspirin (100 mg/day) was continued.

Coronary angiography showed acute occlusion of middle RCA due to “very late” thrombosis in the 3-year-old stent (Figure 1A). In consideration of suspected high thrombotic burden in this peculiar clinical setting, we decided to perform manual thromboaspiration (Figure 1B) with significant clot extraction (Figure 1F). PCI was completed with 2 zotarolimus-eluting stents (Figure 1C and 1D) and good angiographic result (Thrombolysis in Myocardial Infarction flow 3) (Figure 1E). Unfractionated heparin (6000 U) was administered before the PCI, followed by glycoprotein IIb/IIIa inhibitor (tirofiban) in consideration of high thrombotic burden. A ticagrelor loading dose (180 mg) was administered after guide-catheter removal.

Hymenoptera stings can induce hypersensitivity acute coronary syndrome in susceptible individuals. Kounis and Zavras first described allergic angina syndrome in 1991. Several etiologic factors have been reported, including drugs, hymenoptera, ants, fish, seafood, jellyfish, and mushrooms.

Hymenoptera venom is made by bioactive allergenic proteins (phospholipase A1, hyaluronidases, acid phosphatases) and vasoactive and thrombogenic substances able to induce vasospasm and coronary thrombosis. Histamine can promote platelets activation, increase aggregatory response of other agonists (adrenaline, 5-hydroxytryptamine, and thrombin), and induce proinflammatory cytokine production from endothelial cells.

Three types of Kounis syndrome have been described:

• type 1: coronary vasospasm with or without progression to myocardial infarction in absence of coronary artery disease;

• type 2: plaque erosion or rupture complication after allergic insult in patients with preexisting atheromatous disease; and

• type 3: stent thrombosis in response to allergic reaction.

Our case confirms that an allergic insult can cause an acute myocardial infarction in a stable coronary disease setting. It also suggests that type 3 Kounis syndrome must be suspected in cases of apparently unexplained “very late” stent thrombosis.