002038 - Exercise-Associated Anaphylaxis Complicated by Type II Kounis Syndrome in a Patient With Chronic Coronary Artery Disease

Kounis syndrome(KS) or allergic acute coronary syndrome, is characterized by myocardial ischemia triggered by mast cell mediator release during allergic or anaphylactic reactions. While commonly associated with identifiable IgE-mediated allergens,KS may occur in patients without demonstrable allergy, particularly when cofactors such as physical exercise or histamine-liberating foods are present.We report a patient with chronic coronary artery disease who developed generalized urticaria and anaphylactic shock after swimming, following ingestion of tree nuts, despite negative allergy testing and tolerance at oral provocation.Coronary angiography revealed critical in-stent restenosis treated successfully with drug-coated balloon angioplasty, confirming a diagnosis of type II Kounis syndrome.

61-year-old male with a history of chronic coronary artery disease and prior myocardial infarction underwent percutaneous coronary intervention (PCI) with stent placement approximately 23 years ago. He also had dyslipidemia and hypertension..The index event occurred after swimming in an indoor pool. The patient reported ingestion of tree nuts and honey at breakfast. Shortly after exercise, he developed generalized urticaria followed by pre-lipothymia and anaphylactic shock. Emergency medical services administered intramuscular epinephrine, systemic corticosteroids, and H1-antihistamines. Upon arrival at the hospital, a significant elevation of cardiac troponin was noted. The patient was admitted to the cardiology ward with a working diagnosis of NSTEMI occurring during anaphylactic shock, raising suspicion of type II Kounis syndrome.

Coronary angiography revealed critical in-stent restenosis of the right coronary artery, which was successfully treated with drug-coated balloon angioplasty. This confirmed the diagnosis of type II KS, linking myocardial injury to mast cell mediator release in the context of anaphylaxis. The allergic tests shows: Total IgE: 301 U/mL Basal tryptase: 2.5 µg/mL Specific IgE to common foods, tree nuts, and hymenoptera venoms: negative or within normal limits. Prick tests and prick-by-prick tests for walnut, almond, pistachio, pine nut, hazelnut, peanut, and cashew were negative. We perform an oral provocation tests with walnut and almond, were tolerated The patient was advised to avoid exercise within 4 hours of food intake, particularly histamine-liberating foods.

KS occurred without demonstrable IgE-mediated food allergy, consistent with previously reported cases where mast cell activation occurs via non-IgE-dependent mechanisms, such as exercise, histamine-liberating foods, or cofactor-mediated mast cell hyperreactivity. This overlap resembles food-dependent exercise-induced anaphylaxis (FDEIA), wherein food ingestion alone is tolerated but triggers systemic reactions can be favors.

We highlights the intersection of FDEIA and type II Kounis syndrome, emphasizing that exercise and histamine-liberating foods can act as cofactors for anaphylaxis and myocardial injury even in the absence of positive allergy testing.