Abstract
Abstract
Kounis syndrome (KS) is a hypersensitivity-associated acute coronary syndrome. Food-associated KS remains poorly characterized, and its clinical presentation may be mimicked by non-immune food-related toxic reactions. To characterize the food exposures, clinical and cardiovascular presentations, allergological assessment, potential cofactors, KS phenotypes, management, and outcomes reported in food-associated KS. PubMed, Scopus, and Web of Science Core Collection were searched from inception to August 22, 2026. Original case reports, case series, and sufficiently informative conference reports describing objective coronary involvement temporally associated with a food or food-derived exposure were included. Patient-level data were synthesized qualitatively. KS diagnostic certainty, coronary phenotype, food causality, and presumed mechanism were assessed separately. Planned sensitivity analyses restricted the synthesis to confirmed or suspected food allergy, definite or probable KS, and cases without epinephrine administration before coronary onset or its first objective documentation. The synthesis included 50 publications or reports describing 53 unique patients. Food-related mechanisms comprised confirmed food allergy in 20 patients, clinically suspected food allergy in 26, scombroid poisoning in six, and a Coprinopsis atramentaria-alcohol interaction in one. The reported coronary spectrum ranged from transient vasospasm and nonobstructive presentations to plaque-related myocardial infarction, native-coronary thrombosis, and stent or graft thrombosis. Type I was the most frequently assigned phenotype. Allergological assessment, paired acute and baseline tryptase measurements, treatment chronology, and long-term follow-up were inconsistently reported. The main cardiovascular patterns remained broadly consistent across the planned sensitivity analyses. Food-associated KS encompasses a heterogeneous spectrum of allergic coronary presentations. Clinically similar non-immune food-related toxic reactions, including scombroid poisoning, should be recognized as differential diagnoses and analyzed separately from true allergic KS. Diagnosis requires integration of exposure chronology, objective cardiovascular findings, coronary substrate, allergological evidence, potential cofactors, and competing exposures. Intramuscular epinephrine remains the first-line treatment for anaphylaxis, and temporal precedence should not be interpreted as evidence that epinephrine caused the coronary event.