To the Editor: In the very important report published in Chinese Medical Journal,[1] a 50-year-old male patient, stented with a bare metal stent followed by 3 overlapping drug-eluting stents, developed anaphylactic reaction following a bee sting that was treated with intravenous 0.1 mg epinephrine at a 1:100,000 together with intravenous methylprednisolone, chlorpheniramine maleate, and ranitidine. He developed, immediately after, an anterior wall myocardial infarction, and subsequent coronary arteriography revealed total occlusion in the proximal left anterior descending stent and 90% stenosis with tissue growth in the mid-stent. The authors concluded that the acute myocardial infarction occurred due to acute stent thrombosis caused by exogenous epinephrine administration. This report, however, raises important questions related to the cause and pathophysiology of these events.First, could bee sting anaphylaxis be aggravated by concurrent anti-allergic therapy in atopic diathesis individuals? The described patient was given intravenously, apart from epinephrine, methylprednisolone, chlorpheniramine maleate, and ranitidine. These 4 drugs that are given to treat anaphylaxis have been incriminated, paradoxically, as inducing mild or severe allergic reactions! Indeed, most epinephrine preparations contain sulfite as a preservative and antioxidant, which itself may trigger anaphylaxis in atopic individuals.[23] We must always bring in mind that allergens have additive effects and the more allergens an atopic patient is exposed to, the easier and quicker anaphylactic shock and Kounis syndrome appear.[3]Second, the administration of epinephrine was the cause of stent thrombosis or the anaphylactic reaction? The described patient was stented with a bare metal stent followed by 3 overlapping drug-eluting stents. Bare metal and drug-eluting stents have components namely stainless steel that is a combination of nickel, chromium, titanium, manganese, molybdenum, polymer coating, and eluted antiproliferative drugs such as paclitaxel, zotarolimus, and accompanying antiplatelet therapy that constitute an allergenic complex. This allergenic complex embedded in the coronary intima is applying continuous, persistent, and chronic hypersensitivity inflammation able to induce stent thrombosis manifesting as the Kounis hypersensitivity coronary syndrome.[4] Several reports have shown that stents attract, such as magnet eosinophils and mast cells that release inflammatory mediators locally and in the systemic circulation able to induce coronary spasm and stent thrombosis. For example, acute myocardial infarction, in the stented area, manifesting as Kounis syndrome has coincided with allergic reactions from contrast material, insect and larvae stings, nonsteroidal anti-inflammatory agents, and even with allergy to clopidogrel the drug that is given to prevent stent thrombosis![56]Third, can we always give epinephrine intravenously? Epinephrine is the cornerstone of treatment for anaphylaxis but it can aggravate the ischemia, prolong QTc interval, promote platelet aggregation, and induce coronary vasospasm and arrhythmias. According to the current guidelines, there is no absolute contraindication to epinephrine use in anaphylaxis. However, the use of intravenous epinephrine is still controversial in severe allergic reactions. It should be considered in patients with severe hypotension or cardiac arrest who do not respond to aggressive fluid resuscitation. Intramuscular use of epinephrine is the safer and preferred route of administration unless the patient has severe anaphylaxis.[7]All above support the view that the described patient's acute myocardial infarction due to stent thrombosis following the intravenous epinephrine for bee sting-induced anaphylaxis was due to Kounis syndrome rather than to intravenous epinephrine administration.