Kounis syndrome risk factors, pathophysiology, and management

Abstract

The combination of acute coronary syndromes, illnesses associated with mast cell activation, interconnected and interacting inflammatory cells, allergic or hypersensitive reactions, and anaphylactic or anaphylactoid episodes is known as the Kounis syndrome. Non-steroidal anti-inflammatory drugs (such as ibuprofen, alclofenac, diclofenac, and naproxen) are the most frequently observed medications that cause Kounis syndrome, followed by antibiotics like ampicillin, azithromycin, ampicillin/sulfactam, amoxicillin, amikacin, cefazolin, cefoxitin, cefuroxime, cephradine, cinoxacin, lincomycin, penicillin, cefopera (5-fluorouracil, capecitabine, carboplatin, denileukin, interferons, paclitaxel, vinca alkaloids). There are three main types of Kounis syndrome: type 1 is allergic vasospastic angina, which is caused by endothelial dysfunction and is one of the causes of non-obstructive myocardial infarction; type 2 is allergic myocardial infarction; and type 3 is allergic stent thrombosis with an occluding thrombus (subtype a) or stent restenosis (subtype b). The first step in treating Kounis syndrome is to stop the allergic reaction, then use medicinal or interventional methods to stabilize the coronary arteries. Strong immunosuppressive and anti-inflammatory drugs, corticosteroids play a significant part in the management of allergic responses. Kounis syndrome is treated with intravenous corticosteroids, such as hydrocortisone, at a dosage of 5 mg/kg/day.