Kounis syndrome presenting with acute inferior wall myocardial infarction and cardiogenic shock secondary to intravenous ampicillin/sulbactam administration

To the Editor,

Kounis syndrome (KS) is induced by allergic and anaphylactic reaction, and is considered a rare cause of coronary artery spasm (1) A 44-year-old male patient was admitted to our center with complaint of severe chest pain lasting for 1 hour. He was administered treatment of 1 g intravenous ampicillin/sulbactam with diagnosis of upper respiratory tract infection. He did not have history of allergy or traditional risk factors for coronary artery disease. Ten minutes after the injection, he felt severe, squeezing retrosternal chest pain. On physical examination, he was pale. He did not have pruritus or rash. His blood pressure (BP) and heart rate were 77/48 mm Hg and 104 bpm, respectively. Electrocardiogram (ECG) showed ST segment elevation in leads D2, 3, aVF, V4R, V5R, and V6R. Echocardiogram revealed moderate reduction in left ventricular ejection fraction (45%), inferior and inferoseptal wall hypokinesia, and right ventricular systolic dysfunction. Coronary angiography (CAG) revealed diffuse constriction of left anterior descending artery and left circumflex artery, and total occlusion of right coronary artery. All constrictions were considered coronary artery spasm, and despite deep hypotension, intracoronary nitroglycerin was administered to confirm spasms. Subsequently, BP rose to 108/73 mm Hg. By this time, chest pain was alleviated and follow-up CAG showed complete normalization of coronary artery spasm. Combination treatment of intravenous 25 mg prednisolone, 50 mg ranitidine, and 50 mg diphenhydramine was administered with diagnosis of KS. He felt better and chest pain was completely resolved over the next 15 minutes. Second ECG showed resolution of ST segment elevation. Isosorbide-5-mononitrate and ciprofloxacin 400 mg once a day were administered to manage KS. Patient’s eosinophil count was in normal range (120/µL), and cardiac biomarkers were elevated as follows: troponin I: 3 ng/dL, creatine kinase-MB: 52 U/L. Additionally, serum tryptase level was elevated at 146 ng/mL (reference range: <11.4 ng/mL). Patient was observed closely over the next 2 days and did not develop further chest pain or complication. There are 3 types of KS; type I variant is described as coronary artery spasm in patients with normal coronary arteries without traditional risk. In these patients, coronary artery spasm is triggered by acute release of inflammatory mediators (1–3). Although cardiac marker elevation is not expected in type I variant, our patient suffered severe myocardial infarction due to crucial diffuse coronary artery spasm. Ampicillin/sulbactam-induced KS is very rarely reported. First intravenous antibiotic administration resulted in catastrophic complication in our patient. Although adrenalin is a traditional drug used for anaphylactic shock, it causes both coronary vasodilatation and myocardial oxygen demand by direct inotropic and chronotropic effects (4). Due to serious side effects of adrenalin, we administered antihistaminic and corticosteroid combination. In selected patients, intracoronary nitroglycerine may be used to reverse vasospasm. In patients with coronary vasospasm related to allergic reaction, treatment with vasodilators such as nitrates and calcium channel inhibitors is choice of treatment for case of coronary vasospasm (5).