Yusif Shakanti

Stockport NHS Foundation Trust, United Kingdom

Abstract Title: Kounis Syndrome Following Co-amoxiclav-Induced Anaphylaxis

Biography:

Research Interest: Background: Kounis syndrome, or allergic myocardial infarction, is an uncommon but potentially life-threatening entity in which acute coronary events are triggered by hypersensitivity reactions. Mast cell–mediated release of inflammatory mediators can cause coronary vasospasm, myocardial ischaemia, or infarction. Case Presentation: An 80-year-old woman with no prior coronary artery disease developed anaphylaxis minutes after intravenous co-amoxiclav in the emergency department. She had no documented penicillin allergy. Symptoms included acute dyspnoea, hypotension (systolic BP 70 mmHg), and widespread urticaria. An ECG performed within 15 minutes showed new ST-segment elevation in the inferior and anterior leads. Intramuscular epinephrine (0.5 mg) led to rapid haemodynamic stabilisation and symptom resolution. ST elevation partially resolved within 30 minutes and normalised completely within 12 hours. High-sensitivity cardiac troponin I was 10 ng/L (reference: 0–54 ng/L) on admission and 23 ng/L at 12 hours, indicating a non-dynamic pattern. Echocardiography revealed normal left ventricular function without regional wall motion abnormalities. Coronary angiography was not performed, as findings were consistent with transient coronary vasospasm rather than obstructive disease. Discussion: This case illustrates Type I Kounis syndrome, in which allergic mediators induce coronary vasospasm in angiographically normal vessels. Prompt recognition of the allergic trigger, the transient nature of ECG changes, and the absence of biomarker rise/fall can prevent unnecessary invasive intervention. Conclusion: Kounis syndrome should be considered in patients presenting with acute ECG changes following an allergic reaction. Timely treatment of the hypersensitivity response may reverse cardiac involvement without the need for coronary intervention.