Kounis Syndrome Triggered by Intravenous Co-Amoxiclav: A Case of Transient ST Elevation in the Context of Anaphylaxis.

Kounis syndrome, also known as allergic myocardial infarction, is a rare but potentially life-threatening condition in which acute coronary events are triggered by an allergic reaction. The pathophysiology involves mast cell degranulation and the release of inflammatory mediators such as histamine, leukotrienes, and platelet-activating factor, leading to coronary vasospasm, myocardial ischemia, or infarction. We present the case of a female patient in her 80s with no prior history of coronary artery disease who developed anaphylaxis shortly after intravenous administration of co-amoxiclav in the emergency department. She had no documented allergy to penicillin or prior hypersensitivity reactions. Within minutes, she experienced an acute onset of dyspnoea, hypotension (systolic BP dropped to 70 mmHg), and widespread urticaria. The patient was treated promptly with intramuscular epinephrine (0.5 mg), leading to hemodynamic stabilization and resolution of ECG changes. She was admitted for observation and recovered without further cardiac complications. Simultaneously, her ECG done within 15 minutes of the onset of the allergic reaction showed new ST-segment elevation in the inferior leads and anterior leads. She went on to have serial ECGs performed to monitor disease progression, and the ST elevations showed partial resolution within 30 minutes following treatment, with complete resolution 12 hours later. High-sensitivity cardiac troponin I was initially 10 ng/L (0-54 ng/L) and remained essentially unchanged at 23 ng/L after 12 hours, suggesting a non-dynamic pattern on serial monitoring. Echocardiography showed normal left ventricular function without regional wall motion abnormalities. Coronary angiography was not performed, as the clinical presentation, rapid normalization of ECG changes, normal echocardiographic findings, and non-dynamic cardiac biomarkers strongly supported a vasospastic rather than obstructive coronary pathology. This case illustrates the diagnostic challenge of differentiating Kounis syndrome from typical acute coronary syndromes, particularly in older adults. Recognizing the allergic trigger and observing the transient nature of ECG changes can help avoid unnecessary invasive procedures. Management should focus on treating the allergic reaction, which may be sufficient to reverse myocardial involvement. Kounis syndrome should be considered in patients presenting with ECG changes following an allergic reaction. Treatment should prioritize the management of the hypersensitivity response, which may in fact reverse cardiac involvement without the need for invasive cardiac procedures.