Severe Renal Colic as a Trigger of Coronary Thrombosis on Plaque Erosion

Acute myocardial infarction may result from the complex interplay between transient systemic triggers and vulnerable coronary substrates.

A 37-year-old man presented with persistent chest pain after severe renal colic. Electrocardiography demonstrated lateral ST-segment elevation with diffuse ST-segment depression. Emergency coronary angiography revealed thrombotic occlusion of the proximal left anterior descending artery. Optical coherence tomography (OCT) identified extensive thrombus overlying a mildly atherosclerotic segment without evidence of plaque rupture, consistent with probable plaque erosion. Thrombus aspiration followed by drug-coated balloon angioplasty restored TIMI flow grade 3 without stent implantation.

This case illustrates a possible trigger-substrate interaction, in which severe visceral pain may act as a systemic trigger for coronary thrombosis in a patient with an erosion-prone phenotype. OCT was pivotal in defining the underlying mechanism and guiding a stent-free strategy.

Transient systemic stressors may act as triggers of acute coronary events. OCT enables mechanism-based, stent-free management in selected cases of plaque erosion.