A case report of complex acute coronary syndrome presentation: Plaque rupture and mild coronary artery ectasia presenting as de Winter T-waves morphing into anterior ST-elevation myocardial infarction in a young adult male.

This case report details a rare presentation of acute coronary syndrome in a young adult male with no significant medical history. A 24-year-old male presented with acute chest pain, and his initial ECG revealed the rare de Winter pattern, an underrecognized ST-elevation myocardial infarction (STEMI) equivalent. The de Winter T-wave morphology evolved into anterior STEMI, emphasizing the critical need for prompt recognition and intervention. Coronary angiography demonstrated mild coronary artery ectasia (CAE) with slow blood flow in the left anterior descending (LAD) and left circumflex arteries, alongside intramuscular bridging. Advanced imaging via optical coherence tomography identified ruptured plaque and mild spontaneous dissection as the underlying pathology. Initial treatment involved dual antiplatelet therapy, beta-blockers, statins, and low-molecular-weight heparin, leading to clinical stabilization and normalization of cardiac function. This case underscores the diagnostic challenges associated with CAE, particularly in young patients, and highlights the utility of advanced imaging modalities in personalizing treatment strategies. CAE, affecting 1%-5% of patients undergoing coronary angiography, is characterized by aneurysmal coronary dilation. It poses unique therapeutic challenges due to its association with turbulence, thrombus formation, and vulnerability to ischemic events. The findings revealed that even mild CAE, when coupled with structural abnormalities such as ruptured plaque, can result in significant ischemic complications. The case demonstrates the importance of multidisciplinary care and individualized management, combining medical therapy with advanced diagnostic tools. It also emphasizes the need for familiarity with the de Winter ECG pattern to facilitate timely reperfusion therapy and mitigate adverse outcomes. Further research into CAE pathophysiology, including genetic, inflammatory, and hemodynamic aspects, is essential to enhance risk stratification and optimize treatment approaches for this complex condition.