Kyung Hee University · Medicine
Professor Ik-Kyung Jang's research lab specializes in interventional cardiology and vascular imaging, with a primary focus on understanding the pathological mechanisms underlying acute coronary syndromes (ACS), particularly plaque erosion and its hemodynamic and biological determinants. The lab leverages advanced intravascular imaging techniques—especially optical coherence tomography (OCT) and intravascular ultrasound (IVUS)—to investigate plaque phenotypes, stent healing, and vascular responses in vivo, aiming to refine patient-specific treatment strategies. A key research direction involves distinguishing the pathophysiological mechanisms of plaque erosion from plaque rupture, with implications for tailored anti-thrombotic and interventional therapies. The lab also explores clinical outcomes in special populations, such as women with heparin-induced thrombocytopenia (HIT), highlighting sex-specific differences in treatment response.
Figures are computed from collected data and may differ slightly.
For patients with ACS caused by plaque erosion, conservative treatment with anti-thrombotic therapy without stenting may be an option.
Pathology and in vivo imaging studies have identified superficial plaque erosion as a frequent and important mechanism underlying acute coronary syndromes (ACS). In contrast with plaque rupture, the pathophysiological mechanisms leading to plaque erosion remain poorly understood. The advent of intravascular imaging techniques, particularly optical coherence tomography, has aided understanding of this mode of ACS in vivo by complementing previous insights from pathology studies. Appreciation of t
IVUS (A) and OCT (B) images of the stented right coronary artery are shown.Although IVUS showed a well-deployed stent, the detailed structure around the stent struts is not well visualized.In addition, OCT clearly visualized tissue prolapse between the stent struts (12 to 3 o'clock).The tissue prolapse occurred mainly in an area with lower OCT signal intensity, which is suggestive of a plaque with a large lipid content.
Compared with those with culprit plaque rupture, patients with acute coronary syndrome caused by culprit plaque erosion had a smaller number of nonculprit plaques and the lower levels of panvascular instability, affirming that distinct pathophysiologic mechanisms operate in plaque erosion and plaque rupture.
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