Kyung Hee University · 医学
Professor Ik-Kyung Jang's research lab specializes in cardiovascular thrombosis and interventional cardiology, focusing on the pathophysiology of acute coronary syndromes, thrombus composition, and the efficacy of antithrombotic therapies. The lab employs advanced intravascular imaging techniques such as optical coherence tomography (OCT) to characterize vulnerable atherosclerotic plaques in vivo, particularly in patients with acute myocardial infarction (AMI) or unstable angina (ACS). A key research direction involves evaluating the resistance of different thrombus components—such as platelet-rich and erythrocyte-rich clots—to thrombolytic therapy, as well as testing novel anticoagulants like argatroban in animal models. The lab also investigates immune-mediated thrombosis, notably heparin-induced thrombocytopenia (HIT), aiming to improve diagnostic accuracy and therapeutic strategies for thrombotic complications of anticoagulant therapy.
Figures are computed from collected data and may differ slightly.
OCT is a safe and effective modality for characterizing coronary atherosclerotic plaques in vivo. Thin-cap fibroatheroma was more frequently observed in patients with AMI or ACS than SAP. This is the first study to compare detailed in vivo plaque morphology in patients with different clinical presentations.
Acute myocardial infarction is triggered by coronary artery occlusion that may be recanalized by thrombolytic therapy with a success rate of up to 75% only. The resistance of coronary artery occlusion to thrombolysis may either be due to obstruction of the lumen by a nonthrombotic mechanism or by intrinsic resistance of thrombus to dissolution. Coronary arterial thrombi are composed of platelet-rich and erythrocyte-rich material in variable proportions. To evaluate the relative sensitivity of th
H eparin-induced thrombocytopenia (HIT; sometimes known as HIT type II) is a serious, immune systemmediated complication of heparin therapy often resulting in devastating thromboembolic outcomes. Although nomenclature distinctions have been made historically between this condition and the non-immune system-mediated, asymptomatic transient drop in platelet count in some patients receiving heparin (sometimes known as HIT type I), the term "HIT" is now preferably reserved for the immune system-medi
The effect of heparin and of the synthetic competitive thrombin inhibitor (2R,4R)-4-methyl-1-[N2-(3-methyl-1,2,3,4-tetrahydro-8-quinolinesulfon yl)-L-arginyl]-2-piperidinecarboxylic acid monohydrate (argatroban) on platelet-rich arterial thrombosis was studied in a rabbit model, consisting of a 4-6-mm everted ("inside-out") femoral arterial segment. Intravenous injection of heparin (200 units/kg) failed to prevent occlusion within 60 minutes in all 10 rabbits, whereas intravenous argatroban infu
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