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Articles by S. W Lee
Total Records ( 8 ) for S. W Lee
  D. W Park , S. C Yun , J. Y Lee , W. J Kim , S. J Kang , S. W Lee , Y. H Kim , C. W Lee , J. J Kim , S. W Park and S. J. Park

Background— Although C-reactive protein (CRP) has been proposed as a useful biomarker for predicting atherothrombosis, the association between CRP and stent thrombosis after drug-eluting stent implantation has not been defined.

Methods and Results— We prospectively evaluated 2691 patients treated with drug-eluting stents who had a baseline CRP measurement. The primary outcome was stent thrombosis; secondary outcomes were death, myocardial infarction (MI), death or MI, and target vessel revascularization. During follow-up (median, 3.9 years), 32 patients had definite or probable stent thrombosis, 137 patients died, 227 had an MI, and 195 underwent target vessel revascularization. In multivariable Cox proportional-hazards models, elevated levels of CRP were significantly associated with increased risk of stent thrombosis (hazard ratio, 3.86; 95% confidence interval, 1.82 to 8.18; P<0.001). Elevated CRP levels also significantly predicted the risks of death (hazard ratio, 1.61; 95% confidence interval, 1.13 to 2.28; P=0.008), MI (hazard ratio, 1.63; 95% confidence interval, 1.25 to 2.12; P=0.001), and death or MI (hazard ratio, 1.61; 95% confidence interval, 1.29 to 2.00; P<0.001) but not target vessel revascularization (hazard ratio, 1.20; 95% confidence interval, 0.90 to 1.61; P=0.21). The incorporation of CRP into a model with patient, lesion, and procedural factors resulted in a significant increase in the C statistic for the prediction of stent thrombosis, MI, and the composite of death or MI.

Conclusions— Elevated CRP levels were significantly associated with increased risks of stent thrombosis, death, and MI in patients receiving drug-eluting stents, suggesting the usefulness of inflammatory risk assessment with CRP. Given the relatively infrequent occurrence of stent thrombosis, death, and MI, larger studies with longer-term follow-up are required to confirm the novel relationship.

  M. S Kim , C. S Lee , J Hur , H. J Cho , S. I Jun , T. Y Kim , S. W Lee , J. W Suh , K. W Park , H. Y Lee , H. J Kang , D. S Lee , G. Y Koh , H Nakagami , R Morishita , Y. B Park and H. S. Kim

Background— The low engraftment rate of stem/progenitor cells infused via the intracoronary route to the ischemic myocardium is one of the most important factors limiting the efficacy of cell therapy. We investigated the concept of priming peripheral blood stem cells enriched by granulocyte colony-stimulating factor mobilization and apheresis (mobPBSCs) with angiopoietin-1 (Ang1), to enhance the engraftment into the ischemic tissue and neovasculogenic potential.

Methods and Results— The expression of Tie2, the Ang1 receptor, was significantly higher in mobPBSCs than naïve peripheral blood mononuclear cells (19.2±3.0% versus 1.2±0.8% versus 1.2±0.2%; P<0.001 for mobPBSCs from acute myocardial infarction (AMI) patients with granulocyte colony-stimulating factor treatment for 3 days versus peripheral blood mononuclear cells from AMI patients versus peripheral blood mononuclear cells from stable angina patients). After 4 hours of cartilage oligomeric matrix protein (COMP)-Ang1 stimulation, mobPBSCs committed to the endothelial lineage with the induction of CD31 and VE-cadherin expression, mediated by Tie2/Ets-1 pathway. Priming of mobPBSCs with COMP-Ang1 induced the expression of 4β1 and 5β1 integrins, which are also Ets-1 downstream molecules, leading to enhanced adhesion to endothelial cells or fibronectin. In a rabbit ear ischemia/reperfusion model, priming of mobPBSCs with COMP-Ang1 improved first-pass engraftment to the distal vascular bed after intraarterial delivery. In a murine ischemic hind-limb model, intravascular delivery of primed mobPBSCs enhanced both engraftment and neovascularization.

Conclusions— The short-term priming with COMP-Ang1 may be a feasible and promising option to activate mobPBSCs by enhancing differentiation and adhesiveness and to improve the efficacy of cell therapy for ischemic diseases.

  S. J Park , Y. H Kim , D. W Park , S. W Lee , W. J Kim , J Suh , S. C Yun , C. W Lee , M. K Hong , J. H Lee , S. W Park and for the MAIN COMPARE Investigators

Background— Although intravascular ultrasound (IVUS) guidance has been useful in stenting for unprotected left main coronary artery stenosis, its impact on long-term mortality is still unclear.

Methods and Results— In the MAIN-COMPARE registry, patients with unprotected left main coronary artery stenosis in a hemodynamically stable condition underwent elective stenting under the guidance of IVUS (756 patients) or conventional angiography (219 patients). Patients with acute myocardial infarction were excluded. The 3-year outcomes between the 2 groups were primarily compared using propensity-score matching in the entire and separate populations according to stent type. In 201 matched pairs of the overall population, there was a tendency of lower risk of 3-year morality with IVUS guidance compared with angiography guidance (6.0% versus 13.6%, log-rank P=0.063; hazard ratio, 0.54; 95% CI, 0.28 to 1.03; Cox-model P=0.061). In particular, in 145 matched pairs of patients receiving drug-eluting stent, the 3-year incidence of mortality was lower with IVUS guidance as compared with angiography guidance (4.7% versus 16.0%, log-rank P=0.048; hazard ratio, 0.39; 95% CI, 0.15 to 1.02; Cox model P=0.055). In contrast, the use of IVUS guidance did not reduce the risk of mortality in 47 matched pairs of patients receiving bare-metal stent (8.6% versus 10.8%, log-rank P=0.35; hazard ratio, 0.59; 95% CI, 0.18 to 1.91; Cox model P=0.38). The risk of myocardial infarction or target vessel revascularization was not associated with the use of IVUS guidance.

Conclusions— Elective stenting with IVUS guidance, especially in the placement of drug-eluting stent, may reduce the long-term mortality rate for unprotected left main coronary artery stenosis when compared with conventional angiography guidance.

  Y. H Jeong , J. Y Hwang , I. S Kim , Y Park , S. J Hwang , S. W Lee , C. H Kwak and S. W. Park

Background— Optimal platelet inhibition is an important therapeutic adjunct in patients acute myocardial infarction (AMI) undergoing coronary stenting. Whether adjunctive cilostazol to dual antiplatelet therapy (triple antiplatelet therapy) can inhibit enhanced platelet reactivity in patients with AMI yet has not been determined. The aim of this study was to assess the degree of platelet inhibition by triple antiplatelet therapy in patients with AMI.

Methods and Results— Immediately after emergency room arrival, patients with AMI received clopidogrel (600-mg loading dose, followed by 75 mg daily) and aspirin (300-mg loading dose and 200 mg daily throughout the study period). After patients underwent coronary stenting (n=90), they were randomly assigned to 1 of 3 groups before discharge: standard group, clopidogrel of 75 mg daily (n=30); high maintenance dose (MD) group, clopidogrel of 150 mg daily (n=30); and triple group, adjunctive cilostazol of 100 mg twice daily to clopidogrel of 75 mg daily (n=30). Platelet reactivity was assessed at predischarge and 30-day follow-up by conventional aggregometry and the VerifyNow P2Y12 assay. Predischarge platelet reactivities were similar in the 3 groups. At 30-day follow-up, inhibition of maximal aggregation with 20 µM ADP stimuli was 6.0% in the standard group, 19.1% in the high-MD group, and 42.4% in the triple group (P<0.001), whereas inhibition of late aggregation with 20µM ADP stimuli was 10.8%, 38.1%, and 66.4%, respectively (P<0.001). Similar results were demonstrated when 5 µM ADP was used. Furthermore, percent changes of P2Y12 reaction unit were significantly different among regimens (10.6% in the standard group, 30.7% in the high-MD group, and 43.0% in the triple group; P<0.001). With respect to high-postclopidogrel platelet reactivity (prespecified as 20 µM ADP-induced maximal aggregation >50% of light transmission), fewer patients in the triple group (13.3%) met the criteria as compared with those in the standard (76.7%) and high-MD groups (56.7%) at 30-day follow-up (P<0.001). In the triple group, there were more potent and consistent platelet inhibitions by all parameters as compared with the high-MD group except for percent changes of P2Y12 reaction unit (P=0.071).

Conclusions— Among patients with AMI undergoing coronary stenting, triple antiplatelet therapy results in a greater antiplatelet effect at 30 days as compared with a high-MD clopidogrel or standard dual antiplatelet therapy.

  S. Y Min , D. W Park , S. C Yun , Y. H Kim , J. Y Lee , S. J Kang , S. W Lee , C. W Lee , J. J Kim , S. W Park and S. J. Park

Background— The clinical characteristics that identify high-risk subsets of patients with unprotected left main coronary artery disease undergoing percutaneous coronary intervention (PCI) or coronary artery bypass grafting (CABG) have not been well established.

Methods and Results— Between January 2000 and June 2006, 2240 patients with unprotected left main coronary artery disease underwent PCI (n=1102) or CABG (n=1138). Twenty-six preprocedural parameters were evaluated by univariate and multivariate Cox regression analysis to identify independent predictors of all-cause mortality and target-vessel revascularization. Interaction tests were performed to compare heterogeneities of effects of preprocedural parameters depending on the revascularization methods. During follow-up (median of 3.1 years), 187 patients died (78 PCI and 109 CABG) and 149 patients had target-vessel revascularization (121 PCI and 28 CABG). EuroSCORE ≥6 was an independent predictor of death in both groups. Additional independent predictors were chronic renal failure and previous congestive heart failure in the PCI group and age ≥75 years, atrial fibrillation, right coronary artery disease, and left main distal bifurcation disease in the CABG group. Interaction analysis showed no heterogeneities of the effects of variables depending on the revascularization methods. Independent predictors of target-vessel revascularization were acute coronary syndrome and left main distal bifurcation disease in the PCI group and history of coronary intervention in the CABG group. The interaction between previous PCI and treatment remained after adjustment for all independent predictors of target-vessel revascularization (interaction P=0.0345).

Conclusions— Several clinical characteristics were identified as important preprocedural predictors of long-term adverse outcomes after percutaneous or surgical revascularization in patients with unprotected left main coronary artery disease.

  S. J Kang , G. S Mintz , D. W Park , S. W Lee , Y. H Kim , C. W Lee , K. H Han , J. J Kim , S. W Park and S. J. Park

The long-term natural history of acquired malapposition continues to be the subject of debate.

Methods and Results—

Using volumetric intravascular ultrasound analyses, we evaluated serial (poststenting, 6-month, and 2-year follow-up) changes in drug-eluting stent–treated vascular segments with acquired malapposition. External elastic membrane, stent, lumen, malapposition, and peristent plaque+media (P+M=external elastic membrane –stent– malapposition) areas were measured; and volumes were calculated and divided by stent length (normalized volume). Among 250 lesions in which complete serial intravascular ultrasound data were available, stent malapposition was identified in 19 lesions (7.6%) at 6 months, and an additional 13 malapposition lesions were newly detected at 2 years (5.2%). Because no malapposition sites resolved, the malapposition rate at 2 years was 12.8%. Malapposition areas and volumes were correlated to the increases in external elastic membrane (positive remodeling) throughout the study period, from immediately after stenting to 6 months and from 6 months to 2 years, both in the group that developed malapposition at 6 months and in the group that developed malapposition at 2 years. Clinical follow-up beyond the 2 year intravascular ultrasound study was done in all patients. Overall, there were 2 cardiac deaths and 1 noncardiac death. Two patients presented with acute myocardial infarction associated with very late stent thrombosis (1 definite stent thrombosis, 1 probable stent thrombosis). Three patients underwent repeat revascularization owing to in-stent restenosis developed after the 2-year follow-up.


Expansive vascular remodeling may play a role in the development and dynamic progression of acquired drug-eluting stent malapposition, not only during the first 6 months after implantation but thereafter.

  W. J Lee , E. S Cha , M Ha , Y. W Jin , S. S Hwang , K. A Kong , S. W Lee , H. K Lee , K. Y Lee and H. J. Kim

This study details the distribution and trends of doses of occupational radiation among diagnostic radiation workers by using the national dose registry between 1996 and 2006 by the Korea Food and Drug Administration. Dose measurements were collected quarterly by the use of thermoluminescent dosemeter personal monitors. A total of 61 732 workers were monitored, including 18 376 radiologic technologists (30 %), 13 762 physicians (22 %), 9858 dentists (16 %) and 6114 dental hygienists (9.9 %). The average annual effective doses of all monitored workers decreased from 1.75 to 0.80 mSv over the study period. Among all diagnostic radiation workers, radiologic technologists received both the highest effective and collective doses. Male radiologic technologists aged 30–49 y composed the majority of workers receiving more than 5 mSv in a quarter. More intensive monitoring of occupational radiation exposure and investigation into its health effects on diagnostic radiation workers are required in South Korea.

  Y Xia , P Ongusaha , S. W Lee and Y. C. Liou

In response to various environmental stresses, the stress-responsive MAPKs p38 and JNK are activated and phosphorylate ATF2 and c-Jun transcription factors, thereby affecting cell-fate decision. Targeted gene disruption studies have established that JNK-c-Jun signaling plays a vital role in stress-induced apoptosis. The oncogenic phosphatase Wip1 acts as an important regulator in DNA damage pathway by dephosphorylating a spectrum of proteins including p53, p38, Chk1, Chk2, and ATM. In this study we show that Wip1 negatively regulates the activation of MKK4-JNK-c-Jun signaling during stress-induced apoptosis. The loss of Wip1 function sensitizes mouse embryonic fibroblasts to stress-induced apoptosis via the activation of both p38-ATF2 and JNK-c-Jun signaling. Here we reveal that Wip1 has dual roles in alternatively regulating stress- and DNA damage-induced apoptosis through p38/JNK MAPKs and p38/p53-dependent pathways, respectively. Our results point to Wip1 as a general regulator of apoptosis, which further supports its role in tumorigenesis.

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