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Articles by J. J Kim
Total Records ( 5 ) for J. J Kim
  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.

  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
  Background—

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.

Conclusions—

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.

  J. J Kim , P Li , J Huntley , J. P Chang , K. C Arden and J. M. Olefsky
  OBJECTIVE

Forkhead box O (FoxO) transcription factors represent evolutionarily conserved targets of insulin signaling, regulating metabolism and cellular differentiation in response to changes in nutrient availability. Although the FoxO1 isoform is known to play a key role in adipogenesis, its physiological role in differentiated adipose tissue remains unclear.

RESEARCH DESIGN AND METHODS

In this study, we analyzed the phenotype of FoxO1 haploinsufficient mice to investigate the role of FoxO1 in high-fat diet–induced obesity and adipose tissue metabolism.

RESULTS

We showed that reduced FoxO1 expression protects mice against obesity-related insulin resistance with marked improvement not only in hepatic insulin sensitivity but also in skeletal muscle insulin action. FoxO1 haploinsufficiency also resulted in increased peroxisome proliferator–activated receptor (PPAR) gene expression in adipose tissue, with enhanced expression of PPAR target genes known to influence metabolism. Moreover, treatment of mice with the PPAR agonist rosiglitazone caused a greater improvement in in vivo insulin sensitivity in FoxO1 haploinsufficient animals, including reductions in circulating proinflammatory cytokines.

CONCLUSIONS

These findings indicate that FoxO1 proteins negatively regulate insulin action and that their effect may be explained, at least in part, by inhibition of PPAR function.

  Y. D Kim , C. B Park , J. J Kim , C. K Kim and S. W. Moon
 

Complications after performing mediastinoscopy are uncommon, but they may occur even for an experienced surgeon. The major complications have the potential to be life-threatening injuries, such as major vascular or airway injury. A 51-year-old man presented to our hospital due to mediastinal node enlargement on follow-up after he had undergone gastric cancer surgery 2 years previously. An iatrogenic bronchial rupture occurred while performing mediastinoscopic biopsy, and this injury was primarily repaired with multiple direct interrupted sutures, along with the aid of a homemade knot pusher under video mediastinoscopy, and we did not have to convert to an open thoracotomy.

 
 
 
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