BACKGROUND: There are many evidences that inflammation is an important determinant of the development of atherosclerosis and one of the systemic markers of inflammation, C-reactive protein(CRP), is associated with extent of coronary artery disease and risk of coronary events. We assessed the time response of CRP response after coronary angioplasty and it's influence on the clinical restenosis in angina patients. MATERIALS AND METHODS: Patients included 36 angina patients undergoing single vessel angioplasty. Levels of CRP were measured before and 12, 24, 48, and 72 hours after angioplasty. Clinical restenosis was assessed at 6 months after procedure. RESULTS: Baseline CRP level was 0.30+/-0.01 mg/dL in stable and 0.46+/-0.28 mg/dL in unstable angina patients(p<0.05). After angioplasty, CRP level was increased with peak at 24 hour and persisted to 72 hours after angioplasty. At 24 hour after angioplasty, the magnitude of CRP change was 0.32+/-0.31 mg/dL in stable and 0.79+/-0.73 mg/dL in unstable angina patient(p<0.05). The change of CRP level was not associated with troponin-T after angioplasty. In unstable angina patients, clinical restenosis was developed in 8% of patients with low baseline CRP levels and in 50% of those with high baseline CRP levels more than 0.6 mg/dL(p<0.05). CONCLUSION: In unstable angina patients, inflammatory response is more increased than stable angina patients, and increased inflammatory response effects on the restenosis after coronary angioplasty.
Angina, Stable ; Angina, Unstable ; Angioplasty* ; Atherosclerosis ; C-Reactive Protein* ; Coronary Artery Disease ; Humans ; Inflammation ; Troponin T

BACKGROUND AND OBJECTIVES: Percutaneuous transvenous mitral commissurotomy(PTMC) has been performed as an effective non-surgical treatment modality of rheumatic mitral stenosis. Mitral regurgitation(MR) as a complication of the procedure occur in 20-53% of the patients. The moderate to severe mitral reguargitation, created by the PTMC, sometimes leads to the requirement for mitral valve replacement, but most of the MR limits the optimal dilation of mitral commissure due to the worry about the progression of the MR. This study was designed to evaluate the occurrence of mitral regurgitation and predictive factors for the moderate to severe mitral regurgitation(grade> or =2) induced by PTMC. METHODS: This study enrolled 46 patients(female 42, mean age 45 years) who have performed PTMC in Yeungnam University Hospital from May 1996 to May 1999. We analyzed the occurrence rate of mitral regurgitation(MR) and predictive factors for MR grade> or =2 after procedure. RESULTS: MR was detected in 35% of the patients prior PTMC, and in 56% after the procedure(grade 1, 30%; grade 2, 15%; grade 3, 11%). 21 cases of the MR was commissure MR as a grade< or =2. MR grade 3, occured in 5 patients, was non-commissure MR caused by the unilateral rupture of the lateral commissure in 4 patients and tearing of the annulus in one patient. On the univariate analysis, patients with MR grade> or =2 showed more frequent atrial fibrillation, mitral regurgitation and fluoroscopic calcification, and had more severe symptoms than patients with MR grade<2 before the procedure. On the analysis of the calcification, there was no significant difference of the leaflet calcification score, but the commissure calcification score was significantly higher in MR> or =2 group than MR<2 group(1.5+/-0.54 vs 2.5+/-0.96, p=.02). On the multivariate logistic regression analysis, independent predictor of MR grade> or =2 was fluoroscopic mitral calcification(OR 6.38, p=.048). CONCLUSION: Mild to moderate commissure MR was observed in most of the patients after PTMC. Commissure calcification have more influence on the development of MR grade> or =2 than valvular calcification, and the fluoroscopic mitral calcification can predict the occurrence of MR grade> or =2 mitral regurgitation after PTMC.
Atrial Fibrillation ; Humans ; Logistic Models ; Mitral Valve ; Mitral Valve Insufficiency* ; Mitral Valve Stenosis ; Rupture

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Recent laboratory data indicate that the adenosine during the ischemic period may trigger protection via A1 or A3 adenosine receptor and also protein kinase C(PKC) plays a central role. This study was designed to determine the role of adenosine receptor subtypes and PKC in the preconditioning protection. METHODS: All cat heart groups were subjected to 40min ischemia and 30min reperfusion. The preconditioning protocol consists of 4min ischemia and then 10min of reperfusion 4 times. The effects of ischemic preconditioning, nonselective adenosine receptor blocker(SPT), an A1 specific antagonist(DPCPX) and protein kinase C inhibitor(Polymyxin B), on ischemic preconditioning were determined by infarction size. There were 5 groups : (1) control group (Group 1, n=10)(2) Ischemic preconditioned group(Group 2, n=9)(3) DPCPX pretreatment group(Group 3, n=6)(4) SPT preteatment group(Group 3, n=6)(5) Polymyxin B pretreatment group(Group 5, n=6). SPT and DPCPX were given intravenously 5 min before ischemic preconditioning. Polymyxin B was administered to cats for 30min during ischemic preconditioning period. RESULTS: Ischemic preconditioning only or pretreatment with DPCPX prior to preconditioning demonstrated a significant reduction in infarct size(22.6+/-1.5, 25.4+/-0.9% infarction of the risk zone, respectively, p<0.05) with respect to control, SPT-pretreatment, and polymyxin B-pretreatment groups(44.0+/-1.7, 43.0+/-2.0 and 40.3+/-0.4% infarction of the risk zone, respectively). CONCLUSIONS: Ischemic preconditioning protects heart from subsequent ischemia. Protection was blocked by SPT and protein kinase C inhibitor(polymyxin B), but not by A1 antagonist DPCPX. The cardioprotective effects by ischemic preconditioning in the in vivo cat heart appear to be dependent on A3 adenosine receptors and activation of protein kinase C.
Adenosine* ; Animals ; Arrhythmias, Cardiac ; Cats* ; Heart* ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Polymyxin B ; Polymyxins ; Protein Kinase C* ; Protein Kinases* ; Receptors, Purinergic P1* ; Reperfusion

BACKGROUND: It is well known that ischemic preconditioning protects the heart against infarction or arrhythmias from a subsequent ischemic injury. Two phases of the effect of preconditioning has been explored, early protection and second window of protection at 24 hours. The late protection was seen in some animal model, but the precise mechanism is controversal. This study was designed to evaluate the late cardioprotective effect and role of HSP70 in ischemic preconditioning of cat heart. METHODS: Two groups of cats were studied. Control animals were subjected to an episode of 40-min coronary artery occlusion followed by 30-min reperfusion. Experimental animals were subjected to ischemic preconditioning before the 40-min ishcemia/reperfusion. The preconditioning protocol was comprised of three 5-min episodes of ischemia interspersed by 10-min episodes of reperfusion. After sustained ischemia and reperfusion, left ventricular risk area and infart area were measured by injection of Evans blue bye and triphenyltetrazolium staining, and myocardial HSP70 mRNA was examined in risk(left ventricular anterior wall) and nonrisk(left ventricular posterior wall) area using northern blot hybridization. HSP70 mRNA expression was quantified as a percent of GAPDH. The late cardioprotective effects of ischemic preconditioning were determined by infarct size (% area at risk). RESULTS: Infarct size was markedly limited by ischemic preconditioning when compared with the control group (18.5+/-6.9% vs 38.5+/-11.1%; p<0.001). HSP70 mRNA expression in risk area was much higher in preconditioning group than control group(78+/-12% vs 41+/-11%; p<0.01). But, there was no significant difference of HSP70 mRNA expression in the posterior wall between control and ischemic preconditioning group. CONCLUSIONS: These data suggest that ischemic preconditioning have delayed myocardial protective effect from ischemia. The increase in myocardial HSP70 mRNA may be one of the contributing factors to the delayed cardioprotective effects of ischemic preconditioning in cats.
Animals ; Arrhythmias, Cardiac ; Blotting, Northern ; Cats* ; Coronary Vessels ; Evans Blue ; Heart* ; Heat-Shock Proteins* ; Hot Temperature* ; HSP70 Heat-Shock Proteins ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Models, Animal ; Reperfusion ; RNA, Messenger

BACKGROUND: To study the prognosis of patients with lung cancer, many investigators have reported the methods to detect cell proliferation in tissues including PCNA, thymidine autoradiography, flow cytometry and Ki-67. PCNA, also known as cyclin, is a cell related nuclear protein with 36KD intranuclear polypeptide that is maximally elevated in S phase of proliferating cells. In this study, PCNA was identified by paraffin-embedding tissue using immunohistochemistry which has an advantage of simplicity and maintenance of tissue architecture. The variation of PCNA expression is known to be related with proliferating fraction, histologic type, anatomic(TNM) stage, degree of cell differentiation, S-phase fraction and survival rate. We analyzed the correlation between PCNA expression and S-phase fraction, survival. METHODS: To investigate expression of PCNA in primary lung cancer, we used immunohistochemical stain to paraffin-embedded sections of 57 resected primary non-small cell lung cancer specimen and the results were analyzed according to the cell type, cell differentiation, TNM stage, S-phase fraction and survival. RESULTS: PCNA expression was dMded into five group according to degree of staging(-, +, ++, +++,++++). Squamous cell type showed high positivity than in adenocarcinoma. Nonsignificant difference related to TNM stage was noticed. Nonsignificant difference related to degree of cell differentiation was noticed. S-phase fraction was increased wit advance of PCNA positivity, but t could not reach the statistic significance. The 2 year survival rate and median survival time were -50% 13 months, +75% 41.3 months, ++73% 33.6 months, +++67% 29.0 months, ++++25% 9 months with statistic significance (P<0.05, Kaplan-Meier, generalized Wilcox). CONCLUSION: From this study. PCNA expression was high positive n squamous cell cancer. And, there was no relationship between PCNA positivity and TNM stage, cellular differentiation or S-phase fraction. But, the patients with high positive PCNA staining showed poor survival rate than the patients with lower positive PCNA. It was concluded that PCNA immunostaining is a simple and useful method for survival prediction in paraffin embedded tissue of non-small cell lung cancer.
Adenocarcinoma ; Autoradiography ; Carcinoma, Non-Small-Cell Lung* ; Cell Differentiation ; Cell Proliferation ; Cyclins ; Flow Cytometry ; Humans ; Immunohistochemistry ; Lung Neoplasms ; Neoplasms, Squamous Cell ; Nuclear Proteins ; Paraffin ; Prognosis ; Proliferating Cell Nuclear Antigen* ; Research Personnel ; S Phase ; Survival Rate* ; Thymidine

No abstract available.
Neurofibroma* ; Scalp*

BACKGROUND: It is well known that intracoronary thrombolysis during the early period of acute myocardial infarction leads to the limitation of myocardial necrosis, preserves left ventricular function, and improves survivals. The recanalization rate of intracoronary rrokinase infusion into infarct-related coronary artery was known as 62-94 percents in previos studies. The various factors influence the outcome of intracoronary thrombolysis, including total dose of urokinase, time from onsrt of chest pain to thrombolysis. The purpose of this study was to evaluate whether the occlusion site morphology influences recanalization rates of intracoronary thrombolysis. METHODS: We evaluated infarct-related coronary artery morphology of 56 acute mycardial infarction patients who performed intracoronary thrombolytic therapy within 6-12 hours after the onset of acute myocardial infarction. Intracoronary urokinase infusion was performed at a rate of 25000 IU/minute. The presence of calcification, collaterals, side branches and the stump site morphologies(thrombus type, pencil type, cutting type) were identified on magnified 35mm cine frames. RESULTS: Reperfusion was successed in 34 patients and failed in 22 patients. There were no statistically significant difference in the pressure of calcification, collaterals, and side branches between success and failure groups. Intracoronary thrombus was identified in 21 percent of success group, but not in failure group. The reperfusion rates according to stump site morphology were 76% in thrombus type, 58% in cutting type, and 42% in pencil type(p<0.05). CONCLUSION: Our study indicates the presence of intracoronary thrombus and the morphology of thrombus type is more effective in intracoronary thrombolysis in acute myocardial infarction. The identification of types of the coronary obstruction will be helpful for the selection of intracoronary thrombolysis in acute myocardial infarction patients. And the results suggest that the difference of stump composition show different stump morphologies.
Chest Pain ; Coronary Vessels* ; Humans ; Infarction ; Myocardial Infarction* ; Necrosis ; Reperfusion ; Thrombolytic Therapy ; Thrombosis ; Urokinase-Type Plasminogen Activator ; Ventricular Function, Left

No abstract available.
Dermatitis, Contact*

No abstract available.
Humans ; Inpatients* ; Pediatrics ; Retrospective Studies*

No abstract available.
Hyperplasia ; Scrotum