As prediction of rapidly aging society, bone health is considered increasingly important and received more attention than ever. Bone health is regulated by balancing between bone resorptive osteoclasts and bone formative osteoblasts. Disruption of balance between bone-resorbing osteoclasts and bone-forming osteoblasts results in bone disease. Natural products have recently received much attention as an alternative tool for the development of novel therapeutic strategy. Baicalein is reported it has anti-cancer, anti-inflammatory and antioxidant effects. Baicalein also has been known that it has both promotive effect on MC3T3-E1 cell line and inhibitory effect on RAW 264.7 cell line. However, the inhibitory mechanism of baicalein using bone marrow derived macrophages (BMMs) on osteoclast differentiation remains not clear. In this study, the suppressive mechanism by baicalein on osteoblast differentiation was evaluated. Bicalein inhibited receptor activator of nuclear factor-kappaB ligand (RANKL)-induced osteoclast differentiation in BMMs in a dose dependent manner without any toxicity. Baicalein suppressed phosphorylation of protein kinaseB (Akt), c-Jun N-terminal kinases (JNK) and phosphoinositide-specific phospholipaseCgamma2 (PLCgamma2). Furthermore, Baicalein suppressed the induction of RANKL-induced c-Fos and Nuclear factor of activated T cell c1 (NFATc1), essential genes on osteoclastogenesis. In BMMs, Bicalein inhibited the mRNA expression of tartrate-resistant acid phosphatase (TRAP), osteoclast-associated receptor (OSCAR), cathepsinK, dendritic cell-specific transmembrane protein (DC-STAMP). Moreover, baicalein promoted differentiation of osteoblast on bone marrow stromal cells (BMSCs). Taken together, these results suggest that baicalein has a potential for treating bone lytic diseases, such as osteoporosis, periodontitis, and rheumatoid arthritis.
Acid Phosphatase ; Aging ; Antioxidants ; Arthritis, Rheumatoid ; Biological Products ; Bone Diseases ; Bone Marrow* ; Cell Line ; Genes, Essential ; Macrophages* ; Mesenchymal Stromal Cells ; Osteoblasts ; Osteoclasts* ; Osteoporosis ; Periodontitis ; Phospholipase C gamma ; Phosphorylation ; Phosphotransferases ; RANK Ligand ; RNA, Messenger

BACKGROUND AND OBJECTIVES: Recent studies have implicated inflammation in the pathogenesis of coronary artery disease. The aim of this study was to determine whether C-reactive protein (CRP) levels are predictive of major adverse cardiac events (MACE) following stenting. SUBJECTS AND METHODS: The study comprised 193 patients (90 men, 152 unstable angina, mean age 63 years) between October 1999 and March 2001. The patients were classified into 2 groups according to their MACE, [group A; MACE (+), n=46 and group B; MACE (-), n=147]. RESULTS: During clinical follow-up at a mean duration of 15 months, there was 1death, 7 myocardial infarctions, 25 cases of revascularization therapy, and 13 recurrent anginas. At 24 hours after stenting, the CRP levels were significantly higher in group A compared to group B (5.4, 0.6-15.2 vs. 3.1, 0.1-9.8 mg/L, respectively, p<0.01), with the elevation of the CRP level ( >8.0 mg/L) occurring more commonly in group A than group B (24% vs. 9%, p<0.05). The differences in the CRP levels between the baseline and 24 hours following stenting (CRP 24h-base ) were also significantly higher in group A than in group B. After adjustment for age, sex, and cardiovascular risk factor, multi-variate analysis using logistic regression revealed the CRP levels 24 hours after stenting were predictive of MACE, with an odd ratio of 1.6 (95% CI 1.1-2.2, p=0.01). CONCLUSION: CRP levels, 24 hours following intervention, are powerful predictor of cardiac events in patients with stable or unstable angina undergoing coronary stenting. These results suggest that the inflammatory responsiveness to coronary intervention can plays an important role in predicting cardiac events.
Angina, Unstable ; Angioplasty, Balloon, Coronary ; C-Reactive Protein* ; Coronary Artery Disease ; Follow-Up Studies ; Humans ; Inflammation ; Logistic Models ; Male ; Myocardial Infarction ; Risk Factors ; Stents*

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.
Adenosine Diphosphate ; Adenylyl Cyclases ; Agranulocytosis ; Aspirin ; Cardiovascular Diseases* ; Cerebral Infarction ; Dipyridamole ; Humans ; Myocardial Ischemia ; Neutropenia* ; Platelet Aggregation ; Pneumonia ; Recurrence ; Stroke ; Sulfinpyrazone ; Thromboxane A2 ; Ticlopidine

Ticlopidine is an antiplatelet agent used as a drug to prevent the recurrence of cerebral infarction or ischemic heart disease. Close attention has recently been paid to the superiority of this drug to aspirin in the prevention of stroke. Its mechanism of action differs from aspirin, dipyridamole, and sulfinpyrazone. Inhibition of the adenosine diphosphate induced pathway of platelet aggregation, along with the activation of adenylate cyclase and suppression of platelet-activating factor and thromboxane A2, are the postulated mechanisms of action of ticlopidine. Because ticlopidine causes neutropenia and agranulocytosis in roughly 1% of treated patients, usually within the first 3 months of treatment, this drug has been reserved for patients intolerant to aspirin therapy. We reported two cases of ticlopidine-induced neutropenia and one patient hospitalized with severe neutropenia and pneumonia.
Adenosine Diphosphate ; Adenylyl Cyclases ; Agranulocytosis ; Aspirin ; Cardiovascular Diseases* ; Cerebral Infarction ; Dipyridamole ; Humans ; Myocardial Ischemia ; Neutropenia* ; Platelet Aggregation ; Pneumonia ; Recurrence ; Stroke ; Sulfinpyrazone ; Thromboxane A2 ; Ticlopidine

BACKGROUND: Insulin resistance syndrome has been proposed as a major promotor of atherosclerotic disease and earlier studies have implied the hyperinsulinemia itself may enhance coronary vasomotor tone. In patients with vasospastic angina, previous studies have been inconclusive whether to basal coronary artery tone is elevated at the spasm related and nonspasm related artery. This study was performed to investigate whether basal coronary artery tone is elevated ans insulin resistance syndrome correlates to vasospastic angina. If insulin resistance syndrome correlates to vasospastic angina, we also investigated whether insulin resistance syndrome correlates to basal coronary artery tone. METHODS: The study comprised 27 patients with vasospastic angina(M/F ; 19/8, mean age ; 52+/-2 year) and 21 control subjects with atypical chest pain(M/F ; 9/8, mean age ; 47+/-3 year). We assessed basal coronary artery tone by obtaining the percent increase in coronary artery diameter induced by nitroglycerin and also examined glucose and insulin response to an oral glucose load of 75g. RESULTS: 1) There were no significant differences in body surface area, abdominal hip ratio, body mass index, incidence of hypertension, lipid profile, von-Willebrand factor, fibrinogen, and microalbumin except smorking incidence [vasospastic angia ; 16(50%) vs control ; 5(24%), p<0.05)] between vasospastic angina group and control. 2) Basal coronary artery tone was greater at the nonspastic site of the spasm-related artery(28.1+/-2.2% vs 13.1+/-0.9%, p<0.0001) and non-spasm related artery(23.7+/-1.6% vs 13.1+/-0.9, p<0.0001) in the patients with vasospstic angina than in control subjects. In the patients with vasospastic angina, high activity group had a greater basal coronary artery tone than low activity group at the nonspastic site of the spasm-related artery(31.7+/-2.6 vs 20.4+/-2.7%, p<0.001) and non-spasm related artery(26.8+/-2.0 vs 19.4+/-5.8%, p<0.001). 3) Plasma glucose and serum insulin response to an oral glucose load were similar between vasospastic angina group and control subjects, and glucose area, insulin area, and insulinogenic index(delta sigma Glucose / delta sigma Insulin)(330+/-12 vs 328+/-20 mg/dl *hour, 107+/-14 vs 96+/-17uU/ml*hour, and 2.18+/-0.33 vs 2.63+/-0.46, respectively, p=NS) also did not between both groups. 4) Two group did not differ siginificantly in the prportion of glucose intolerance but glucose area and insulin area were significantly high in vasospastic angina patients with glucose intolerance than in control subjects with normal glucose tolerance(366+/-22 vs 257+/-17mg /dl*hour, 127+/-19 vs 52+/-15uU*hour, respectively, p<0.05), but basal coronary artery tone did not differ significantly between vasospastic angina patients with glucose intolerance and control subjects with normal glucose tolerance. CONCLUSION: 1) These results revealed that basal coronary artery tone is elevated at the nonspastic site of the spasm related artery and non-spastic vessel, and the disease activity associated with elevated basal coronary artery tone in vasospastic angina. 2) But these results did not reveal the correlation of hyperinsulinemia with vasospastic angina, and so we did not determine the role of hyperinsulinemia as a pathogenesis of coronary spasm and the relation between hyperinsulinemia and basal coronary artery tone.
Arteries ; Blood Glucose ; Body Mass Index ; Body Surface Area ; Coronary Vessels* ; Fibrinogen ; Glucose ; Glucose Intolerance ; Hip ; Humans ; Hyperinsulinism ; Hypertension ; Incidence ; Insulin Resistance* ; Insulin* ; Nitroglycerin ; Spasm ; Thorax

Torsade de Points is unique polymorphic ventricular tachycardia associated with QT interval prolongation. The mechanism of Torsade de Points was not defined exactly but triggered activity associated with afterdepolarization and/or dispersion of repolarization were known possible explanation. Torsade de points is most often induced by various drugs such as antiarrythmic agents, antipsychotic agents, antibiotis, and antihistamines. Astemizole(Hismanal(R)) and Terfenadine among antihistamines are reported that cause leading to a Torsade de Points. We experienced the case of Torsade de Points which was induced with Piprinhydrinate(Diphenylpyraline, Plokon(R)), antihistamine of ethanolamine derivatives, expressed recurrent syncope and dizziness in a young lady.
Antipsychotic Agents ; Dizziness ; Ethanolamine ; Histamine Antagonists ; Syncope ; Tachycardia, Ventricular* ; Terfenadine

BACKGROUND: Percutaneous transluminal coronary angioplasty(PTCA) is one of the most widely used therapeutic procedures in the treatment of patients with coronary artery disease. However, acute closure and late restenosis remain a major limitation of PTCA despite extensive efforts to prevent. Coronary artery stents have been proposed as a treatment modality for acute closure and restenosis. We evaluated the initial success rate, complications, the restenosis rate, and the clinical outcomes after coronary artery stenting. METHODS: We implanted 56 stents(Palmaz-Schatz(PS) stent : 38 ; #3.0-14, #3.5-7, #4.0-17, Gianturco-Roubin(GR) stent : 18 ; #2.5-4, #3.0-10, #3.5-1, #4.0-3) in 51 patients(male : 40, mean age : 58+/-1 year). The clinical characteristics of the subjects were unstable angina in 26(51%), stable angina in 2, and myocardial infarction in 23(45%) patients(acute : 18). Follow-up angiography was done at a mean duration of 5.4 month(1-12) after coronary stenting for 34 lesions(61%) of 30 patients. RESULTS: 1) The indications of stenting(n=56) were De novo in 33(59%), bailout procedure in 15(27%), suboptimal result after PTCA in 6, and restenosis after PTCA in 2 stents. The location of lesions were LAD in 24, RCA in 27, and circumflex artery in 5 lesions. Angiographic morphologic characteristics were type B in 38(BI : 3, B2 : 35) and type C in 18 lesions. 2) The angiographic and clinical success rate was 96%(54/56) and 94%(52/56). There were no significant difference in stent modality, lesion site and morphology, and indication of stent. 3) Procedural complications were 1 acute closure which was recanalized by emergency coronary artery bypass graft(CABG), 1 death with subacute closure, 2 dissection, and 5 hemorrhages requiring transfusion. 4) The overall restenosis rate was 26%(9/34). The restenosis rate was reduced significantly in PS stent[PS : 9%(2/22) vs GR : 58%(7/12), P < 0.05], > or =3.5mm of stent size[> or =3.5mm : 6%(1/18) vs 3.5mm : 50%(8/16), p < 0305], and high pressure ballooning group(poststenting adjunct balloon dilation pressure > 12atm) [High pressure(+) : 7%(1/14) vs High pressure(-) : 40%(8/20), p<0.05]. 5) The restenosis sites were managed with re-PTCA in 4, elective CABG in 1, and medical follow-up in 4 patients. CONCLUSION: Coronary stenting is an effective and safe procedure for the management of coronary artery disease. The PS stent and GR stent are considered as a safe means for bail-out, and the PS stent can reduces the restenosis rate especially.
Angina, Stable ; Angina, Unstable ; Angiography ; Arteries ; Coronary Artery Bypass ; Coronary Artery Disease ; Coronary Vessels* ; Emergencies ; Follow-Up Studies* ; Hemorrhage ; Humans ; Myocardial Infarction ; Stents*

The association between nephrotic syndrome and intravascular coagulation has been known for more than a century, but it was not until 1948 that a thrombotic diathesis in nephrotic patients was proposed. The prevalence of thrmbo-embolic complications is much higher in adult patients. Deep vein thrombosis of the leg is the most common complications in nephrotic adult and was responsible for one-third of the thrombo-embolic complications of nephrotic children. Arterial thrombosis occurs less frequently and is seen primarily in childern. We present a case of acute anterior myocardial infarction in a young man with nephrotic syndrome, secondary to minimal change glomerulonephritis, in which thrombosis of the proximal left anterior descanding artery was the actual cause of acute myocardial infarction.
Adult ; Arteries ; Child ; Disease Susceptibility ; Humans ; Leg ; Myocardial Infarction* ; Nephrosis, Lipoid ; Nephrotic Syndrome* ; Prevalence ; Thrombosis ; Venous Thrombosis

BACKGROUND: The endothelium is an important regulator of vascular tone via release of relaxing and constricting substances. The regulatory effect of the endothelium has been shown to be impaired in atherosclerotic arteries in human and animal models of hypertension. But there are some debates on extent and developing time of endothelium dysfunction in patients with hypertension, and the determining factors for endothelium dysfunction also were not defined. The objects of this study are to determine whether endothelial function is impaired in coronary and peripheral arteries, and to investigate the predicting factors for endothelial dysfunction in patients with essential hypertension. METHODS: The study patients comprised 14 patients with essential hypertension(M : 7, Mean age : 50+/-2 year) and 6 normal control (M :2, Mean age : 45+/-4 year). We assessed the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the infusion of acetylcholine, from 10(-9M) to 10(-6M) in coronary artery and 7.5, 15, and 25ug/min in left superficial femoral artery, and on intracoronary injection of 200ug nitroglycerin after acetylcholine infusion. RESULTS: 1) There were no significant differences in sex, age, body mass index and ventricular mass index, except systolic(174+/-5 vs 118+/-7mmHg, p<0.001) and distolic blood pressure(106+/-5 vs 75+/-5mmHg,p<0.001) between patients with hypertension and normal control. 2) There were no significant differences in laboratory date of total cholesterol, HDL-cho-lesterol, lipoprotein(a), microaluminuria and von-Willebrand Factor but Fibrinogen level was raised significantly in patients with hypertension than normal control(299+/-26 vs 192+/-23ng/dl, p=0.04). 3) The vasoconstrictor response to acetylcholine, 10-8 to 10-6 M concentration, at proximal, mid, and distal left anterior descending coronary artery were increased significantly in hypertensive patients than normal control(p<0.05). At rest superficial femoral artery, the vasodilator response to acetylcholine, only 25ug/min, was decreased in patients with hypertension(p<0.05). There was no signficant difference in the vasodilator response to nitroglycerin at coronary artery between two groups but in superficial femoral artery, the vasodilator response to nitroglycerin was decreased significantly in hypertensive patients(p<0.05). CONCLUSIONS: The results of this study suggest that endothelium dependent vascular relaxation is impaired in both coronary and superificial femoral artery and it remained to be investigated the predicting factors for endothelial dysfunction in patients with essential hypertension.
Acetylcholine ; Arteries ; Body Mass Index ; Cholesterol ; Coronary Vessels ; Endothelium ; Femoral Artery ; Fibrinogen ; Humans ; Hypertension* ; Lipoprotein(a) ; Models, Animal ; Nitroglycerin ; Relaxation

BACKGROUND: Uncomplicated myocardial infarction is often the harbinger of future cardiac events such as unstable angina, recurrent myocardial infarction or death. The prognostic utility of exercise test(pre-discharge low level exercise test) in patients recovering from acute myocardial infarction(AMI) has been documented by many studies. However there are few data of the safety and value of a symptom-limited exercise test early after AMI. We performed this study to assess the safety of test and the prevalence of abnormal response to symptom-limited exercise test and to determine the ability to predict future cardiac events. METHODS: The study group comprised 91 patients(male ; 73, Anterior infarction ; 43, Q-wave infarction ; 68, Thrombolysis ; 58, Age ; 57+/- years) with uncomplicated AMI. Symptom-limited exercise tests were performed before discharge(8.7+/-0.5 days after infarction) using modified Bruce protocol. Exercise test was considered positive if there was new > or =1mm horizontal or downsloping ST segment depression at 0.08sec after J point compared with baseline. The patients were followed for the development of new cardiac events. RESULTS: 1) The mean duration of exercise test was 14.2 min(range 4.3 - 21.5)and the mean workload(Metabolic Equivalents : METs) was 6.0 METs(range 2.1 - 17.0). There were no complications during exercise test and post-recovery phase. 2) There were positive test in 31 patients(34%), ST segment elevation in 10(11%), and inadequate blood pressure(BP) response in 10 patients(11%). 3) During the follow-up period(1-50 months, mean 12.5 months), 9 patients experienced post-myocardial infarction angina and revascularization therapy, respectively, and 1 patient had cardiac death and recurrent myocardial infarction, respectively. 4) The patients with cardiac events had a significantly higher degree in stenosis of infarct-related artery(90+/-3 vs 78+/-3, p<0.05) and lower systolic BP on peak exercise(136+/-7 vs 156+/-4, p<0.05). 5) The positive exercise test was associated with cardiac events in the follow-up period but ST-segment elevation, inadequate BP response, the use of thrombolytic agents, and non-Q wave infarction did not predict future cardiac events. CONCLUSIONS: The symptom-limited exercise tests early after acute myocardial infarction appear to be safe and will identify more patients with inducible myocardial ischemia relatively. The posive test can predict cardiac events and the prognosis of patients of this group can be improved with aggressive management and careful follow-up.
Angina, Unstable ; Constriction, Pathologic ; Death ; Depression ; Exercise Test* ; Fibrinolytic Agents ; Follow-Up Studies ; Humans ; Infarction ; Myocardial Infarction* ; Myocardial Ischemia ; Prevalence ; Prognosis