No abstract available.

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.
Sinusitis*

No abstract available.
Foreign Bodies* ; Skull Base* ; Skull*

No abstract available.
Myelodysplastic Syndromes*

BACKGROUND: It is known that QT dispersion represents asynchronous repolarization of ventricle which is related to ventricular fibrillation. The incidence of ventricular arrhythmia is increased after acute myocardial infarction. So this study compared QT dispersion and other repolarization indexes for detection of asynchronous repolarization in acute myocardial infarction. We also investigated which portion of repolarization is the key portion of the asynchrony. METHODS: In 37 acute myocardial infarction patients and 38 angina patients dispersion of QT, JT, JTpeak and QTpeak were measured. We also measured maximum adjacent dispersion of same parameters in precordial leads. In 20 survived patients and 17 dead patients after acute myocardial infarction were also compared. We also investigated correlation of PVC's on Holter monitoring with these repolarization parameters. RESULTS: 1) All ventricular repolarization indexes(QT, QTc, JT, JTpeak, QT peak and TpeakTend dispersion) were significantly increased in acute myocardial infarction group than compared with those of angina group(p<0.05). 2) Maximal precordial dispersion(QT, QTc, JT, JTpeak and QTpeak) were also significantly increased in acute myocardial infarction group than angina group(p<0.05). 3) Dead patient group after myocardial infarction showed significantly increased QTc and TpeskTend dispersion compared with those of survived patient group(p<0.05). 4) Multivariate linear correlation showed that TpeakTend dispersion and JT dispersion was correlated with QT dispersion. CONCLUSIONS: There were asynchronous myocardial repolarization changes in acute myocardial infarction. Our study demonstrated that T wave change was major determinant of dispersion of myocardial repolarization.
Arrhythmias, Cardiac ; Electrocardiography, Ambulatory ; Humans ; Incidence ; Myocardial Infarction* ; Ventricular Fibrillation

BACKGROUND: Hyperlipidemia has been known as an independent risk factor in the develop-ment of coronary artery disease. This study was carried out to compare nutrient intakes, smo-king status, antioxidant vitamins, and plasma lipids in patients with coronary heart disease (CHD) and in normal healthy subjects among Korean population in Taegu. Possible causes of this dis-ease in patients are discussed. METHODS: Anthropometric assessments included mean intakes of nutrients, and the levels of plasma lipids (apolipoprotein [Apo] A - I, Lipoprotein [Lp] [a]), and antioxidant vitamins (such as vitamins A and E) were measured in female and male subjects with CHD against healthy con-trols. RESULTS: Dietary cholesterol and fat intakes were significantly higher in CHD groups in men and women. Total plasma cholesterol, LDL-C, triglyceride, thiobarbituric acid reactive subst-ance (TBARS), atherogenic index and Lp (a) levels were significantly higher in CHD patients than in the normal group in both men and women. Apo A-I, HDL-C and vitamin E levels were lower in CHD patients than in the normal group. The number of smokers was higher in CHD patients than in the normal group in both sexes of subjects. CONCLUSION: High fat and high cholesterol intakes seemed to be a major factor for the hyperlipidemia in the CHD patients. Their abnormal lipoprotein profile, which appeared in pati-ent plasma, corresponded well to dietary intake patterns. However, long term studies are need-ed to investigate the effects of smoking on lipid metabolism in CHD patients among the Korean population.
Apolipoprotein A-I ; Cholesterol ; Cholesterol, Dietary ; Coronary Artery Disease ; Coronary Disease* ; Daegu ; Female ; Humans ; Hyperlipidemias ; Lipid Metabolism ; Lipid Peroxidation ; Lipoprotein(a)* ; Lipoproteins* ; Male ; Plasma* ; Risk Factors ; Smoke* ; Smoking* ; Triglycerides ; Vitamin A ; Vitamin E ; Vitamins

Objectives: Bladder storage symptoms including nocturia is the most common cause of sleep disturbance in all age groups.Sleep disturbance is also a main cause of nocturia so that sleep recovery can clinically improve nocturia. Melatonin has main action to induce sleep and additional effects of smooth muscle relaxation, free radical scavenging, anti-inflammation, et cetera. This study was evaluated the improvement of sleep quality after administrating prolonged-release melatonin in elderly patients with overactive bladder and chronic insomnia. Methods: This clinical trial was performed with a randomized single open study. Thirty-seven patients with overactive bladder and chronic insomnia were initially enrolled in this study. After 4 or 12 weeks treating with 2 mg of prolongedrelease melatonin, clinical outcomes were evaluated with OABSS, IPSS, PSQI and WHO 5 well-being index. Results: Of the 37 patients, 34 (91.9%) were included in the ITT group and 26 (76.5%) in the PP group. In the primary outcome of PP group, significant improvements were observed in total OABSS and nocturia frequencies at 12 weeks, respectively. Secondary outcome measurement including in voiding, storage symptoms, and total IPSS scores showed the improvement at 4 and 12 weeks and in total and sleep quality PSQI scores at 12 weeks, and in quality of life scores of the WHO 5 well-being index at 12 weeks. Only one (3.8%) adverse event was observed. Conclusions These results suggest clearly that prolonged-release melatonin in elderly patients with overactive bladder and chronic insomnia has the potential to control concomitant voiding and sleep difficulty.

Objectives: Bladder storage symptoms including nocturia is the most common cause of sleep disturbance in all age groups.Sleep disturbance is also a main cause of nocturia so that sleep recovery can clinically improve nocturia. Melatonin has main action to induce sleep and additional effects of smooth muscle relaxation, free radical scavenging, anti-inflammation, et cetera. This study was evaluated the improvement of sleep quality after administrating prolonged-release melatonin in elderly patients with overactive bladder and chronic insomnia. Methods: This clinical trial was performed with a randomized single open study. Thirty-seven patients with overactive bladder and chronic insomnia were initially enrolled in this study. After 4 or 12 weeks treating with 2 mg of prolongedrelease melatonin, clinical outcomes were evaluated with OABSS, IPSS, PSQI and WHO 5 well-being index. Results: Of the 37 patients, 34 (91.9%) were included in the ITT group and 26 (76.5%) in the PP group. In the primary outcome of PP group, significant improvements were observed in total OABSS and nocturia frequencies at 12 weeks, respectively. Secondary outcome measurement including in voiding, storage symptoms, and total IPSS scores showed the improvement at 4 and 12 weeks and in total and sleep quality PSQI scores at 12 weeks, and in quality of life scores of the WHO 5 well-being index at 12 weeks. Only one (3.8%) adverse event was observed. Conclusions These results suggest clearly that prolonged-release melatonin in elderly patients with overactive bladder and chronic insomnia has the potential to control concomitant voiding and sleep difficulty.

BACKGROUND AND OBJECTIVES: The myocardial protective effect of ischemic preconditioning is well known. However, the mechanism is remains unclear. The purpose of this study is to determine the role of adenosine, protein kinase C, KATP channel and the change of monophasic action potential duration on cardioprotective effect of ischemic preconditioning in cat. Materials AND METHODS: In this experiment, 66 cats were allocated into 7 groups:control (n=10), ischemic preconditioning (n=10), adenosine pre-treated (n=10), SPT (8-p-sulfophenyl theophylline) pre-treated (n=9), polymyxin B pre-treated (n=9), glibenclamide pre-treated (n=9) and nicorandil pre-treated (n=9) groups. Ischemic preconditioning was performed in ischemic preconditioning, SPT pre-treated, polymyxin B pre-treated and glibenclamide pre-treated groups by 3 episodes of 5 minutes ischemia and 10 minutes reperfusion. All animals were subjected to 40 minutes of ischemia and 40 minutes reperfusion. Monophasic action potential duration at 50% repolarization (MAP50) was measured in the ischemic and non-ischemic area respectively by epicardial probe throughout the experiment. The effect of ischemic preconditioning was determined by infarct size (% area at risk). RESULTS: Ischemic preconditioning, adenosine pre-treatment and nicorandil pre-treatment groups demonstrated a significant reduction in infarct size (26+/-4%, 25+/-4% and 34+/-8% infarction of the risk zone, respectively, p<0.01, p<0.01 and p<0.05 vs. control) with respect to control (41+/-8% infarction of the risk zone). However, pretreatment with SPT, polymyxin B or glibenclamide abolished the effect of ischemic preconditioning. Ischemic preconditioning group exhibited a significant reduction of MAP50 duration in the ischemic area during preconditioning;at the first preconditioning 128+/-11 msec vs. 144+/-10 msec control, at the second preconditioning 110+/-10 msec vs.147+/-10 msec control (p<0.01), at the third preconditioning 114+/-10 msec vs. 145+/-11 msec control (p<0.05). But, pretreatment with SPT, polymyxin B and glibenclamide prevented the reduction of MAP50 in the ischemic area during ischemic preconditioning. During 40 minutes ischemia, the shortening of MAP50 was more pronounced in the preconditioned group than in control group;at 5 minutes 112+/-13 msec vs. 124+/-10 msec control, at 10 minutes 89+/-12 msec vs. 133+/-11 msec control (p<0.05 ), at 20 minutes 93+/-12 msec vs. 136+/-11 msec control (p<0.05), and at 30 minutes 107+/-19 msec vs. 144+/-14 msec control (p<0.05). In adenosine pre-treated group, the MAP50 was significantly shortened than control group throughout 40 minutes occlusion period;at 5 minutes 90+/-8 msec (p<0.05), at 10 minutes 77+/-9 msec (p<0.05), at 20 minutes 92+/-8 msec (p<0.05), and at 30 minutes 103+/-8 msec (p<0.05). Nicorandil pretreatment pronounced the ischemic shortening of MAP50 in ischemic area and the effect was significant during early ischemic period;at 10 minutes 98+/-22 msec (p<0.05 vs. control). In pretreatment groups with SPT, polymyxin B or glibenclamide, the ischemic preconditioning of MAP50 measured in non-ischemic area was not significantly different compared with control group. MAP50 measured in ischemic area during reperfusion was not significantly different between groups. CONCLUSION: Based on this study, adenosine receptor-protein kinase C-KATP channel activation and monophasic action potential duration shortening during ischemia play an important role in myocardial protection during ischemic injury.
Action Potentials* ; Adenosine* ; Animals ; Cats* ; Glyburide ; Infarction ; Ischemia ; Ischemic Preconditioning* ; Nicorandil ; Phosphotransferases ; Polymyxin B ; Protein Kinase C* ; Protein Kinases* ; Receptors, Purinergic P1* ; Reperfusion