Amiodarone hydrochloride is a benzofuran derivative used for the treatment of cardiac arrhythmias. It is associated with a number of side effects, including thyroidopathy, neuropathy, cutaneous pigmentation, photosensitivity, pulmonary toxicity, hepatotoxicity and keratopathy. Amiodarone keratopathy hasbeen classified into four stages. Corneal pigmentation varies from stage 0, which is a clear cornea without pigment deposition, to stage 3, that is, corneal pigmentation encroaching upon the pupil. We present a case of amiodarone induced keratopathy of stage 3 who received low dose oral amiodarone maintain therapy.
Amiodarone* ; Arrhythmias, Cardiac ; Cornea ; Pigmentation ; Pupil

BACKGROUND: It has been well known that the bone and kidney are the principle organs of parathyroid hormine (PTH) actions. Although patients with primary hyperparathyroidism show a high incidence of LVH and trophic effects of PTH on adult rat ventricular cardiomyocytes were investigated in vitro, effect of PTH on the cardiac tissue in vivo is unknown. METHODS: We examined the effects of PTH on the cardiomyocyte and interstitial tissue using adult rat heart. Twenty-two female Sprague-Dawley rats were ovariectomized bilaterally at three months old and weighing in 250 - 300 gm in order to exclude the trophic effect of estrogen. We administrated human parathyroid hormone (20 ug subcutaneously 5 times per week) to 12 rats for 4 weeks after raising for 8 weeks (PTH group):the remaining 10 rats received only normal saline (control). We measured left ventricular thickness [IVS+LVPW)/2] and number of cardiomyocytes and interstitial fibrosis on LM (H & E and Masson's trochrome stain) and EM. RESULTS: 1) LV wall thickeness tended to increase in PTH group as compared with control (2.16+/-0.31 vs 1.12+/-0.21 mm, p=0.099). 2) The number of cardiomyocyte in PTH group was significantly less than that of control (61.2+/-13.1 vs 70.5+/-14.9, p=0.003, Magnification x 400). 3) There was no significant change of interstitial fibrosis between PTH group and control. CONCLUSION: These results shggest that PTH may produce left ventricular hypertrophic effects in aged ovariectomized rat that resulted form hypertrophy of cardiomyocyte without increase of interstitial connetive tissue.
Adult ; Animals ; Estrogens ; Female ; Fibrosis ; Heart ; Humans ; Hyperparathyroidism, Primary ; Hypertrophy ; Hypertrophy, Left Ventricular* ; Incidence ; Kidney ; Myocytes, Cardiac ; Ovariectomy ; Parathyroid Hormone* ; Rats* ; Rats, Sprague-Dawley

The incidence of angina pectoris(AP) in patients with severe aortic stenosis(AS) and normal coronary arteries has been reported to be 30 to 40%. The pathophysiologic mechanism suggests marked decrease in coronary rederve with left ventricular hypertrophy secondary AS and mismatched oxygen demand-supply by valvular pressure gradient, but only 1 case of acute myocardial infarction(AMI) was reported in severe AS and normal coronary arteries as far as we are concerned. We report a case of AMI occuring in a patient with severe AS and left ventricular hypertrophy. A coronary angiogram excluded coronary obstruction and spasm as the cause of AMI in this patient.
Aortic Valve Stenosis* ; Coronary Vessels* ; Humans ; Hypertrophy, Left Ventricular ; Incidence ; Myocardial Infarction* ; Oxygen ; Spasm

BACKGROUND: Coronary angiography have become important and integral components in the investigation of patients with cardiovascular disease. Technical improvement combined with an increased need of coronary angiography, and efforts to decrease the length of inpatient hospital stay have prompted the development of outpatient coronary angiography. In this study, we compared the procedure-related complications and costs of inpatient and outpatient coronary angiography when performed at the same institution. In addition, we attempted the coronary angiography as outpatient setting in patients with unstable angina, old age, and anticoagulation therapy, who have been regarded as contraindication for outpatient procedure. METHODS: Diagnostic coronary angiography was performed in 199 cases as inpatient setting, and 225 cases as outpatient setting at Korea University Guro Hospital From January through July 1996. There was no significant difference in sex, age, risk factor, blood pressure, cholesterol level, and ejection fraction. We did not give the heparin during the procedure and, use the Judkins' method in all patients. After the procedure, pressure dressing was done with compressor device for 15 minutes, then sandbag was applied on the puncture site. In outpatient, they took bed rest for 6 hours in one-day care room. RESULTS: 1) In the inpatient group, there were 6 cases(3.0%) of catheterization-related complication, and there were 7 cases(3.1%) of complication in the outpatient group. There was no major complication in both groups, such as death, myocardial infarction, stroke, and perforation of heart and great vessels. In the inpatient group, 2 cases of arrhythmia, 3 cases of hematoma at puncture site, and 1 case of femoral artery pseudoaneuryrsm occurred. In the outpatient group, 2 cases of arrhythmia, 1 case of hematoma at puncture site, 2 cases of skin rash, 1 case of acute febrile reaction, and 1 case of femoral artery dissecting aneurysm developed. There was no significant difference in the rate of complications between two groups(p=0.947). 2) In the outpatient group, there were 28 cases of unstable angina, 6 cases of old age more than 75 years, and 5 cases of anticoagulant has been taken. No catheterization-related complication occurred in those groups. 3) The costs and duration of hospital stay in the inpatient group were won480,230+/-86,800 and 50.3+/-12.3 hours and those in the outpatient group were won276,870+/-32,050 and 8.3+/-1.2 hours. There was significant difference between two groups in the costs and duration of hospital stay(p<0.01, p<0.01). CONCLUSIONS: Outpatient coronary angiography could be done safely with low complication rate, and could reduce the costs and hospital stay. For high risk group such as unstable angina, old age, and anticoagulation therapy, there was no complication in this study, but more experiences and available data should be accumulated to be accepted as a general guideline.
Aneurysm, Dissecting ; Angina, Unstable ; Arrhythmias, Cardiac ; Bandages ; Bed Rest ; Blood Pressure ; Cardiovascular Diseases ; Cholesterol ; Coronary Angiography* ; Exanthema ; Femoral Artery ; Heart ; Hematoma ; Heparin ; Humans ; Inpatients ; Korea ; Length of Stay ; Myocardial Infarction ; Outpatients* ; Punctures ; Risk Factors ; Stroke

Antithyroid drugs (ATD) has been widely used to treat Graves' disease. However agranulocytosis, a serious fatal complication of ATD treatment, occurs in about 0.5 percent. The symptoms may mimic viral infections (fever, sore throat), and the potentially life-threatening pyogenic infections can go unrecognized initially. The median duration of drug exposure before the onset of acute agranulocytosis is within 30 days in most cases. We report a case of agranulocytosis with secondary soft tissue infection and abscess occuring after increasing the dose of methimazole in a woman who had taken methimazole for more than 10 years. We administered broad-spectrum antibiotics and aspirated the soft tissue abscess. A review of the medical literature regarding agranulocytosis in the setting of ATDs is presented.
Abscess ; Agranulocytosis ; Anti-Bacterial Agents ; Antithyroid Agents ; Female ; Graves Disease ; Humans ; Hydrazines ; Methimazole ; Soft Tissue Infections

BACKGROUND AND PURPOSE: Although thrombolytic strategies with streptokinase(STK) and tissue-type plasminogen activator(t-PA) in the treatment of acute myocardial infarction(AMI) have been studied in large-scale clinical trials in the western countries, such large-scale studies with urokinase(UK) are scanty. Even though UK is most commonly used thrombolytic agent for the treatment of AMI in Korea, there is no consensus on the dosage and the way of administration of UK in patients with AMI. Accordingly, a prospective clinical study was performed to evaluate the effects of thrombolytic strategies of intravenous double bolus method and standard double-infusion method with different dosage of UK in the treatment of AMI. SUBJECTS AND METHODS: Ninety there patients with AMI(male 75, female 18, age 57.5+/-10.8 years) were studied. The patients were divided into 3 groups according to dosage of UK and method of administration. Group I : 19 patients who received 1.5 million U of UK IV bolus, followed by 1.5 million U IV infusion for an hour(High Dose Group). Group II : 34 patients received 20,000U/kg body weight of UK IV bolus, followed by 20,000U/kg IV infusion for an hour(Double Dose Group). Group III : 40 patients received 1.5 million U of UK IV bolus and followed by 20,000U/kg IV bolus in 30 minutes with total dose of no more than 3 million U(Double Bolus Group). Coronary angiography(CAG) and left ventriculography(LVG) were performed 90 minutes after the administration of UK and post-AMI 7-10 days to investigate the patency of infarct-related artery(IRA) and LV function. Patency of IRA was graded according to the extent of flow of IRA. TIMI grade 0-1 was regarded as occluded, and grade 2-3 flow as patent. LV ejection fraction(EF) by echocardiography was measured on day 1, day 7-10 and 1 month after AMI. Indirect clinical parameters of thrombolysis were evaluated and were compared with CAG findings. RESULTS: 1) The 90 minutes IRA patency in Group III(Double bolus ; 79.0%) was higher than that in Group 1, but showed no statistically significant difference(High dose ; 61.5%, p=0.790). The 90 minutes IRA patency in Group III showed borderline significance with Group II(Double dose ; 57.1%, p=0.057). TIMI flow III in Group III(60.6%) was significantly higher than that in Group II(53.6%, p=0.0468) but showed no statistically significant difference with Group I(61.5%, p=0.158). 2) The EF by LVG were 49.1% in Group I, 41.7% in Group II and 49.2% in Group III. The difference in EF between Group I and Group III vs Group II was significant(p=0.008 in Group I, p=0.014 in Group III vs Group II). 3) Fatal bleeding complications(1 intracranial hemorrhage and 1 gastric ulcer bleeding) developed in Group II (Double dose). 4) Pain to door time, pain to needle time and door to needle time tended to be shorter in open(TIMI flow II-III) IRA group than in closed IRA group. 5) Initial EF were similar between open IRA group and closed IRA group(46.1% and 42.1% ; p=NS). The EF of open IRA group measured by LVG on initail coronary angiography(41.8% in closed IRA vs 48.0%, in open IRA, p=0.03) and by 2D-Echo on 7-10 day(41.7% in closed IRA vs 51.0% in open IRA, p=0.004) were better than those of closed IRA group. 6) Indirect clinical indices of reperfusion such as mean CPK peak, time to CPK peak significantly lower in open IRA group than in closed IRA group. 7) Fatal bleeding complications(1 intacranial hemorrhage and 1 gastric ulcer bleeding) developed in closed IRA group. CONCLUSION: The findings we observed in this trial showed that earlier initiation and more rapid infusion of UK were associated with more increased 90min patency of infarct-related artery and more improved LV function without any obviously increased bleeding complications or other serious life-threatening complications than conventional UK therapy. Specifically, double bolus IV injection of UK(1.5 million U bolus followed by 20,000 U/Kg bolus in 30min)was more effective method of thrombolysis than conventional method for achieving optimal reperfusion in AMI patients. Also, IRA patency at 90 minutes after the initiation of thrombolysis was important in preserving global LV function in early recovery phase of AMI. Further trials may be needed to determine more effective thrombolysis with UK in AMI.
Arteries ; Body Weight ; Consensus ; Echocardiography ; Female ; Hemorrhage ; Humans ; Intracranial Hemorrhages ; Korea ; Myocardial Infarction* ; Needles ; Plasminogen ; Prospective Studies ; Reperfusion ; Stomach Ulcer ; Urokinase-Type Plasminogen Activator*

BACKGROUND: Thrombotic and fibrinolytic factors which change in women following menopause, may be of pathogenetic importance in atherogenetic and thrombotic cardiovascular diseases by altering fibrinolysis on vascular surfaces. We investigated whether parameters of thrombosis and fibrinolysis were different before and after menopause. METHODS: Thrombotic factors such as plasma plasminogen activator inhibitor type 1(PAI-1), fibrinogen, a2 antiplasmin, lipoprotein(a) were measured. In addition, fibrinolytic factors such as plasma tissue-type plasminogen activator(t-PA), plasminogen, antithrombin-III were also assessed in 41 premenopausal women, 174 menopausal women and 201 men. RESULTS: PAI-1 and fibrinogen and t-PA were significantly higher in menopausal women than in premenopausal women(13.1+/-6.6 vs 16.9+/-9.5ng/ml, p=0.046, 293.6+/-83.3 vs 347. 5+/-256.9mg/dl, p=0.001, 10.1+/-4.4 vs 12.5+/-5.6ng/ml, p=0.003). A positive significant correlation was found between PAI-1 and any other thrombogenic and fibrinolytic factors. CONCLUSIONS: PAI-1, fibrinogen, t-PA were higher in menopausal women than in premenopausal women. The findings suggest that increase of athersclerotic and thrombotic cardiovascular diseases after menopause may be influenced by these changes.
Cardiovascular Diseases ; Female ; Fibrinogen ; Fibrinolysis ; Humans ; Lipoprotein(a) ; Male ; Menopause ; Plasma ; Plasminogen ; Plasminogen Activator Inhibitor 1 ; Plasminogen Activators ; Thrombosis

BACKGROUND: Lipoprotein (a) concentration is mainly determined by apo (a) genotype, but elevated in the atherosclerotic vascular disease more than in normal group with the same apo (a) phenotype. It has been known that Lp (a) has independent metabolism in contrast with other lipoproteins and that the use of cholesterol lowering agent such as HMG-CoA reductase inhibitor for 6 months does not change the level of Lp (a). The results of several studies suggests that Lp (a) may be related to inflammation of atherosclerotic plaque and therefore, long term use of cholesterol lowering agents make plaque stable by reduction of inflammation at plaque. We hypothesized that there is a relationship between long term use of HMG-CoA reductase inhibitor and change of Lp (a) level. We prospectively measured Lp (a), lipids and inflammatory markers before and after long term use of HMG-CoA reductase inhibitor to examine our hypothesis. METHODS: Forty-nine subjects (M:F=28:21, age=59.1+/-12.0) with hyperlipidemia were administered HMG-CoA reductase inhibitor for 15 months (minimum 6 months, maximun 44 months), and Lp (a), lipids and inflammatory markers were measured before and after use of the HMG-CoA reductase inhibitor. In control group (ninty-nine subjects, M:F=60:39, age=61.2+/-9.2), these parameters were measured more than 6 months. RESULTS: In the hyperlipidemia group who were given HMG-CoA reductase inhibitor, baseline levels of total cholesterol, TG, LDL were significantly elevated more than those of the control group, but Lp (a) and inflammatory markers were not significantly different. After use of HMG-CoA reductase inhibitor, the level of Lp (a) was reduced significantly (before 28.9+/-29.3 mg/dl, after 20.0+/-19.0 mg/dl, p=0.009), but not significantly in the control group. There was a minimal relation between baseline Lp (a) levels and percent changes of Lp (a) levels. Total cholesterol and LDL levels reduced significantly after use of the drug, but inflammatory markers did not. CONCLUSION: These data showed that Lp (a) level in the hyperlipidemia group after the long term use of HMG-CoA reductase inhibitor decreased significantly. We suggest that these changes of Lp (a) level may be one of reliable markers for plaque stability in atherosclerotic vascular disease.
Atherosclerosis ; Cholesterol ; Genotype ; Hyperlipidemias ; Inflammation ; Lipoprotein(a) ; Lipoproteins ; Metabolism ; Oxidoreductases* ; Phenotype ; Plaque, Atherosclerotic ; Prospective Studies ; Vascular Diseases

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.
Animals ; Arginine ; Arrhythmias, Cardiac ; Heart Rate ; Heart* ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Myocardial Stunning ; Nitric Oxide ; Rats* ; Reperfusion

BACKGROUND: Brief episodic ischemias prior to subsequent prolonged ischemia limit infarct size and attenuate the reperfusion arrythmia. But the effect of ischemic preconditioning on post-ischemic myocardial dysfunction, coronary flow and nitric oxide (NO) remains unclear. METHODS: To investigate the effect of ischemic preconditioning on myocardial function and coronary flow during reperfusion after 15 minutes of global myocardial ischemia, 30 isolated hearts of Sprague-Dowley rats were perfused under constant pressure. Two episodes of three minutes global ischemia followed by 12 minutes of reflow were employed to precondition the hearts. The hearts were randomized to one of three groups : group I had no preconditioning, group II had preconditioning, group III had preconditioning as well as L-arginine pretreatment. Left ventricular developed pressure (LVDP), LV dp/dt, perfused coronary flow, concentration of NO and heart rate were continuously measured. RESULTS: In preconditioning groups (Group II, Group III), LVDP decreased during reflow and was lower than that of the control group. LV dp/dt decreased after reflow and gradually recovered with time but recovered was less in preconditioning groups. Coronary flow increased in the first few minutes after reflow in all groups, but decreased gradually. The decrease of coronary flow was greater in preconditioning groups. NO increased during the first 10 minutes after reflow and then decreased. In preconditioning groups, NO tends to be lower than that in the non-preconditioning group. CONCLUSION: Ischemic preconditioning was not beneficial to post-ischemic myocardial dysfunction, coronary flow and NO concentration in the flow. Cummulative effect of stunning due to repetitive ischemia for preconditioning may be an explanation for worse post-ischemic myocardial dysfunction and coronary flow in preconditioning groups.
Animals ; Arginine ; Arrhythmias, Cardiac ; Heart Rate ; Heart* ; Ischemia ; Ischemic Preconditioning* ; Myocardial Ischemia ; Myocardial Stunning ; Nitric Oxide ; Rats* ; Reperfusion