BACKGROUND AND OBJECTIVES: Unstable angina is an inhomogenous syndrome. A substantial percentage of patients, ranging from 12 to 30% in most series, develops acute myocardial infarction or dies suddenly soon after their hospitalization, while the remainder have a benign prognosis without adverse coronary events. Unstable angina is a complex condition such as angina at rest, crescendo angina, new onset angina and postinfarction angina. These variable clinical presentations suggest that unstable angina have a heterogenous pathogenesis and prognosis. We divided unstable angina into 5 groups and studied the relationship between clinical presentations and coronary angiographic morphology. METHODS: One hundred sixty six patients were selected from the patients who were diagnosed as an unstable angina between January 1989 and March 1991, at Hallym University Hospital. Angiography was performed in patient with typical angina symptoms and transient ECG changes of myocardial ischemia. Coronary angiogram was done as usual method. Calcification of coronary artery as well as the presence of collateral circulation were recorded. Ergonovine test was performed in patients with near normal or normal angiogram. Coronary lesions were morphologically classified as follows; type A is simple lesion such as symmetric, concentric narrowing and smooth border. and type B is complex lesion such as asymmetric, eccentric, ulcerated narrowing and irregular border. RESULTS: These groups were classified as follows; Group I(represented the patients with angina at rest but typical Prinzmetal angina was excluded) 30 patients, Group II(represented the patients with crescendo angina) 24 patients, Group III(represented the patients with new onset angina) 62 patients, Group IVA(represented the patients with early postinfarction angina within 2 weeks after AMI) 34 patients, Group IVB(represented the patients with delayed postinfarction angina) 16 patients, There were no significant differences in age and sex among the 5 groups. Locations of involved vessel were similar among the five groups, and left anterior descending artery was most frequently(mean 60%) involved. Single vessel disease was frequently observed in new onset angina and early postinfarction angina(Group III*, IVa** 48%, 65% VS Group II, IVB 25%, 19% respectively, *p<0.05, **p<0.005) whereas multivessel disease was frequent in crescendo angina and delayed postinfarction angina(Group II, IVB 51%, 76% VS Group II, IVA 16%, 27% respectively, p<0.005). More than two third of patients with unstable angina had complex B lesion of coronary artery (77%), but in new onset angina simple A lesion was frequently observed (Group III 45% VS Group I, IVA, IVB 16%, 10%, 13% respectively, p<0.05). The frequency of calcification increased in early postinfarction angina(Group IVA 18% VS Group III 3%, p<0.05). The frequency of coronary collateral circulation increased in cresendo angina, early postinfarction and delayed postinfarcion angina(Group II*, IVA*, IVB** 38%, 35%, 50% VS Group III 10% respectively, *p<0.005.**p<0.0001). Incidence of coronary vasospasm was higher in resting angina than the others(Group I*, III 30%, 19% VS Group II, IVA 4%, 6% respectively, *p<0.02). The coronary vasospasm was frequently observed in an insignificant lesion(insignificant lesion/total vasopasm: 12/24(50%)). Early postinfarction angina had frequent intracoronary thrombus in infact-related artery(incidence of thrombus : Group IVA*, IVB 21%, 13% VS Group I, II, III 3%, 4%, 5% respectively, *p<0.05). CONCLUSION: This study suggests that patients with unstable angina pectoris may be heterogeneous groups. Coronary angiography must be performed in patients with unstable angina, in order to classify the clinical correlates with each possible angiogrphic finding that could affect treatment modality and outcome of cardiac events.
Angina Pectoris, Variant ; Angina, Unstable* ; Angiography ; Arteries ; Collateral Circulation ; Coronary Angiography ; Coronary Vasospasm ; Coronary Vessels ; Electrocardiography ; Ergonovine ; Hospitalization ; Humans ; Incidence ; Myocardial Infarction ; Myocardial Ischemia ; Prognosis ; Thrombosis ; Ulcer

We described a giant chroioangioma of the placenta that caused premature rupture of membranes at 31 weeks of gestation in a 31-year-old primiparous woman and a subsequent neonatal death of the baby. The placental mass, weighing 820 gm and measuring 21.5x15x4.5 cm, was easily shelled out from a edematous 1280 gm-placenta. The mass had a thin fibrous capsule and a solid fibromatous appearance. The infant, weighed 2175 gm, appeared edematous oon the whole body and had Apgar scores of 4 and 5 at 1 and 5 minutes respectively. The baby expired 4 days after birth due to high output cardiac failure and respiratory failure. Postmortem examination revealed markedly dilatated umbilical vein, inferior vena cava and right atrium with patent froamen ovale, congestive hepatosplenomegaly, pulmonary hemorrhages, and meconium aspiration pneumonia. Microscopically, the mass revealed a variety of histologic patterns, reflecting entire spectrums of villous vasculogenesis from loose myxomatous connective tissue and undifferentiated hemangioblastic cell nests to well-developed capillaries with hematopoietic cells in the lumen.
Infant ; Male ; Female ; Infant, Newborn ; Humans

A 45 year old male patient complained of mucous fluid drainage in the vicinity af the manubrium sterni for 5 years. Skin around the lesion had normal appearance except pinpoint sized sinus opening. H.istopathology showed a cyst in the upper and mid-dermis which consisted of pseudoetratified columnar epithelium with interspersed goblet cells. Goblet; cells were confirmed by positive stain to D-PAS and alcian blue and by metachromatic stain to toluidine blue. VFe present here a case of cutaneous bronchogenic cyst clinically and histopathologically which is thought to be the first cace in Korea.
Alcian Blue ; Bronchogenic Cyst* ; Drainage ; Epithelium ; Goblet Cells ; Humans ; Korea ; Male ; Manubrium ; Middle Aged ; Skin ; Tolonium Chloride

No abstract available.
Hyperlipidemias* ; Obesity* ; Risk Factors* ; Urolithiasis*

No abstract available.
Hyperlipidemias* ; Obesity* ; Risk Factors* ; Urolithiasis*

Constrictive pericarditis is caused by fibrosis of the pericardium leading to decrease in ventricular compliance. The diagnosis is often delayed due to nonspecific signs and symptoms. The authors experienced eight cases of constrictive pericarditis detected on chest CT scan while being treated for considerable length of time under the clinical impressions of intrathoracic tumor, tuberculous pleural effusion, liver cirrhosis, etc. Constrictive hemodynamics of these patients were confirmed by echocardiogram and cardiac catheterization. Among them five cases were due to tuberculosis. In four cases with pathologically proven tuberculous granuloma, the pericardium was markedly thickened and intensely enhanced. Associated pericardial effusion (n=3), and mediastinal lymphadenitis (n=3) were present, but pericardial calcifications were not seen. On the other hand, the fibrosis group (n=3) displayed mild pericardial thickening. All the three patients showed pericardial calcifications, mild or absent enhancement of pericardium, but no mediastinal lymphadenitis. The cardiovascular changes such as inferior or superior vena caval distension, left ventricular deformity, interventricular septum angulation, and biatrial enlargements were more severe than those in patients with active granuloma. In patients with constrictive pericarditis with nonspecific signs and symptoms, CT scan is very helpful in making the diagnosis and can give informations about the evolution of the disease.
Cardiac Catheterization ; Cardiac Catheters ; Compliance ; Congenital Abnormalities ; Diagnosis* ; Fibrosis ; Granuloma ; Hand ; Hemodynamics ; Humans ; Liver Cirrhosis ; Lymphadenitis ; Pericardial Effusion ; Pericarditis, Constrictive* ; Pericardium ; Pleural Effusion ; Tomography, X-Ray Computed ; Tuberculosis

Constrictive pericarditis is caused by fibrosis of the pericardium leading to decrease in ventricular compliance. The diagnosis is often delayed due to nonspecific signs and symptoms. The authors experienced eight cases of constrictive pericarditis detected on chest CT scan while being treated for considerable length of time under the clinical impressions of intrathoracic tumor, tuberculous pleural effusion, liver cirrhosis, etc. Constrictive hemodynamics of these patients were confirmed by echocardiogram and cardiac catheterization. Among them five cases were due to tuberculosis. In four cases with pathologically proven tuberculous granuloma, the pericardium was markedly thickened and intensely enhanced. Associated pericardial effusion (n=3), and mediastinal lymphadenitis (n=3) were present, but pericardial calcifications were not seen. On the other hand, the fibrosis group (n=3) displayed mild pericardial thickening. All the three patients showed pericardial calcifications, mild or absent enhancement of pericardium, but no mediastinal lymphadenitis. The cardiovascular changes such as inferior or superior vena caval distension, left ventricular deformity, interventricular septum angulation, and biatrial enlargements were more severe than those in patients with active granuloma. In patients with constrictive pericarditis with nonspecific signs and symptoms, CT scan is very helpful in making the diagnosis and can give informations about the evolution of the disease.
Cardiac Catheterization ; Cardiac Catheters ; Compliance ; Congenital Abnormalities ; Diagnosis* ; Fibrosis ; Granuloma ; Hand ; Hemodynamics ; Humans ; Liver Cirrhosis ; Lymphadenitis ; Pericardial Effusion ; Pericarditis, Constrictive* ; Pericardium ; Pleural Effusion ; Tomography, X-Ray Computed ; Tuberculosis

No abstract available.
Congenital Hypothyroidism*

BACKGROUND AND OBJECTIVES: Ischemic preconditioning (IP) has been shown to reduce the infarct size and severity of arrhythmia in a post-ischemic reperfused heart. Angina before myocardial infarction reflects brief episodes of myocardial ischemia and may be a marker of ischemic preconditioning. We studied the effect of a history of previous angina on early outcomes (infarct size, left ventricular (LV) function and residual myocardial ischemia) for patients with acute myocardial infarction (AMI) after thrombolytic therapy. MATERIALS AND METHOD: We examined prospectively 58 consecutive patients who had AMI and arrived hospital within 6 hours after chest pain developed. IP was defined as prodromal angina within 24 hours before myocardial infarction. Patients were divided 2 groups:Group I (Gr I, 30 cases) without IP, Group II (Gr II, 28 cases) with IP. Thrombolytic therapy was done 23 cases (77%) and 21 cases (75%) respectively in each groups. Thereafter, electrocardiographic findings, infarct size on the basis of peak creatine kinase, LV function on the 2-D echocardiographic findings, recurrent myocardial ischemia were examined between 2 groups. RESULTS: In predischarge 2-D echocardio-graphic findings, LV dilatation and normal regional wall motion did not differ between two groups. But, there were significantly smaller creatine kinase (CK)-determined infarct size in Gr II than that in Gr I (peak CK level, Gr I:1566.3+/-960.0 IU/L vs Gr II:1066.9+/-773.2; p<0.05). The time interval between the onset of infarction and peak CK level was shorter in Gr II than that in Gr I (Gr I:18.3+/-8.3 vs Gr II:10.7+/-3.4 hours; p<0.001). There were significantly more common incidences of residual myocardial ischemia in Gr II (Gr I:26.7% vs Gr II:60.7%; p<0.01). CONCLUSION: Patients with a history of prodromal angina preceding myocardial infarction had small infarct size and earlier reperfusion of infarct related artery. However, there were significantly more common residual myocardial ischemia in these patients and a trend toward re-infarction on same previous infarction sites.
Angina Pectoris* ; Arrhythmias, Cardiac ; Arteries ; Chest Pain ; Creatine Kinase ; Dilatation ; Echocardiography ; Electrocardiography ; Heart ; Humans ; Incidence ; Infarction ; Ischemic Preconditioning* ; Myocardial Infarction* ; Myocardial Ischemia ; Prospective Studies ; Reperfusion ; Thrombolytic Therapy

No anstract available.
Magnetic Resonance Imaging* ; Spine*