Amniotic fluid embolism (AFE) is a rare peripartum complication with a mortality rate of 61 to 86%. The main clinical manifestations include shock, acute pulmonary edema, neurologic signs, and coagulopathies. Most diagnosis of AFE is made on the postmortem examination of the maternal pulmonary vasculature, but antemortem confirmation of amniotic fluid material by aspiration of pulmonary blood is rare. We report the first case in Korea who survived from amniotic fluid embolism confirmed by the identification of amniotic fluid debris in pulmonary artery blood. Serial echocardiographic changes of left ventricle systolic dysfunction are also described with a brief review of literatures.
Amniotic Fluid* ; Autopsy ; Diagnosis ; Echocardiography ; Embolism, Amniotic Fluid* ; Female ; Heart Ventricles* ; Korea ; Mortality ; Neurologic Manifestations ; Peripartum Period ; Pregnancy ; Pulmonary Artery ; Pulmonary Edema ; Shock

BACKGROUND: Large series of patients with symptomatic mitral stenosis have undergone percutaneous mitral balloon valvuloplasty(PMV) with use of the Inoue or double balloon technique. But to date the result of the two procedure have not been compared with a single series prospectively. METHODS: In order to assess the immediate hemodynamic results and the longterm efficacy of two different PMV technique, a prospective, randomized trial of PMV was performed using the Inoue balloon(Toray, I group) in 59 patients and the double balloons(a pair of Mansfield balloon. D group) in 61 patients with moderate to severe mitral stenosis. Before valvuloplasty, the patients series were comparable with regard to average age. gender, most clinical and echocardiographic variables. All the patients(120 patients, M/F 38/82, mean age 41+/-11 year) were preselected with good echoscore> or =9. RESULTS: The success rate was 83% in the I group and 89% in the D group when the success defined as mitral valve area(MVA)> or =1.5cm2 with 25% gain in MVA and mitral regurgitation> or =2+ at the end of procedure. The magnitude of increase of mitral valve area and decrease of mitral gradient, left atrial pressure and pulmonary arterial pressure were not significantly different in the Inoue and double balloon series(1.0+/-0.4 and 1.1+/-0.4cm2 for mitral vale area, 10.2+/-6.6 and 11.7+/-6.4mmHg for mitral gradient, 10.5+/-6,4 and 12.9 +/-7,3mmHg for left atrial pressure, and 8.7+/-7.3 and 10.1+/-9.4 mmHg for pulmonary artrial pressure respectively). Immediatly after dilation, the long diameter changes of the mitral orifice was more prominent in the D group(from 1.0+/-0.2 to 2.6+/-0.4cm p<0.01) than those in I series(from 1.1+/-0.4 to 2.3+/-0.3cm) Moreover, the magnitude of increase in the EF slop was significantly larger in the D group(31.9+/-17.0 vs 21.8+/-14.2mm/sec, p<0.001). The duration of total procedure(56+/-20 vs 84+/-24 min, p<0.002) and the fluoroscopic time (15+/-6 vs 25+/-11min, p<0.002) was significantly shorter in group I. The incidence of left to right shunt at the atrial level(Qp/Qs>1.5) was 3.4% in group I and 4.9% in group D. Severe mitral regurgitation> or =3+ occurred in 2 patients in each I(3.4%) and D(3.3%) group respectively. At follow-up, the mitral valve area was significantly decreased(1.6 in group I vs 1.8cm2 in group D, P<0.001 vs immediate after MVA) at 6 months and well maintained at 1 year follow-up in both groups. Until 6 months after valvuloplasty, the long diameter of orifice was greater in group D, however the difference was not apparent at 1 year follow-up. CONCLUSION: The Inoue and double balloon techniques obtained equivalent results of the success rate and the frequently of complications. However, the Inoue balloon technique reduced significantly fluoroscope time and total procedure duration. Double balloon technique afforded a longer longitudinal splitting of the commissure immediatly and 6 months after valvuloplasty. However the differences was not apparent at 1 year follow-up. Increased MVA was well maintained at 1 year in both groups. The severity of the newly developed mitral regurgitation immediately after valvuloplasty reduced significantly in 53% of the Inoue and 43% in the double balloon group at 6 months follow-up. In the view point of similiar immediate and late results of the two methods, the stepwise dilation with Doppler echocardiographic monitoring during the Inoue procedure appeared to be cumbersome.
Arterial Pressure ; Atrial Pressure ; Balloon Valvuloplasty* ; Echocardiography ; Follow-Up Studies* ; Hemodynamics ; Humans ; Incidence ; Mitral Valve ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Prospective Studies

BACKGROUND: Intimal tear or dissection is a serious complication after coronary angioplasty,sometimes which may develop an acute ischemic event. We evaluate the factor that may predict the development of dissection after angioplasty. METHODS: To identify the factors that development of dissection after angioplasty, the data of 52 patients identified as having dissection with or without immediate vessel closure were examined. Follow-up coronary angiogram was obtained in 22 out of 58 lesions at mean 5.6 month after angioplasty. RESULTS: Intimal dissection developed 58 lesion(31%) out of 177 lesions in 122 patients after PTCA. Ischemic complications, defined as ischemic chest pain, myocardial infarction, the need for coronary bypass surgery occured in 5 patients(9.6%) out of 52 patients with dissections. Significant correlates of a development of dissection were the lesion morphology of type C(P<0.01), more tight diameter stenosis before PTCA(P<0.01), and right coronary artery(P<0.02), especially in the proximal portion (P<0.05). There were no significant correlations of clinical pictures, whether complex or simple angioplasty and PTCA in single vessel disease or in multivessel disease. Morphologic feature of dissection was type A(radiolucency) in 22(38%), B(filling defect)in 14(24%), C(extra-luminal "cap")in 8(14%), D(spiral dissection)in 5(9%), E(filling defect with delayded antegrade flow)in 7(12%) and F(total occlusion) in 2(3%). Twenty-two(38%) dissection out of 58 were obtained follow-up angiogram at mean 5.6 month. Angiographic restenosis occured in 9(41%) lesions, which included more type A dissections (7/9,78%) compared to lesions with dissection healing (3/13, 23%)(P<0.001) at follow-up. Thirteen lesions with dissection healing at follow-up included more B and C dissection(B;54%,C;15%)and E dissection in 1. Furthermoremore restenosis occurred more prevalent in the infarct-related artery(P<0.001) and left anterior decending coronary artery lesion(P<0.01). There was somewhat higher diameter residual stenosis after angioplasty (32+/-11% vs 26+/-10%) in the lesions with restenosis, but there was no statistical significance. CONCLUSION: Intimal dissection after angioplasty occurred in 58(31%) leisions out of 122(177leisions) consecutive patients underwent PTCA developments if intimal dissection after PTCA significantly correlated with the lesions if type C, more tight diameter stenois before PTCA and right coronary artery. At mean 5.6months follow-up,angiographic restenosis occured in 41% of dissections, which had more included type A(radiolucency)dissections, infarct-related artery and left anterior descending coronary artery leision.
Angioplasty* ; Arteries ; Chest Pain ; Constriction, Pathologic ; Coronary Vessels ; Follow-Up Studies* ; Humans ; Myocardial Infarction

There are several EKG changes in cerebrovascular disease(CVD). The wide prominent of inverted T wave is frequently developed in patients with CVD. There were case reports for CVD in patient with ST-segment elevation without myocardial infarction, but the exact mechanism is unknown. EKG abnormalities associated with subarachnoid hemorrhage were first described by Byer et al, in 1947.1 We report the case of 72 years old female patient who developed subarachnoid hemorrhage and intraventricular hemorrhage with ST-segment elevation.
Aged ; Electrocardiography ; Female ; Hemorrhage ; Humans ; Myocardial Infarction ; Subarachnoid Hemorrhage*

The coronary arteriovenous fistula (CAVF) is a rare congenital anomaly but constitutes the most common hemodynamically significant coronary artery anomaly. Transcatheter embolization is as an effective alternative to surgery even though procedure may be complicated by migration of the coil into peripheral vessels or pulmonary arteries. To our knowledge, the association of CAVF with Turner syndrome was not reported. We report a case of successful coil embolization of CAVF using a complex, helical-fibered platinum coil in patient with Turner phenotype with 46,XX.
Arteriovenous Fistula* ; Coronary Vessels ; Embolization, Therapeutic* ; Humans ; Phenotype* ; Platinum ; Pulmonary Artery ; Turner Syndrome

BACKGROUND: During and immediately after percutaneous transluminal coronary angioplasty(PTCA), reversible ischemic electrocardiographic change and/of left ventricular dysfunction are developed. But it is not investigated whether there are potential myocardial cell damages following PTCA or not, and the clinical Significance of myocardial cell damage following PTCA. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial damage. The object of this study is to investigate whether potential Myocardial damage following PTCA was occurred and the utility of cardiac Tropoin-T for predicting the complications during and immediately after PTCA. METHODS: The study group comprised 12 patients(M/F;8/4mean age;60 +/- 4year,AMI in 6) undergoing PTCA, Samples for Troponin-T were obtained before, directly after, after 2 hours, 6 hours, and after 12 hours and was determined by enzyme immunoassay on an ES 300 analyzer(Boehringer Mannheim). Discrimination limit for myocardial cell damage is 0.1 ng/ml in normal baseline level but if the baseline level is elevated such as acute myocardial infarction or unstable angina, myocardial cell damage is defined with further increase of cardiac Troponin-T(>0.1 ng/ml) compare to baseline level. RESULTS: 1) The mean duration of total balloon inflation is 10.7 +/- 2(3-22) minutes and the mean duration of single maximal inflation is 3.9 +/- 0.6(1-8) minutes. There are no significant change in concentration of Troponin-T by inflation time. None of the patients showed electroca rdiographic evidence for myocardial infarction. 2) Troponin-T were increased in 2 patients with unstable angina(0.01 vs 0.11 ng/ml) which were developed major dissection including acute closure during PTCA, and 2 patients with acute myocardial infarction(2.37 vs 3.73 ng/ml) which didn't developed dcomplication. The increase of cardiac Troponin-T were observed in 2 of 10 patients with uncomplicated PTCA(20%). 3)The subacute complications were not developed. CONCLUSION: The cardiac Troponin-T were increased significantly in two AMI patients with uncomplicated PTCA(2/10,20%). The increase of cardiac Troponin-T following PTCA is associated with periprocedural complications but the prognostic significance to detect postprocedural complication did not define in this study because there were no subacute complications after PTCA and may be limited value due to time course of complication(usaully within 1 hour after PTCA) and relatively long analytic time.
Angina, Unstable ; Discrimination (Psychology) ; Electrocardiography ; Humans ; Immunoenzyme Techniques ; Inflation, Economic ; Myocardial Infarction ; Troponin T* ; Ventricular Dysfunction, Left

BACKGROUND: Microalbuminuraia is a strong prognostic factor for cardiovascular morbidity and mortality in type I and II diabetics. Recent data suggest that microalbuminuria predicted cardiovascular disease independent of hypertension in one of two large-scale studies performed in non-diabetics. Additional possibilities could be a previously documented association with other major and interconnected cardiovascular risk factors, such as insulin resistance, and elevated cardiac mass, abnormal circulation lipid levels, and overweight. The object of this study os to investigat the incidence of microalbuminuria, and to define the pathophysiologic mechanism of microalbuminuria to contribute coronary heart disease in non-diabetic patients with angiographiclly documented coronary artery disease(CAD). METHODS: The study group comprised 31 patients(M;21, mean age 60+/-30 year) with angiographically documented CAD and 15 normal control(m;9, mean age 62+/-7 year). Urinary albumin excretion, blood pressure, echocardiographic left ventricular mass indes, plasma abdominal/hip circumference ratio, fasting glucose, insulin, and c-peptide were studied. The microalbuminuria was defined urinary albumin more than 20ug/min. RESULTS: 1) Six of 31 patients with CAD(19.4%) and none of 15 normal control had microalbuminuria. Hypertension were documented 13 of 31 patients with CAD, and none of 15 normal control(p<0.01). Five of 6 patients with CAD and microalbuminuria and 8 of 25 patients with non-microalbuminuric aptients had hypertension (p<0.05). 2) In the microalbuminuric subjects with CAD, body mass index(29.0+/-3.2vs 24.8+/-3.5), systolic blood pressure(138+/-31 vs 118+/-15mmHG), lipoprotein(a) (69+/-31vs 32+/-32mg/dl), fastion C-peptide(5.5+/-2.2 vs 2.7+/-1.6ng/ml), and microalbumin(221+/25 vs 9.6+/-7.9mg/day)were significantly greater than in normal control(p<0.05). But no difference in left ventricular mass, lipid profile, and abdominal/hip circumference ratio existed between the microalbminuric patients with CAD and normal control. 3) Between the microalbuminuric patients with CAD and without CAD, no signficant difference were noted excepr lipoprotein(a) lever(69+/-31 vs 29+/-29mg/dl), fasting C-peptide(5.5+/-2.4 vs 2.5+/-1.2ng/ml), and microalbumin(221+/-247 vs 8.6+/-6.7mg/day). CONCLUSION: Microalbuminuria was associated with history of hypertension or concurrent antihypertension therapy and insulin resistance in non-diabetics with CAD. But left ventricular cardiac mass, central obesity inedw, and lipid profile were not related with microalbuminuria. The underlying presence of a major risk factor such as hypertension and insulin resistance might be explain the previously reported predictive value of microalbuminuria for cardiac events.
Blood Pressure ; C-Peptide ; Cardiovascular Diseases ; Coronary Artery Disease* ; Coronary Disease ; Coronary Vessels* ; Echocardiography ; Fasting ; Glucose ; Humans ; Hypertension ; Incidence ; Insulin ; Insulin Resistance ; Lipoprotein(a) ; Mortality ; Obesity, Abdominal ; Overweight ; Plasma ; Risk Factors

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

BACKGROUND: Reperfusion of ischemic myocardium is clinically encountered during thrombolytic therapy of acute myocardial infarction, percutaneous transluminal coronary angioplasty(PTCA), and coronary artery bypass graft(CABG). Reperfusion results in endothelial dysfunction characterized by a reduced release of endothelium-derived relaxing factor(EDRF) in animal studies. Studies with experimental animals have emphasized the role of oxygen free radicals and lipid peroxidation in pathophysiology of reperfusion injury and myocardial stunning. The object of this study is to determine whether endothelial dysfunction was developed after open heart surgery and to evaluated the role of oxygen free radical and lipid peroxidation in reperfusion injury. METHODS: The study group was comprised 13 patients who underwent open heart surgery(male/female : 2/11, mean age : 43+/-4 year, Atrial septal defect in 4, Ventricular septal defect in 1, Mitral regurgitation in 2, Tetralogy of Fallot in 1, and Aortic stenosis and Regurgitation with Mitral stenosis in 5 patients). The endothelial function was evaluated with the vasomotor response to acetylcholine and nitroglycerin by change of arterial diameter during the continous infusion of acetylcholin, from 10(-9) to 10(-6) molar concentration to the coronary artery and intracoronary injection of 200microg nitroglycerin after acetylcholine infusion. The infusion study was performed before and 10 days after surgery. For analysis of the role of oxygen free radical and lipid peroxidation in reperfusion injury, blood samples for malondialdehyde and neutrophil respiratory burst test(hydrogen peroxide amount of neutrophils) were obtained in pre-declamping of aorta and 5 min, 10 min, and 20 min after declamping of aorta from coronary sinus. RESULTS: 1) The vasoconstrictor response to acetylcholine, 10(-9) to 10(-6)M concentration, at proximal and distal left anterior descending coronary artery, were increased significantly in post-operation infusion study but there was no singnificant difference in vasodilator response to nitroglycerin. 2) The mean absorbance value of malondialdehyde(MDA) in pre-declamping and 5min, 10min, and 20min after reperfusion were 96+/-12, 73+/-12, 89+/-11 and 77+/-12, respectively. There was no significant difference in plasma MDA level and hydrogen peroxide amount of neutrophils after reperfusion(aortic declamping). CONCLUSION: These data suggest that endothelium dependent vascular relaxation is impaired in patients with open heart surgery and post-ischemic reperfusion injury may be responsible for the abnormal response. But we did not determine the role of lipid peroxidation and oxygen free radical in reperfusion injury.
Acetylcholine ; Animals ; Aorta ; Aortic Valve Stenosis ; Coronary Artery Bypass ; Coronary Sinus ; Coronary Vessels ; Endothelium ; Free Radicals ; Heart Septal Defects, Atrial ; Heart Septal Defects, Ventricular ; Heart* ; Humans ; Hydrogen Peroxide ; Lipid Peroxidation* ; Malondialdehyde ; Mitral Valve Insufficiency ; Mitral Valve Stenosis ; Molar ; Myocardial Infarction ; Myocardial Stunning ; Myocardium ; Neutrophils ; Nitroglycerin ; Oxygen* ; Plasma ; Relaxation ; Reperfusion Injury* ; Reperfusion* ; Respiratory Burst ; Tetralogy of Fallot ; Thoracic Surgery* ; Thrombolytic Therapy

BACKGROUND: The exercise stress testing(Treadmill Test) is one of the preferred noninvasive methods of identifying patients with coronary artery disease. ST-segment elevation during or immediately after exercise is uncommon and in most patients, it was associated with prior infarction, left ventricular hypertrophy or left bundle branch block, Exercise-induced ST-segment elevation has been attributed to ventricular wall motion abnormalities, and ischemia due to either coronary vasospasm or ervere proximal coronary stenosis. We examined the clinical, angiographic, and prognostic significance of 16 patients with exercise induced ST-segment elevation. METHODS: 16 patients with exercise-induced ST-segment elevation were retrospectively reviewed. The symptom-limited exercis testing was performedn using a modified Bruce protocol and in patients with acute myocardial infarction(AMI), low level exercise testing(Myocardial infarction protocol) was used. The significant ST-segment elecation was defined as a > or =1mm change present in >1 lead measured at 0.08 sec after J point and in > or =3 consecutive beats. Coronary arteriogram and percutaneous transluminal coronary angioplasty(PTCA) was performed using standard techniques within 7 days of initial exercise testing and a luminal diameter stenosis of >50% was considered significant. RESULTS: 1) We have studied 2076 exercise tests and 16 patients(M/F:15/1, Mean age : 58 years) developed exercise-induced ST-segment elevation. The initial diagnosis were acute myoca rdial infarction(AMI) in 12, variant angina in 2, effort angina in 1 and unstable angina in 1 patient. 9 of 12 patients with AMI were treated with thrombolytic agent(Urokinase 2.5 to 3 million unit) within 6 hours from the onset of chest pain. 2) Mean maximal ST-segment elevation was 2.6mm(range 1-5mm). The leads which showed exercise-induced ST-segment elevation were corresponded to the location of severe coronary stenosis in typical effort angina, to spasm site in variant angina, and to infarction site in AMI. 11 Patients had follow-up exercise testing and showed abolition of exercise-induced ST-segment elevation in 4 of 5 patients with AMI and 1 patient with effort angina after PTCA, and 1 patient with variant angina and 3 of 4 patient with AMI after medication. 3) In 12 patients, coronary angiography was performed, and showed 95% and 90% stenosis at proximal LAD in 2 patients with effort angina and >80% stenosis at proximal or mid lesion of infarct-related artery in 7 patients with AMI. In variant angina, one patient showed normal coronary artery and another patient showed 60% stenosis at mid LAD. On LV angiogram, there were moderate to severe hypokinesia instead of akinesia or dyskinesia at infarction site in all patients with AMI and showed normal LV contractility in patients with effort or variant angina. PTCA were successfully performed in 7 patients(effort angina 2, AMI 5). 4) The clinical follow up for 16 patients were obtained for mean follow-up duration of 17 months and during the clinical follow-up, 1 variant angina patient with mild stenosis at proximal LAD was died with ventricular fibrillation after discontinution of medication. There were CABG due to restenosis in 1 patient and cerebrovascular accident in 1 patient. CONCLUSION: 1) The exercise-induced ST-segment elevation signifies severe ischemia due to either severe proximal coronary stenosis or coronary arterial spasm. In AMI, this findings suggests the residual ischemia(or residual viable myocardium) in addition to left ventricular dyssynergy or aneurysm. 2) Adverse cardiac events can be provented by revascularization in patients who had critical coronary stenosis and by medical therapy in those with coronary vasospasm or mild coronary stenosis.
Aneurysm ; Angina, Unstable ; Arteries ; Bundle-Branch Block ; Chest Pain ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease ; Coronary Stenosis ; Coronary Vasospasm ; Coronary Vessels ; Diagnosis ; Dyskinesias ; Exercise Test ; Follow-Up Studies ; Humans ; Hypertrophy, Left Ventricular ; Hypokinesia ; Infarction ; Ischemia ; Phenobarbital ; Retrospective Studies ; Spasm ; Stroke ; Ventricular Fibrillation