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

A total of 30 cases of cerebral gliomas, including 6 cases of low grade astrocytomas, 6 anaplasticastrocytoomas and l8 glioblastomas multiforme, was examined immunohistochemically to demonstrate the overexpression of mutant forms of p53 protein and to evaluate their relationships with histological subtypes. A p53 monoclonal antibody was applied to the routine formalin fixed, paraffin-embedded tissues for this study using microwave-assisted avidin-biotin method. Overexpression of p53 protein was identified in 4 out of 6 anaplastic astrocytomas (66.7%) and in l3 out of l8 glioblastomas multiforme (72.2%). No immunohistochemical positivity of p53 was found in adjacent normal brain tissue, gliosis and 6 cases of astrocytoma. These results suggest that overexpression of mutant p53 may be an important step in the development and progression of malignant astrocytoma, especially of the aggressive subtypes of glioma, including glioblastoma multiforme.
Humans

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: 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*

BACKGROUND: Unstable angina is a critical phase of ischemic heart disease, but there are no reliable noninvasive methods of assigning patients to different prognostic actegories. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial injury. We investigated the value of the Troponin-T in unstable angina to determine whether the increase of cardiac Troponin-T might be a useful predictor of prognosis. METHODS: Unstable angina is defined as Braunwald classification(Class I, II, III). CLass I is new onset of severe angina or accelerated angina and no rest pain, class II is angina at rest but not within preceding 48 hour, and class III is angina at rest within 48 hour. We studied 16 cases of unstable angina(male:10, mean age:57+/-2year). We measured Troponin-T and CK-MB at admission, after 6 hours, and every 8 hour for 2 days. For the determination of serum Troponin-T, an enzyme immunosorbent assay (Boehringer Mannheim, ES 300 analyzer) was used. Above 0.1ng/ml was regarded as positive. During the admission, we investigated the myocardial infartion, sudden death, and the need of emergency PTCA and CABG. RESULTS: 1) Among 16 unstable angina patients, there are 12 patients in Class I(range 0.001-0.13, mean SD 0.04 0.01, median 0.02ng/ml) and 4 patients in Class III(range 0.03-1.56, mean SD 0.39 0.2, median 0.27ng/ml) and 4 patients showed positive value of Troponin-T. One was in Class I and the others were in Class III. 2) During the admission, one patient expired due to cardiogenic shock preceding inferior myocardial infarction, and 2 patients progressed non-Q wave myocardial infarction(NQMI). These 3 patients were in unstable angina Class III and had positive Troponin-T value. In Class I, one patient performed emergency CABG due to consistent chest pain at the sixth hospital day. These patient had negative Troponin-T value. 3) CK-MB increased in one patient with NQMI, and the other patients were not increased. CONCLUSION: Cardiac Troponin-T in serum appears to be a more sensitive indicator of myocardial cell injury than serum creatine Kinase MD activity, and its detection in the circulation may be a useful porgnostic indicator in patients with unstable angina.
Angina, Unstable* ; Chest Pain ; Creatine Kinase ; Death, Sudden ; Emergencies ; Humans ; Inferior Wall Myocardial Infarction ; Myocardial Ischemia ; Prognosis ; Shock, Cardiogenic ; Troponin T*

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

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

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: Uncomplicated myocardial infarction is often the harbinger of future cardiac events such as unstable angina pectoris,recurrent myocardial infarction or death. The feasibility and safety of exercise testing performed soon after myocardial infarction have been established but the prognostic value of exercise test after myocardial infarction remain inconclusive. The object of this study is to determine whether exercise test results can be utilized to predict of future cardiac events after uncomplicated myocardial infarction. METHODS: The study group comprised 149 patients with an uncomplicated myocradial infarction. A low level exercise test was performed before discharge from the hospital 8 to 10 days after myocardial infarction. The exercise thst results was considered positive if there was new > or =1mm horizontal or downsloping ST segment depression at 0.08 sec after the J point compared with baseline. The patients were followed for the development of new cardiac events. RESULTS: 1) The exercise test after acute myocardial infarction was performed in 149 patients without complication. The mean duration of exercise test was 14 min(range 1-20 min) and the mean work-load(Metabolic equivalents) was 3.7+/-1.1 METs. 2) 37 patients had ST-segment depression, 13 had ST-segment elevation and 27 had an inadequate blood pressure response to exercise. During the exercise, there were angina in 5 patients, dyspnea in 17 and no symptom in 127 patients. 3) During the follow-up period(1 to 75 month, mean 27.4 month), 29 patients experienced post-myocardial infarction angina, 1 had recurrent myocardial infarction, 4 had revascularization therapy(PTCA 2, CABG 2),5 had ischemic cardiomyopathy and 5 died a cardiac death. 4) The patients with cardiac events such as cardiac death, myocardial infarction and post MI angina had a significantly shorter exercise duration(13.1+/-4.0 and 14.6+/-2.7min, p<0.05), lower exercise tolerance(3.5+/-1.0 and 3.9+/-1.0 METs, p<0.05) and lower peak heart rate(117 +/- and 126+/-5, p<0.05). 5) The ST-segment depression, lower exercise tolerance(<3.0 METs) and history of hypertension were associated significantly with cardiac events(p<0.05) but ST-segment elevation, inadequate blood pressure response to exercise, the use of thrombolytic agents and non-Q wave infarction did not predict future cardiac events. Conclusions: The exercise test after acute myocardial infarction is safe and of limited value for predicting patients at risk of cardiac events in the follow-up period. The ST-segment depression and lower exercise tolerance(<3.0 METs) can predict cardiac events and the prognosis of the patients of this group can be improved with aggressive management and careful follow-up.
Angina, Unstable ; Blood Pressure ; Cardiomyopathies ; Death ; Depression ; Dyspnea ; Exercise Test* ; Fibrinolytic Agents ; Follow-Up Studies ; Heart ; Humans ; Hypertension ; Infarction ; Myocardial Infarction* ; Prognosis

BACKGROUND: An earlier index of reperfusion is desirable to determine whether additional therapy is necessary for myocardial salvage. Using the washout phenomenon of biochemical markers, many investigator have reported noninvasive methods for detection coronary reperfusion in patients with acute myocardial infarction. Recently cardiac Troponin-T has been developed as a new myocardial specific marker, especially myocardial damage. The object of this study is to investigate the utility of cardiac Troponin-T for early assessment of reperfusion therapy. METHODS: The study group comprised 10 patients with acute myocardial infarction and reperfusion therapy that was initiated within 6 hours after the onset of symptoms. Blood samples were taken before treatment, every 30 min interval for 3 hours and then 6, 24, 72 hours after the onset of reperfusion therapy to measuring Troponin-T, Creatin Kinase(CK), and CK-MB level. Serum concentration of cardiac Troponin-T level was measured with immunoassed using ES-300, Boehringer Mannheim. We compared the real reperfusion that was assessed by coronary angiogram, chest pain disappearence and resolusion of St-segment elevation with an index of coronary reperfusion, the increase in Troponin-T(big up tri, open Troponin-T) 60, 90 min after repefusion therapy(Successful Reperfusion Index : Tn-T 60(90)-0>0.3 ng/ml) and the sensitivity, specificity, Positive, and negative predictive value were calculated using this threshold(Successful Reperfusion Index). RESULTS: 1) The studied patients(M/F : 7/3, mean age 54+/-12 year) were treated within 3 hour with thrombolytic therapy(7 patients, t-PA) or emergency angioplasty(3 patients). 2) The cardiac Troponin-T levels in eight patients with successful reperfusion showed early peak within 24 hours after reperfusion therapy were initiated but in 2 patients without successful reperfusion showed sustained increase without early peak within 24 hours. The CK-MB levels in patients with successful reperfusion also showed early peak within 24 hours but 5 of 8 patients showed no significant increase until 2 hours after reperfusion therapy. 3) The sensivity, specificity, positive and negative predictive value for detecting reperfusion using a threshold value of 0.3 ng/ml of big up tri, open Troponin-T 90 min(60 min) after reperfusion therapy was 100%(56%), 50(100%), 89%(100%), and 100%(20%), respectively. CONCLUSION: Serial measurements of cardiac Troponin-T, especially reperfusion index(0.3 ng/ml of big up tri, open Troponin-T 90 min after reperfusion therapy) are useful for early assessment of reperfusion therapy in acute myocardial infarction.
Biomarkers ; Chest Pain ; Emergencies ; Humans ; Myocardial Infarction* ; Myocardial Reperfusion ; Reperfusion* ; Research Personnel ; Sensitivity and Specificity ; Troponin T*