BACKGROUND: Oxygen free radicals have been implicated as a cause of deleterious effects in the setting of coronary reperfusion, and they are believed to be generated by the xanthine oxidase system, from activated neutrophiles and from mitochondria. We evaluate the contribution of mitochondria to the production of oxygen free radicals and clarify the mechanism of cellular damage in ischemic reperfused hearts. METHODS: Mitochondria isolated from the ischemic rabbit hearts were incubated in the reaction conditions with different oxygen tensions. Generation of superoxide anion and activities of defensive enzymes aginst oxidative stress were mesured. RESULTS: Superoxide anion genertion by mitochondria incubated in 21% oxygen condition were 0.54+/-0.09 and 0.27+/-0.04(O2./min/mg protein) in ischemic mitochondria and in control respectively(P<0.05). Activites of defensive enzymes against oxidative stress, superoxide dismutase and glutathione peroxidase, were significantly reduced in mitochondria isolated from either ischemic or reperfused hearts. With the lapse of respiration in 21% oxygen condition, ADP-stimulated state 3 oxygen consumption(306.4+/-31.5 vs 214.4+/-11.4n atoms O/min/mg protein) at 30 minutes, P : O ratio and phosphorylation rate were significantly decreased in ischemic mitochondria. CONCLUSION: Elevation of oxygen free radical generation as well as the reduction of defensive enzyme activities in ischemic reperfused mitochondria are injurious to mitochondrial respiratory function. It may contribute to the mechanism of cellular damage in ischemic reperfused hearts.
Free Radicals ; Glutathione Peroxidase ; Heart* ; Mitochondria* ; Myocardial Reperfusion ; Neutrophils ; Oxidative Stress ; Oxygen ; Phosphorylation ; Respiration ; Superoxide Dismutase ; Superoxides* ; Xanthine Oxidase

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*

To evaluate the cardiac functions we examed the M-mode echocardiography with measurements of blood pressure, heart rate and body surface area in 55 normal Korean adults(male 30 persons, female 25 persons) of mean age, 41.7+/-12.3 years. (1) Interventricular septal thickness is 9.5+/-1.7mm and left ventricular posterior wall thickness are 8.6+/-1.5mm at end-diatole, 14.0+/-2.1mm at end-systole. (2) Diastolic and systolic left ventricular internal dimensions are 49.1+/-4.8mm and 31.3+/-5.0mm, respectively. (3) Left ventricular mass by Penn Convention method is 174.4+/-52.1g and left ventricular mass index is 103.2+/-28.8g/m2. (4) Relative wall thickness is 0.35+/-0.06. (5) Left ventricular volumes by Teichholz's method are 114.9+/-27.6ml at diastole and 40.2+/-17.2ml at systole. Therefore, stroke volume is 74.7+/-16.9ml and stroke volume index is 44.5+/-10.7 ml/m2. (6) Cardiac output is 4944+/-1058 ml/min and cardiac index is 2951+/-666 ml/min/m2. (7) Total peripheral resistance is 1454+/-356 dynes-sec-cm(-5) and total peripheral resistance index is 2472+/-623 dynes-sec-cm(-5).m2. (8) Fractional shortening is 36.5+/-6.0% and pressure-volume ratio is 3.27+/-1.19 mmHg/ml. (9) End-systolic wall stress is 61.3+/-19.7x10(3) dynes=cm2. (10) Atrial emptying index is 0.66+/-0.18.
Adult* ; Blood Pressure ; Body Surface Area ; Cardiac Output ; Diastole ; Echocardiography* ; Female ; Heart Rate ; Humans ; Stroke Volume ; Systole ; Vascular Resistance

Ventricular arrhythmia and left ventricular dysfunction after hospital discharge in acute myocardial infarction are powerful predictors of sudden death. We evaluated the ventricular extrasystoles with 24 hour ambulatory electrocardiography at convalescent phase in 34 patients of acute myocardial infarction. Ventricular extrasystoles were observed in 19 patients (56%) and classified by Lown's grading system as grade 1 for 8 cases, grade 2 for 3 cases, grade 3 for 3 cases, grade 4 for 3 cases, and grade 5 for 2 cases. There was no relation between the develoment of ventricular extrasytoles and the risk factors of ischemic heart discase such as smoking, hypertension, hyperlipidemia, diabetes mellitus, and male sex. Also, the development of ventricular extrasystoles was independent to infarct site, regional wall motion abnormalities, and clinical manifestations of left ventricular dysfunction such as congestive heart failure and cardiomegaly. In conclusion, ventricular arrhythmia might independently predict the prognosis in survivors of acute myocardial infarction.
Arrhythmias, Cardiac ; Cardiomegaly ; Chymopapain ; Death, Sudden ; Diabetes Mellitus ; Electrocardiography, Ambulatory ; Heart ; Heart Failure ; Humans ; Hyperlipidemias ; Hypertension ; Male ; Myocardial Infarction* ; Prognosis ; Risk Factors ; Smoke ; Smoking ; Survivors ; Ventricular Dysfunction, Left ; Ventricular Premature Complexes*

Torsades de pointes is characterized by paroxysms of ventricular tachycardia at rates typically greater than 200 beats/min in which QRS morphology shows alternating polarity in an undulating pattern so that the complexes appear to be twisting about the beseline;this arrhythmia is virtually always associated with prolongation of the QT interval. Its importance lies not in its unusual structure but in the potentially fatal outcome if conventional treatment is administred. Torsades de pointes was diagnosed in 4 patients;the first with hypokalemia, the second with congenital QT prolongation syndrome, the third with amiodarone, the fourth with organophosphorous and hypokalemia. Treatment of these patients consisted of potassium supply, isoproterenol, lidocaine, phenobarbital, tenormin, phenytoin, cardioversion, atropine. Three patients improved successfully, but one patient died, as a direct result of the ensuing ventricular fibrillation and cardiac arrest on one hour after admission.
Amiodarone ; Arrhythmias, Cardiac ; Atenolol ; Atropine ; Electric Countershock ; Fatal Outcome ; Heart Arrest ; Humans ; Hypokalemia ; Isoproterenol ; Lidocaine ; Phenobarbital ; Phenytoin ; Potassium ; Tachycardia, Ventricular ; Torsades de Pointes* ; Ventricular Fibrillation

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

The ambulatory electrocardiographic examinations were performed in 31 patients (mean age of 59.4+/-9.3 yrs : male 16 cases, female 15 cases) with ischemic heart disease to evaluate the clinical features of ST segment more than 1 mm persisting for 45 seconds or longer. The incidence of associated disease are angina pectoris 14 cases, acute myocardial infarction 3 cases, old myocardial infarction 7 cases, hypertension 19 cases, diabetes mellitus 5 cases, cerebrovascular disease 4 cases, aortic regurgitation 2 cases, ventricular arrhythmia 1 case and chronic renal faliure 1 case. 93.7% of 252 monitored episodes of transient myocardial ischemia were silent. The incidence and duration of transient myocardial ischemia were 8.1+/-6.7 episodes/day (7.6+/-6.5episodes/day for silent myocardial ischemia, 0.5+/-0.9 episodes/day for silent ischemia, 7.6+/-14.1mins/day for symptomatic ischemia). The heart rate at the onset of ST segment depression is higher in symptomatic episode than silent episode (94.6+/-19.7 vs 82.1+/-17.4/min,. p<0.05). But duration of ST segment depression is longer in silent episode than symptomatic episode(32.4+/-97.7 vs 14.8+/-10.2/min,. p<0.01). Maximal ST segment depression was similar between silent and symptomatic episode (1.61+/-0.65 mm, 1.97+/-0.84 mm, repectively). 55.5% of silent episodes occurred during sleep or resting state and 60% of symptomatic episodes occurred during strenuous effort, exercise or eating (p<0.01). Transient myocardial ischemia developed not more frequently in the morning probably because the 24 hour Holter electrocadiographic examination was performed during hospitalization in the majority of cases.
Angina Pectoris ; Aortic Valve Insufficiency ; Arrhythmias, Cardiac ; Depression ; Diabetes Mellitus ; Eating ; Electrocardiography ; Female ; Heart Rate ; Hospitalization ; Humans ; Hypertension ; Incidence ; Ischemia ; Male ; Myocardial Infarction ; Myocardial Ischemia*

Anti-thrombin III deficiency is known as a disease of autosomal dominant trait and relatively common, but in Korea, exact incidence and mortality is not known, In general, Anti-thrombin III deficiency is expressed to venous thromboembolism like deep vein thrombosis or pulmonary embolism. But, arterial embolism is very rare. We experienced a case of Antithrombin III deficiency expressed as myocardial infarction of inferior wall by huge thrombosis in the mid and distal right coronary artery.
Antithrombin III Deficiency ; Coronary Vessels ; Embolism ; Incidence ; Korea ; Mortality ; Myocardial Infarction* ; Pulmonary Embolism ; Thrombosis ; Venous Thromboembolism ; Venous Thrombosis

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: 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