No abstract available.

BACKGROUND: Left ventricular thrombus is a common complication after acute myocardial infarction. Methods and RESULTS: To Study the incidence of left ventricular thrombosis (LVT) after acute myocardial infarction, we performed serial two-dimensional echocardiography (2D-Echo) in 35 consecutive patients with acute myocardial infarction prospectively ; 10 patients had inferior wall myocardial infarction, 25 patients had anterior wall myocardial infarction. 2D-Echo was obtained within 3 days of acute myocardial infarction, at 4-10 days after symptom onset, and 2-4 weeks after symptom onset serially in each case. 19 out of 35 patients received thrombolytic therapy with urokinase. Left ventricular thrombi were identified in 9(25.7%) of the 35 study patients. The location of myocardial infarction was anterior and apical in all cases with left ventricular thrombi. The shape of thrombi was mural in 6 cases and protruding in 3 cases. The incidence of left ventricular thrombi in patients who received urokinase was not significantly different from that in patients who didn't(31.9% vs 18.8%,p=0.22). Wall motion score was significantly higher in patients who developed left ventricular thrombi than in patients who had no left ventricular thrombus(8.2+/-1.9 vs 5.8+/-2.6, p<0.005). All thrombi appeared within 10 days after myocardial infarction. CONCLUSIONS: Thus left ventricular thrombi develops within 10 days following myocardial infarction with large anterior and apical location. The thrombolysis therapy has no effect in the incidence of left ventricular thrombi in this study. But because of confounding effect of thrombolysis and location of myocardial infarction and extent of myocardial infarction, further investigation is needed.
Anterior Wall Myocardial Infarction ; Echocardiography ; Humans ; Incidence* ; Inferior Wall Myocardial Infarction ; Myocardial Infarction* ; Prospective Studies ; Thrombolytic Therapy ; Thrombosis* ; Urokinase-Type Plasminogen Activator

The P19 embryonal carcinoma cell line is a useful model cells for studies on cardiac differentiation. However, its low efficacy of differentiation hampers its usefulness. We investigated the effect of 5-azacytidine (5-aza) on P19 cells to differentiate into a high-efficacy cardiomyocytes. Embryoid-body-like structures were formed after 6 days with 1 micrometer of 5-aza in a P19 cell monolayer culture, beating cell clusters first observed on day 12, and, the production of beating cell clusters increased by 80.1% (29 of 36-wells) after 18 days. In comparison, the spontaneous beating cells was 33.3% (12 of 36-wells) for the untreated control cells. In response to 1 micrometer of 5-aza, P19 cells expressed bone morphogenetic protein-2 (BMP-2), BMP-4, Bmpr1a and Smad1 at day 6 or 9, and also cardiac markers such as GATA-4, Nkx2.5, cardiac troponin I, and desmin were up-regulated in a time-dependent manner after induction of BMP signaling molecules. Immunocytochemistry revealed the expression of smooth muscle a-actin, sarcomeric a-actinin, cardiac myosin heavy chain, cardiac troponin T and desmin, respectively. The proportion of sarcomeric a-actinin positive cells accounted for 6.48% on day 15 after 5-aza exposure as measured by flow cytometry. This study has demonstrated that 5-aza induces differentiation of P19 cells into cardiomyocytes in a confluent monolayer culture in the absence of prior embryoid formation and dimethyl sulfoxide exposure, depending in part on alteration of BMP signaling molecules. These results suggest that 5-aza treatment could be used as a new method for cardiac differentiation in P19 cells.
Animals ; Azacitidine/*pharmacology ; Bone Morphogenetic Proteins/genetics/metabolism ; Cell Differentiation/drug effects/genetics ; Cell Line, Tumor ; Cell Proliferation/drug effects ; DNA-Binding Proteins/genetics/metabolism ; Embryo/cytology ; Gene Expression ; Homeodomain Proteins/genetics/metabolism ; Mice ; Muscle Proteins/analysis/genetics/metabolism ; Myocytes, Cardiac/*cytology/immunology/physiology ; Research Support, Non-U.S. Gov't ; Stem Cells/*drug effects/metabolism ; Transcription Factors/genetics/metabolism

BACKGROUND: The presence of diastolic mitral regurgitation has been described in patients with complete atrioventricular(AV) block, aortic valve regurgitation, hypertrophic and restrictive cardiomyopathy, and in patients with long diastolic filling period in atrial fibrillation. However, because of rare incidence and difficulty in making diagnosis of this phenomenon, the frequency and hemodynamic effects of diastolic AV valve regurgitation(DAVVR) and relationship of electrocardiographic(ECG) parameters with DAVVR in patients with complete heart block have not been reported in Korea. METHODS: To evaluate the frequency, hemodynamic effects of DAVVR and relation of ECG parameters with DAVVR in patients with complete AV block, we studied 14 consecutive patients with complete AV block by means of two dimensional and Doppper echocardiography. RESULTS: The DAVVR was observed in all cases of complete AV block except 3 cases on temporary pacemaker. The peak velocy of diastolic mitral and tricuspid valve regurgitaton were 105+/-23cm/sec and 98+/-30cm/sec, respectively. The peak and mean pressure gradient of diastolic mitral regurgitation were 4.7+/-1.7mmHg and 3.1+/-1.5mmHg respectively, and the peak and mean pressure gradient of diastolic tricuspid regurgitation were 4.1+/-2.6mmHg and 2.7+/-2.1mmHg, respectively. There was regular interval between p-wave of ECG and onset of diastolic AV valve regurgitation, which was 215+/-12msec, Diastolic AV valve regurgitation disappeared immediately after recovery of complete AV block to sinus rhythm or insertion of DDD-type permanent pacemaker in all cases. CONCLUSION: In Conclusion, the DAVVR was observed in all cases of complete AV block except cases on temporary pacemaker insertion and its hemodynamic effect was mild. There was regular interval between p-wave of ECG and the onset of diastolic AV valve regurgitation.
Aortic Valve ; Atrial Fibrillation ; Atrioventricular Block* ; Cardiomyopathy, Restrictive ; Diagnosis ; Echocardiography ; Electrocardiography ; Heart Block ; Hemodynamics ; Humans ; Incidence ; Korea ; Mitral Valve Insufficiency ; Tricuspid Valve ; Tricuspid Valve Insufficiency

BACKGROUND: Although determination of Doppler echocardiographic transmitral inflow patterns(DETIP) is used as an indrect method assessing LV diastolic function. It is known that DETIP can be affected by certain hemodynamic variables. The aim of this investigation is to assess the serial changes of DETIP and to determine the relation of DETIP with clinical parameter such as initial left ventricular end-diastolic volume(LVEDV), ejection fraction(EF), Killip class and thrombolytic therapy in acute myocardial infarction (AMI) patients. METHOD: Four serial Doppler and 2-D echocardiographic studies were performed at 1 day, 1 week, 1mouth, and 3 months after development of AMI in 24 patients(M:F=19:5, aged 58+/-11 year , 15 anterior MI) and 13 normal adults (aged 47+/-9 years) as reference group. On admission 14 patients were in Killip class I and 10 patients in class II. Thrombolytic therapy with IV urokinase were done in 11 patients. E velocity, pressure half-time (PHT), and isovolumic relaxation time(IVRT) were analyzed and LV systolic function was determined in apical 4 chamber view. RESULTS: DETIP did not change until 1month after development of AMI. However, E/A ratio was decreased, and PHT and IVRT were increased at 3 months after AMI. Doppler transmitral flow parameters were not related with Killip class and LV systolic function. Patiens who recieved urokinase intravenously and who had greater intial LVEDV(>118cm3) showed higher E/A ratio and shorter PHTand IVRT than those who did not. These findings indicate that changes in Doppler transmitral inflow pattern in AMI patients are not uniform over a period of 3 months and thrombolytic therapy causes favorable effect on Doppler transmitral flow parameters. CONCLUSION: Changes in Doppler trasmitral inflow pattern may be variable over post-AMI period and this should be taken into account in evaluating LV diastolic function after AMI. Thrombolytic therapy may improve LV diastolic function in AMI patients.
Adult ; Echocardiography ; Hemodynamics ; Humans ; Myocardial Infarction* ; Relaxation ; Thrombolytic Therapy ; Urokinase-Type Plasminogen Activator

BACKGROUND: Although there have been many studies on the risk factors for coronary artery disease, the etiology and risk factor of coronary artery spasm has not yet been determined. The objective of this study was to examine the risk factors for coronary vasospasm through a comparison of patients with angiographically determined vasospastic angina and patients without vasospasm and normal coronary artery. METHODS: Intracoronary injection of acetylcholine in order (20microg, 50microg, 100microg) were administered to all patients (Total 81:34 males, 47 females : mean age 50 years) who had a history of chest pain with normal or near normal coronary arteriographic fingings. After documentation of vasospasm in major epicardial coronary arteries by acetylcholine (Ach)-provocated dcoronary angiography, various risk factors (smoking, hypertension, diabetes, drinking and hyperlipidemia) were compared between patients with vasospasm and patients without vaspasm. RESULTS: 24 patients showed significant luminal narrowing (> or =75%)(Vasospasm group) and 57 patients showed no significant change (Control). Vasospasm group were suffered from typical chest pain in 92% of patients but control complained typical chest pain in 51% of subjects. The sites of vasoconstriction induced by Ach were LAD (11 cases), LCX (4 cases), RCA (11 cases) and vasoconstriction occurred 2 vessels (LAD and LCx) at the same time in two cases. The amount of Ach to provocate vasoconstriction was 20~50microg (90%) and there were no difference between left and right coronary arteries. The ratio of smoker was more frequent in the vasospasm group than control (58.3% vs 30.4%, p=0.046). But total cholesterol, low density lipoprotein, high density lipoprotein, triglycerides, apolipoprotein A, apolipoprotein B, lipoprotein (a), diabetes and body mass index, drinking were not statistically significant between two groups. CONCLUSION: Smoking appears to be a major risk factor for vasospastic angina by endotheilal dysfunction without significant coronary artery narrowing. But other fisk for coronary artery disease may not contribute to coronary vasospasm.
Acetylcholine* ; Angiography ; Apolipoproteins ; Body Mass Index ; Chest Pain ; Cholesterol ; Coronary Artery Disease ; Coronary Vasospasm ; Coronary Vessels* ; Drinking ; Female ; Humans ; Hypertension ; Lipoprotein(a) ; Lipoproteins ; Male ; Phenobarbital ; Risk Factors* ; Smoke ; Smoking ; Spasm* ; Triglycerides ; Vasoconstriction

BACKGROUND: QT dispersion(QTD : QTmax-QTmin) or JT dispersion(JTD:JTmax-JT-min)in 12 leads ECG has been known to reflect regional variations in ventricular repolarization and has been reported to bel one of the marker of regional myocardial ischemia. To evaluate the significance of QTD or JTD of exercise ECG in diagnosis of coronary artery disease, we studied 106 patients(mean age, 56.9 years old, male 63) who were referred for the evaluation of chest pain on exertion. METHOD: Treadmill exercise stress test with modified Bruce protocol and coronary angiography were performed in 106 patients with chest pain on exertion. ST-segment depression by >1.0 mm 0.08 second after J-point during or after exercise in exercise test and >50% stanosis of epicardial artery in coronary angiogram were defined as positive. Of 106 patients, 41 had positive exercise ECG and positive coronary angiogram(true positive, TP), 20 had positive exercise ECG and negative coronary angiogram(false positive, FT), 20 had negative exercise ECG and positive coronary angiogram(faalse negative, FN), and 23 had negative exercise ECG and negative coronary angiogram(true negative, Tn). QT and JT interval in 12 leads were measured at baseline and peakexercise and were corrected for heart rate using Bazett's formula. QTD and JTD were measured by calculation the difference between the maximum QT and mininum QT and that between maximum JT and minumum JT. RESULTS: QTD at baseline for TP(72.8ms)was prolonged compared to Tn(52.2ms,P<0.01), but was not different from that for FT(70.2 ms). At peak exercise, QTD for TP(81.3 msec) was significantly prolonged(p<0.01), while QTD for FP(71.2 msec) was not different from that for TN(56.8 msec). JTD at baseline(78.4 msec) and at peak exercise(88.2 msec) for TP were significantly prolonged compared to those for TN(55.2msec and 55.1msec p<0.01,p<0.01, respectively), but those for FP were not porlonged(77.0msec and 79.0msec, respectively). QTD and JTD at peak exercise were more markedly prolonged in patients with sever stenosis of coronary artery(p=0.053 and p<0.05, repectively) and multivessels diseases(p<0.01, 0<0.05) than those with less severe disease and single vessel disease. Patients with left anterior descending artery lesion had greater QTD and JTD at peak exercise than those with other vessels lesion(p<0.01). In addition to standard criteria with ST segment displacement in exercise EGC, inclusion of exercise induced QTD of more than 60msec increased the sensitivity of exercise ECG from 66.7% to 83.3%, and JTD of more than 70msec increased the specificity from 52% to 76.0%. CONCLUSION: Measurement of QT dispersion and JT dispersion of exercise ECG may be useful method to identify the severity of coronary artery disease and to improve diagnostic accuracy of exercise ECG in coronary artery disease.
Arteries ; Chest Pain ; Constriction, Pathologic ; Coronary Angiography ; Coronary Artery Disease ; Depression ; Diagnosis ; Electrocardiography* ; Exercise Test ; Heart Rate ; Humans ; Male ; Myocardial Ischemia ; Sensitivity and Specificity

BACKGROUND: Dobutamine echocardiography is a useful method to detect myocardial viability in ischemic heart disease. Recently myocardial contrast echocardiography(MCE) is reported to be a new method to evaluate myocardial viability by assessing microvascular integrity of dysfunctional myocardium. We hypothesized if the microvascular integrity is maintained, the dysfunctional myocardium would improve its function by dobutamine infusion. METHOD: 10 myocardial infarction patients (acute : old=8 : 2, M : F=7 : 3, mean age=61+/-11yr) were included in the study. 2 dimensional echocardiography was performed before and during dobutamine infusion and after contrast injection to right and left coronary arteries in the catheterization laboratory. Echocardiographic analysis was done in parasternal short, apical 4 and 2 chamber views. Left ventricule was devided by 20 segments from 3 views. In each segment, will motion score(graded 1, normal, to 5, dyskinesia) before and after dobutamine infusion and opacification grade(0, 0.5, 1 denoting no, intermediate and normal opacification respectively) was compared. RESULTS: The number of segments with abnormal wall motion at baseline were 57 segments. 5 segments was exciuded due to poor image quality. Among 52 segments, 25 segments improved it's function during dobutamine infusion. Improvement of regional function was more frequent in hypokinetic segments than akinetic or dyskinetic segments (69% vs 15%). The improvement of dysfunctional regional wall motion by dobutamine infusion was observed in 80%(19/24), 67%(6/9) and 5%(1/19) of normally, intermediately and none opacified segment respectively. The correlation between wall motion score with opacification grade was 0.598 at baseline and increased to 0.766 after dobutamine infusion. CONCLUSION: In patients with myocardial infarction the dysfunctional segments but intact microvasculature assessed myocardial contrast echocardiography improves function by dobutamine infusion. These findings myocardial contrast echocardiography would be a useful method to detect myocardial viability.
Catheterization ; Catheters ; Coronary Vessels ; Dobutamine* ; Echocardiography* ; Humans ; Microvessels ; Myocardial Infarction* ; Myocardial Ischemia ; Myocardium

BACKGROUND: QT dispersion(QTD=QTmax-QTmin) on the 12 lead ECG has been known to reflect regional variation of ventricular repolarization, and thus a marker of an increased risk of arrhythmia events. Late potential(LP) on signal averagina ECG(SAECG) is independent risk factor of ventricular arrhythmia following acute myocardial infaction(AMI). However, the relation between LP and QTD as indicator of electrophysiologic instability in AMI remains to be determined. METHOD: To determine whether there is a difference in QTD between in parients with AMI during acute phase and in normal control and whether thrombolytic therapy is assiciated with a reduction in QTD, and to determine the relationship between change of QTD and late potential on SAECG, we studied 71 patient with AMI(male 54, female 14, mean age 57yrs) and 23 controls(malw 17, female 6, mean age 58yrs). QT interval was measured on a standard 12 lead ECG in patients with AMI on admission, 2 hours after urokinase IV and 10-14 days post-AMI, and QT dispersion was calculated by difference of maximal and minimal corrected QT interval(QTmax-QTmin). A signal averaged ECG was recorded in 36 patients before discharge and coronary angiogeaphy(CAG) was performed in all patients 10-14 days post-AMI. RESULT: QTD is significantly increased in AMI compared to control(78.7+/-39.5ms vs. 24.6+/-22.3ms, P < 0.01). In patients who received thrombolytic therapy with urokinase, QTD is decreased from 75.0+/-34.4ms to 53.9+/-36.0ms(P < 0.01), whereas there is no significant change in patients who did not received thrombolytic therapy(84.8+/-47.6ms vs. 78.9+/-36.2ms, NS). There in no difference in QTD between patients with positive LP(68.4+/-23.6ms) and those with negative LP(77.8+/-32.1ms) on admission, those with positive LP(66.6+/-27.6ms) and those with negative LP(56.0+/-26.4ms) after 10-14days post-AMI. But magnitude of change of 10-14 days post-AMI QTD in patients with negative LP is larger than those with positive LP(-21.7+/-33.4ms vs. -1.8+/-15.2ms, P=0.06). CONCLUSION: QTD in acute phase of AMI is significantly reduced by the thrombolytic therapy. Patients with negative late potential tent to have greater QTD reduction within 14 days after AMI. These finding suggest that QT dispersion in patients with AMI can be reduced by early recanalization and its reduction is associated with the presence of late potential.
Arrhythmias, Cardiac ; Electrocardiography ; Female ; Humans ; Myocardial Infarction* ; Risk Factors ; Thrombolytic Therapy ; Urokinase-Type Plasminogen Activator

BACKGROUND: It is known that there is a pronounced circardian periodicity for the time of onset of acute myocardial infarction(AMI), with prominent increase in incidence of onset in the morning hours. However, the characteristic circardian variability in AMI is blunted in patients receiving beta-blockers or aspirin therapy before their presentation with AMI. These findings are attributed to the increase in platelet aggregability, blood coagulability, and plasma catecholamine that change coronary tone and myocardial oxygen demand. We hypothesize that, in addition to above physiologic and biochemical parameters, morphologic patterns of the coronary artery lesions are related to the development of circardian variation in AMI. METHOD: Subjects were 160 patients with AMI(male 92, female 68, mean age 56.9 +/-10.5 years old). Patients were classified by the time of onset of typical chest pain(AMI) by 6-hour interval from mid-night. Circardian variability of onset of AMI was compared with clinical findings and coronary angiographic findings. RESULTS: Incidence of onset of AMI was most frequent in the morning hours(6AM-noon,42.5%). There was no difference in degree of stenosis, lesion length, incidence of intraluminal thrombus, among 3 subgroups of AMI according to time of attack. Morning hour group had more frequent ulceration of coronary lesion than that of other groups(22.4% vs. 5.4%, p<0.01), and less frequent calcified lesion than that of other groups(3.0% vs 5.4%, p<0.05). Normal or minimal coronary artery lesion, that is Iess than 25% stenosis, was more frequent in the morning hour group comparing to that of other groups(11.9% vs. 9.78%). Eccentric stenosis(15.7% vs, 11,1%) and diffuse irregular lesion(25.5% vs. 16.7%) tended to be more frequent in the morning hour group. There were no differences in sex, age, incidence of hypertension, cigarette smoking, diabetes, degree of alcohol ingestion, ejection fraction, maximal CK value, preinfarction angina duration, past history of MI, and in incidence of arrhythmia. CONCLUSIONS: There were more ulcerative coronary atherosclerotic lesions, but fewer calcified coronary lesions in the morning group than in afternoon and night group. These findings indicate that morphology of coronary artery lesions may play a role in causing circardian variation in AMI.
Angina, Unstable ; Arrhythmias, Cardiac ; Aspirin ; Blood Platelets ; Constriction, Pathologic ; Coronary Vessels* ; Eating ; Female ; Humans ; Hypertension ; Incidence ; Myocardial Infarction* ; Oxygen ; Periodicity ; Plasma ; Smoking ; Thorax ; Thrombosis ; Ulcer