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

No abstract available.

No abstract available.
Ilizarov Technique* ; Pseudarthrosis* ; Tibia*

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) 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: 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

An acute pulmonary embolism (PE) and the apical ballooning syndrome (ABS) are both critical and need proper management during the acute stage. We experienced a case of recurrent severe dyspnea because serious right ventricular dysfunction due to PE and left ventricular dysfunction due to ABS occurred consecutively in the short-term and bedside echocardiography has an important role in management in acute settings.
Dyspnea ; Echocardiography ; Hemorrhage ; Pulmonary Embolism ; Takotsubo Cardiomyopathy ; Ventricular Dysfunction, Left ; Ventricular Dysfunction, Right

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

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

BACKGROUND: A group of patients with chest pain and normal coronary angiograms without spasm of epicardial artery is known to have decreased coronary flow reserve in response to vasodilatory stimuli, but the mechanisms responsible for the impairment of vasodilatory reserve are undefined. The purpose of this study was to determine whether dysfunction of coronary microvascular endothelium contributes to the reduced vasodilatory responses in patients with chest pain and normal coronary angiograms. METHODS: Twenty patients, 12(group A) with and 8(group B) without ST depression on exercise ECG or 24 hours ambulatory ECG. with chest pain and normal coronary angiograms and no spasm of epicardial coronary artery. were studied. As the endothelium-independent vasodilator, acetylcholine at doses of 20microg, 50microg and 100microg, and as the endothelium-independent vasodilator, nitroglycerin 200microg were infused into left coronary artery. The functional response of coronary vasomotion was studied with atrial pacing. By themodilution pacing catheter. great cardiac vein flow(GCVF) was measured. The changes in the diameter of proximal and distal of left anterior descending artery were analyzed. RESULTS: Intracoronary acetylcholine increased GCVF by 12.3% with 20microg(NS),by 38.9% with 50microg(p<0.05) and by 14.8% with 100microg(NS). The changes in GCVF with 20microg and 50microg dose of acetylcholine were positively related with those with atrial pacing(r=0.59 and r=0.62, respectively), but not at dose of 100microg(r=0.12). Thus, patients with diminished flow response with atrial pacing had reduced endothelium-dependent dilation with low dose acetylcholine. Also changes in GCVF with atrial pacing and acetylcholine were smaller in the patients of group A than group B. However, the changes in GCVF to nitroglycerin was not related with the changes with acetylcholine and did not differ between A and B group, indicating this vasodilatory response was not associated with the endothelium-independent vasodilation. Acetylcholine caused similar degree of change in diameter at proximal and distal epicardial artery in two groups and their changes were not related with changed in GCVF with acetylcholine, suggesting the changes in GCVF with acetylcholine were mainly influenced by the changes at the level of microvasculature. CONCLUSION: In patients with chest pain and normal coronary angiograms without spasm of epicardial artery, reduced vasodilatory response with atrial pacing was associated with the impairment of endothelium-dependent dilation at the level of coronary microvasculature, suggesting the endothelial dysfunction of coronary microvessels is one of the causes of inducible myocardial ischemia.
Acetylcholine ; Arteries ; Catheters ; Chest Pain* ; Coronary Vessels ; Depression ; Electrocardiography ; Endothelium ; Humans ; Microvessels* ; Myocardial Ischemia ; Nitroglycerin ; Spasm ; Thorax* ; Vasodilation ; Veins