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*

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: 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

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: 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: Myocardial contrast two-dimensional echocardiography(MC-2DE) has been known to have the real time capabilities for repeat in vivo assessment of ischemic risk areas and for evaluation of the myocardial perfusion. The aims of this investigation are (1) to evaluate the feasibility of MC-2DE for the delineation and quantitation of the area at risk. (2) to determine the relationship between the extent of the echocontrast defect area(EDA) during reperfusion and the size of myocardial infarction as determined by post-mortem tissue examination, and (3) to observe serial changes in the time echo-intensity characteristics of MC-2DE during coronary occlusion and reperfusion. METHODS: Myocardial contrast echocardiographic images were made by injecting bolus 5mL of two-syringe-agitated mixture of sodium meglumine ioxaglate(Hexabrix(R)) and normal saline(2 : 3 by volume) into the aortic root before and during coronary occlusion of the left anterior descending coronary artery, distal to the first diagonal branch and during reperfusion on eight open-chest dogs. Two-dimensional echocardiographic short axis views were obtained at four anatomic levels : the apex, the low papillary muscle, the high papillary muscle and the mitral valve. The changes in EDA and echo-intensity with its wash-out half time(WHT) at the high papillary muscle level during coronary occlusion and reperfusion were measured every 15 minutes. The total EDA was measured by planimetry at 3 minutes after coronary occlusion and at 60 minutes after reperfusion. Evans blue or methylene blue were used for the measurement of the anatomic area at risk and triphenyl-tetrazolium chloride(TTC) for the measurement of the infarct area. RESULTS: The EDA measured 30 minutes after coronary occlusion(19.6%) was smaller than that at 3 minutes after coronary occlusion(24.0%, p<0.01). Then EDA at 3 minutes occlusion was strongly predictive of the anatomic extent of area at risk(EDA=0.48 Area at risk+16.95, r=0.84, p<0.05). The EDA at 60 minutes after reperfusion, which showed an irregular margin and was located within the subendocardium of the area at risk, also correlated well with the infarct area(IA)(EDA=0.78 IA+3.32, r=0.82, p=0.09). The peak echo-intensity in the ischemic area during coronary occlusion was significantly low(14.2+/-6.5 vs 73.8+/-31.7 in the non-ischemic area, p<0.01) and the WHT was delayed more in the ischemic area than in the non-ischemic area(23.2+/-2.8 sec vs 8.1+/-3.3sec, p<0.01). During the period of reperfusion, WHT in the previously ischemic area was markedly delayed compared to that in the non-ischemic area (p<0.01), although the peak echo-intensity in the ischemic area at 3 minutes after reperfusion increased modestly compared to that in the non-ischemic area(80.9+/-22.8 vs 72.7+/-8.4), suggesting the impairment in the transit of microbubbles is probably due to microvascular damage after reperfusion. There were no adverse hemodynamic or electrocardiographic effects after injection of the contrast agent. CONCLUSIONS: These findings suggest that myocardial contrast echocardiography was useful as a non-invasive technique, first, to delineate the area at risk in vivo during coronary occlusion and, after reperfusion, the infarct area, and secondly, to evaluate indirectly the state of myocardial perfusion during coronary occlusion and reperfusion.
Animals ; Axis, Cervical Vertebra ; Coronary Occlusion* ; Coronary Vessels ; Dogs ; Echocardiography* ; Electrocardiography ; Evans Blue ; Hemodynamics ; Meglumine ; Methylene Blue ; Microbubbles ; Mitral Valve ; Myocardial Infarction ; Papillary Muscles ; Perfusion* ; Reperfusion* ; Sodium

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

Recent studies have shown that side population (SP) cells, isolated from adult myocardium, represent a distinct cardiac progenitor cell population that exhibits functional cardiomyogenic differentiation. However, information on the intrinsic characteristics and endothelial potential, of cardiac SP cells, is limited. The present study was designed to investigate whether cardiac SP cells exhibit endothelial differentiation potential. The cardiac SP cells more highly expressed the early cardiac transcription factors as well as endothelial cell markers compared to the bone marrow-SP cells. After treatment with VEGF, for 28 days, cardiac SP cells were able to differentiate into endothelial cells expressing von Willebrand factor as determined by immunocytochemistry. Furthermore, expression of endothelial cell markers increased several-fold in VEGF-treated cardiac SP cells compared to the control group when assessed by real-time PCR. We also confirmed that cardiac SP cells provided a significantly augmented ratio of ischemic/normal blood flow, in the cardiac SP cell-transplanted group compared with saline-treated controls on postoperative days 7, 14, 21 and 28, in a murine model. These results show that cardiac SP cells may contribute to regeneration of injured heart tissues partly by transdifferentiation into angiogenic lineages.
Animals ; Base Sequence ; Bone Marrow Cells/cytology/drug effects ; Cell Differentiation/drug effects ; Cell Separation ; Colony-Forming Units Assay ; DNA Primers/genetics ; Endothelial Cells/*cytology/drug effects/metabolism/transplantation ; Mice ; Mice, Inbred BALB C ; Myocardium/*cytology/metabolism ; Vascular Endothelial Growth Factor A/pharmacology