De novo acute myelogenous leukemia with trilineage myelodysplasia associated with t(8;21)(q22;q22).

We describe a rare case of de novo acute myelogenous leukemia with trilineage myelodysplasia (AML/TMDS) associated with t(8;21)(q22;q22). The patient was admitted to our hospital with leukocytopenia. AML/TMDS was diagnosed by excess myeloblasts and morphological findings of bone marrow. The karyotype revealed 45, X, -Y, t(8;21)(q22;q22) in 17 of 20 analyzed mitoses, and also AML1/MTG8 transcripts were detected by the reverse transcription polymerase chain reaction (RT-PCR) method. The patient achieved a complete remission with a combination chemotherapy of daunorubicin, cytarabine, and prednisolone. This case suggests that t(8;21)(q22;q22) may participate in the pathogenesis of AML/TMDS, although this type is usually found as one of the chromosomal abnormalities in de novo acute myelogenous leukemia (AML) with maturation.

[An aortic valve-sparing procedures (remodeling) for a patient with annuloaortic ectasia: a case report].

A 51-year-old man with annuloaortic ectasia and aortic regurgitation, who did not have Marfan syndrome, underwent an aortic valve-sparing root reconstruction (remodeling). All three sinuses were excised and then the ascending aorta was replaced with a 30 mm collagen-impregnated Dacron graft, one of which ends were scalloped to reproduce pseudosinus. Each coronary artery orifice was anastomosed to the graft with Carrel patch method. Post-operative angiogram showed no aortic regurgitation and no pseudosinus formation, because the graft was slightly larger than the optimal one. The NYHA functional class has been improved III to I 18 months after the operation.

[A case report: surgical treatment of hypertrophic obstructive cardiomyopathy with acute hemodynamic deterioration due to chordae rupture of the mitral valve].

A 70-year-old woman was found to have new heart systolic murmur and was transferred to our hospital for the treatment of high fever and dyspnea. The chest X ray showed cardiomegaly (CTR 63%) and marked pulmonary congestion. The UCG revealed that there was no evidence of infective endocarditis, but there was hypertrophic obstructive cardiomyopathy with the left ventricular pressure gradient of 90 mmHg accompanied by mitral regurgitation (grade 3/4). Two weeks after the admission, mitral regurgitation progressed due to chordae rupture confirmed by UCG. Transaortic subvalvular myectomy and mitral valve replacement were underwent. Post-operative electrocardiogram demonstrated right and left anterior bandle branch block. Eleven months after the operation left ventricular outflow pressure gradient was not detected by echocardiogram and she has been in I/IV NYHA functional class.

[A case of papillary muscle rupture associated with acute inferior myocardial infarction].

A sixty-year-old man was admitted to our hospital due to prolonged left anterior chest oppression and hypotention. The electrocardiogram revealed acute inferior myocardial infarction, confirmed by the coronary angiography which showed occluded right coronary artery (RCA) at the segment 4AV. The intra-coronary pro-urokinase infusion and coronary angioplasty successfully revascularized the occluded 4AV segment. Although the 4AV segment perfused small area, he developed severe pulmonary edema on the second hospital day. A transesophageal echocardiography revealed severe mitral regurgitation due to posterior mitral valve prolapse by the ruptured tendineae with a mobile mass. The damaged mitral valve was replaced by the prosthetic mechanical valve (SJM 25M), resulted in stable hemodynamic state. He discharged one month after the operation.

Left ventricular thrombosis following coronary artery bypass grafting in a patient with nephrotic syndrome: report of a case.

We present herein the case of a 63-year-old man with nephrotic syndrome who developed an apical infarction 4 days after undergoing coronary artery bypass grafting. Echocardiography done 2 weeks postoperatively revealed a left ventricular thrombus which was successfully removed. He has no further thrombotic events since anticoagulant therapy was initiated.

[Studies on faint attack due to arrhythmias with Holter electrocardiogram].

Out of 1,400 Holter ECGs, 15 records revealed arrhythmias which would be responsible for faint attack, including 8 sick sinus syndrome with cardiac arrest, 4 non-sustained ventricular tachycardia (VT), 2 paroxysmal atrial fibrillation and 1 paroxysmal supraventricular tachycardia. All of cardiac arrest corresponding to faint attack lasted for longer than 4 sec, and an averaged duration of the arrest was 5.8 +/- 2.3 sec. This was significantly longer than that with no subjective symptoms, 3.4 +/- 0.7 sec. Duration and rate of VT did not show any significant relationship with faint attack. The result suggests that cardiac arrest is mostly responsible for arrhythmia-induced involvement of cerebral circulation and faint attack. It is also suggested that cardiac arrest longer than 4 sec should be extensively treated including pacemaker implantation.

[Changes in the ECG and myocardial blood flow of the right and left ventricular walls under acute pulmonary arterial stenosis].

For studying the effect of regional myocardial blood flow changes on the epicardial ECG of right and left ventricular walls under acute right ventricular pressure overload, we mapped the epicardial using 64-channel shock electrodes, and estimated the myocardial blood flow with radioactive microspheres. In 9 anesthetized open-chest dogs, the main pulmonary artery was gradedly constricted to the level of mild (peak RV pressure: PRVP, 50-70 mmHg), moderate (PRVP, 70-80 mmHg) and severe stenosis (PRVP, over 80 mmHg). Labeled microspheres were injected into the left atrium before and after the PA constriction, and the epicardial ECGs were recorded continuously. After the completion of the experiment, 9 areas of each right and left ventricular wall were excised. The myocardium was divided into three layers and the flow data were compared to the changes of ECG parameters. In the cases where there was severe PA stenosis, the right ventricular myocardial blood flow decreased to a significantly greater degree (63% reduction from the control), especially in the subepicardial layer, than the flow in the left ventricle (37% reduction from the control). ST potential, STT and QRST Area Map increased in the right ventricle but decreased in the left ventricle. Activation Recovery Time of the right ventricle decreased due to the severe ischemia of the right ventricle. The value of QRS Area Map of the left ventricle decreased significantly in parallel with the decrease in cardiac output.(ABSTRACT TRUNCATED AT 250 WORDS)