[Advanced sequelae of XXXX : report of two cases with wall motion abnormalities].

@entity1 @entity662 @entity712 @entity82 @entity714 @entity1184 @entity999 @entity299 @entity439 @entity4346 @entity460 @entity1167 @entity955 @entity1121
In view of the paucity of reports describing symptoms of increased degree, and deterioration of left ventricular systolic function in @entity1 with @entity1121 ( @entity1121 ), two cases with @entity712 and progressive thinning of previously hypertrophied apical portions of the left ventricle are reported. These were among 13 @entity1 observed from eight to 10 years. Case 1: A 56-year-old @entity1 was diagnosed as having @entity1121 at the age of 49 years. Severe @entity4346 and prominent ST-T changes were observed on ECG during his first admission. His left ventricular end-diastolic pressure (LVEDP) was 24 mmHg and a left ventriculo-gram revealed a decrease in the left ventricular cavity in the apex and @entity1184 of the apical wall. Moderate @entity82 without @entity1184 or disarray of myocytes was observed in a left ventricular endomyocardial biopsy specimen. In two episodes of @entity1167 he was successfully resuscitated at the age of 50 years. At the age of 55 years, two-dimensional echocardiography revealed thinning and abnormal motion in the apical wall, and a defect in 201T1 accumulation was observed in the same region by perfusion scintigraphy. This @entity1 was readmitted with a diagnosis of @entity999 at the age of 56 years. Cardiac catheterization revealed normal LVEDP (8 mmHg), and a left ventriculogram revealed an @entity439 in the left ventricular apex with normal major epicardial coronary arteries. He has been under treatment with antiarrhythmic medications, @entity460 antagonists and anticoagulants, and has become relatively asymptomatic. Case 2: A 69-year-old- @entity1 was diagnosed as having @entity1121 after a complete evaluation, including cardiac catheterization, at the age of 59 years. His LVEDP was elevated (17 mmHg), and a left ventricular angiogram revealed @entity1184 localized to the apex. Ejection fraction was 64%. A left ventricular endomyocardial biopsy revealed @entity82 without @entity1184 of myocytes. Thereafter, he has been followed as a New York Heart Association functional class III to IV with occasional elevation of cardiac enzymes but without @entity662 or acute changes in his ECGs. However, @entity955 with complete @entity714 developed at the age of 60 years. Apical wall thinning and dyskinesis were diagnosed by 2D echocardiography and a defect in the 201T1 accumulation was observed at about 65 years of age. He was readmitted in severe @entity712 at the age of 69 years, and he was diagnosed as having @entity299 with pulmonary capillary wedge pressure of 35 mmHg.(ABSTRACT TRUNCATED AT 400 WORDS)
