Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UNIPROT:P50583 (asymmetrical)
 12,197 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Cardiomyopathy was diagnosed in several members of two families. This familial cardiomyopathy showed symmetrical or asymmetrical hypertrophy of the ventricular walls with or without obstruction to the left ventricular outflow tract. Certain forms were asymptomatic and were revealed by the family history and echocardiography. Myocardial and intercostal muscle biopsy was performed for a biochemical and ultrastructural analysis. Different myocardial features were observed in the two families: a large increase in the glycogen deposits in the one, without clinical signs of a glycogen storage disease, and intracellular deposits of a filamentous protein substance in the other.
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PMID:[Familial cardiomyopathy: a study of two families with myocardial and skeletal muscle biopsies]. 11 77

An echocardiographic and electrocardiographic evaluation of left ventricular hypertrophy (LVH) was carried out in 50 patients with chronic pressure or volume overload of the left ventricle, and in 16 patients with cardiomyopathy. In contrast to the ECG, echocardiography permitted good differentiation of ventricular dilatation, symmetrical and asymmetrical wall thickening. Positive voltage criteria (SOKOLOFF) were found in 76% of cases with abnormal muscle mass, but the height of QRS amplitude showed no close correlation with the degree of LVH. The presence of absence of ST/T changes was an unreliable index in predicting wall thickness. The practical value of echocardiagraphy in the differential diagnosis of left ventricular disorders is discussed.
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PMID:[Proceedings: Echocardiography for the diagnosis of left ventricular hypertrophy]. 12 54

Cardiomyopathies have been characterized as diseases of the heart muscle of unknown cause. The dilated type [idiopathic cardiomegaly] cannot be regarded as a separate entity, but a uniform final result of myocardial damage due to various factors. Hypertrophic cardiomyopathy [asymmetrical hypertrophy of septum] probably represents a genetically conditioned disease with characteristic clinical and pathological features.
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PMID:[Cardiomyopathies]. 14 11

An experienced marathon runner died suddenly during a competitive race. At necropsy, ventricular hypertrophy but no asymmetrical septal hypertrophy was found. Histological studies showed features of hypertrophic cardiomyopathy. The coronary arteries were normal. We propose that the runner died from myocardial ischaemia, precipitated by marathon running on a background of hypertrophic cardiomyopathy. Excess cardiac work, induced by marathon running in the presence of mild congenital cardiac defects, could have contributed to the development of the cardiomyopathy.
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PMID:Hypertrophic cardiomyopathy associated with sudden death during marathon racing. 15 46

In defining the characteristic abnormalities of obstructive cardiomyopathy (OCM), the echocardiogram appears to offer an excellent method. We have used this technique in 22 adults presenting with this condition, and have compared the results of echocardiography with those taken from 17 normal subjects. All those with OCM had asymmetrical hypertrophy of the septum (meaning hypertrophy of the septum without proportional thickening of the posterior wall of the left ventricle); certain other facts were noted: an undilated left ventricular cavity, good systolic function, and indications of poor diastolic compliance. In addition, from the thickeness of the posterior wall and the movement of the mitral valve complex during systole, it has been possible to draw a distinction between the patients with and those without obstruction while they were all at rest. These results confirm that it is possible to identify obstructive cardiomyopathy and the frequently associated defects of ventricular function by an echocardiographic method.
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PMID:[Echocardiographic criteria of obstructive cardiomyopathy]. 40 65

Obstructive and non-obstructive asymmetrical septal hypertrophy (ASH) is a relatively common disease which has no characteristic clinical symptoms. In only 14 of 71 patients in whom the diagnosis had been confirmed echocardiographically had it been possible to make the diagnosis by clinical means alone. Most of the patients had no specific clinical symptoms (angina, dyspnoea, systolic murmur, non-specific ECG changes) indicating a cardiomyopathy. Every patient with such uncharacteristic signs should therefore be studied by echocardiography in order to exclude ASH. In 17 patients there were no clinical symptoms at all, the diagnosis being made entirely by echocardiography.
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PMID:[Familial asymmetrical septal hypertrophy with and without obstruction: clinical findings in patients with echocardiographically confirmed diagnosis (author's transl)]. 86 24

The auscultatory signs in 90 subjects with hypertrophic obstructive cardiomyopathy are described. The late-onset ejection systolic murmur and its responses to vaso-active manoeuvres reflect a volume-dependent outflow tract obstruction. Late vibrations of the systolic murmur, not uncommonly recorded at the apex, are due to associated mitral incompetence. Non-ejection systolic clicks may occur, and the likely explanation is inequality of the functional length of the mitral chordae tendineae secondary to asymmetrical myocardial hypertrophy. The second heart sound is often abnormal, usually with delay in the aortic component. Some correlation was demonstrated between the relative degrees of left and right ventricular outflow obstruction and the pattern of splitting of the second heart sound. Reversed or partially reversed splitting is usually associated with a more severe left ventricular outflow obstruction. Ejection systolic clicks and early diastolic murmurs occur infrequently, but are not incompatible with the diagnosis of hypertrophic obstructive cardiomyopathy.
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PMID:Auscultatory features of hypertrophic obstructive cardiomyopathy. A study of 90 patients. 116 71

We encountered a 65-year-old female with hypertrophic obstructive cardiomyopathy and mitral valve prolapse who had infective endocarditis and hemolytic anemia. The infecting organism of endocarditis was group A streptococci. With regard to the etiology of the hemolytic anemia, fragmentation hemolysis was considered because fragmented red cells and elevated lactic dehydrogenase were observed. Haptoglobin was markedly decreased. Coombs' test, Ham's test and abnormal hemoglobin were negative. She had not had a hemolytic attack in the past. Ultrasonic cardiography showed asymmetrical septal hypertrophy, mitral valve prolapse and 285 mmHg of calculated pressure gradient in the left ventricle. Cardiac catheterization showed 115 mmHg of left intraventricular pressure gradient and mitral regurgitation (grade 2). Hemolysis was slightly improved after treatment with propranolol. Thus, fragmentation of the normal red cells seemed to be due to shear stress.
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PMID:Fragmentation hemolysis in a patient with hypertrophic obstructive cardiomyopathy and mitral valve prolapse. 140 52

Transient hypertrophic cardiomyopathy has been described in human infants of diabetic mothers. The purpose of this study was twofold: first, to document the features of cardiac hypertrophy in newborns of female rats with streptozotocin-induced diabetes and second, to investigate the natural history of this cardiomyopathy. Marked asymmetrical septal hypertrophy with hypertrophy of myocytes was observed in newborns of diabetic female rats, whether or not the mothers received daily administration of NPH insulin. The abnormal cardiac morphology was no longer apparent 4 weeks after birth. Thus, in this model, the asymmetrical septal hypertrophy was secondary and was not a manifestation of genetically transmitted hypertrophic cardiomyopathy.
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PMID:The cardiomyopathy in infants of streptozotocin-induced diabetic female rats. 207 51

Seven elderly patients with hypertrophic obstructive cardiomyopathy (HOCM), who had the three following characteristics on echocardiograms 1) extremely thickened septum, 2) systolic anterior motion of the mitral valve, 3) mid systolic semi-closure of the aortic valve, were clinically evaluated. Ages ranged from 73 to 86 years old (average 78.9% yr.) and all were women. None had not a family history of hypertrophic cardiomyopathy but they had mild hypertension. Six patients showed a significant high voltage on the ST-segment and T-wave abnormalities ("strain" pattern). The left ventricular posterior wall as well as the septum was thickened in 5 and the remaining 2 showed asymmetrical septal hypertrophy (ASH) on echocardiograms. The left ventricular cavity was narrowed due to left ventricular hypertrophy and the shape of the left ventricular cavity was ovoid in all patients. The aorto-septal angles in these 7 patients were 80 degrees to 120 degrees. In addition, proximal septal bulge in all and anterior displacement of the mitral posterior leaflet due to the mitral ring calcification (MRC) in some patients contributed to the narrowing of the left ventricular outflow tract, and the mitral valve was pulled up toward the septum because of the good left ventricular systolic function (ejection fraction: 70 to 94% by echocardiography) and blood was ejected at a high velocity through a narrowed outflow tract (Venturi effect). Pressure gradients in the left ventricular outflow tract was 38 to 146 mmHg in 5 examined by cardiac catheterization. Biopsy specimens were obtained from 2 patients, showing hypertrophic myocytes (diameter: 20 to 30 micron) in 2 and mild disarray in 1.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[A clinical study of hypertrophic obstructive cardiomyopathy in the elderly]. 226 18


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