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)

Echocardiographic patterns in 15 patients with hypertrophic cardiomyopathy were compared with those in 30 healthy persons. Correlations with angiocardiographic data indicated that most of the anatomical abnormalities in hypertrophic cardiomyopathy can be assessed reliably by echocardiography. These include abnormal mitral valve motion, a reduction of the anteroposterior dimension of the left ventricular outflow tract and of the left and right ventricular cavities, increased thickness of the interventricular septum and the posterior left ventricular wall. Comparision of the haemodynamic and echocardiographic data showed that some degree of abnormal mitral valve motion during systole may occur in the absence of left ventricular outflow tract obstruction. On the other hand, it need not always be present with left ventricular outflow tract obstruction. Other, hitherto unrecognized, abnormalities in hypertrophic cardiomyopathy detected by this technique were: (1) Aortic valve regurgitation in three out of nine patients with evidence of left ventricular cutflow tract obstruction at cardiac catheterization. (2) Left ventricular inflow tract obstruction at the mitral valve level associated with gross septal hypertrophy (five cases). (3) Abnormal forward displacement of the posterior mitral valve leaflet and of the chordae tendineae during systole in 10 patients, in seven of whom there was confirmatory angiocardiographic evidence. Seven patients with miscellaneous cardiac disorders are described in whom asymmetric septal hypertrophy was revealed by echocardiography. In one of these patients coexisting hypertrophic cardiomyopathy was excluded histologically; thus asymmetrical septal hypertrophy is not confined to patients with hypertrophic cardiomyopathy.
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PMID:Echocardiographic spectrum of hypertrophic cardiomyopathy. 13 64

Left ventricular scanning by echocardiography and ultrasono-cardiotomography was performed to search the possible muscular abnormality in 9 cases with giant T wave inversion without documented cause. The deeply inverted T wave was more than 1.2 mV (average was 1.63 mV) in the left precordial leads. All the cases had electrocardiographic left ventricular hypertrophy of obscure origin and ischemic episode was absent. Conventional echo beam direction to measure the short axis of the left ventricle disclosed almost normal thickness and movement of both interventricular septum (IVS) and the posterior wasll (PW), so that the report of these cases is frequently within normal limits. However, ultrasono-cardiotomography (sector B scan) disclosed the fairly localized hypertrophy near the left ventricular apex, and conventional echocardiography also revealed the same area of either IVS or PW or both below the insertion of the papillary muscles, when the scanning towards the apex was performed (asymmetrical apical hypertrophy: AAH). Control study of 9 cases with IHSS showed asymmetrical septal hypertrophy (ASH) with almost equally hypertrophied IVS from base to apex. All cases had inverted T waves, but these were of lesser degree. Three cases had relatively deep T wave compatible with those of AAH, and these cases also had the apical hypertrophy of considerable degree (unusual type of IHSS, i.e., intermediate type between AAH and ASH). The close relationship between the depth of the inverted T waves and the Apex/Mid wall thickness ratios suggests that the altered recovery process of the hypertrophied apical musculature is responsible for the giant T wave inversion of heretofore unsolved origin. Until the connective link of AAH to the other forms of hypertrophic cardiomyopathy is disclosed, the cases with such a T wave and the apical hypertrophy may be designated as asymmetrical apical hypertrophy (AAH).
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PMID:Giant T wave inversion as a manifestation of asymmetrical apical hypertrophy (AAH) of the left ventricle. Echocardiographic and ultrasono-cardiotomographic study. 13 32

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

On the grounds of clinical, electro- and echo-cardiographic examination of 39 patients with hypertrophic cardiomyopathy from 3 to 15 years of age three types of this pathological condition are distinguished: asymmetrical septal hypertrophy, idiopathic hypertrophic subaortic stenosis and symmetrical hypertrophic cardiomyopathy. The value of signs of hypertrophic myopathy obtained on clinical and instrumental examination is discussed. The high diagnostic value of echocardiography in the examination of patients is emphasized.
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PMID:[Hypertrophic cardiomyopathy in children (clinico-echocardiographic study)]. 15 5

The pathological findings and available clinical data in 15 necropsy cases of HOCM, aged over 61 years, are reported. Three patients were in the eighth decade and 4 in the ninth; 8 were women. Five presented as sudden death, 2 died in congestive cardiac failure, and 7 died of unrelated conditions and HOCM was an apparently incidental postmortem finding. Compared with cases under 60 years, the hearts of the elderly patients were heavier and less likely to show typical asymmetrical hypertrophy, the free wall of the left ventricle also being thickened in two-thirds of the cases over 60 years. Most of the elderly cases showed a distinctive band of fibrous thickening over the upper part of the interventricular septum. This lesion had a "mirror image" relation to the lower part of the aortic surface of the anterior mitral cusp, with the histological features of a friction lesion. It appears to be a morphological expression of the systolic contact of anterior mitral cusp and interventricular septum seen on cineangiography and thus diagnostic of HOCM. Once formed, the fibrous band appears to persist even if the obstructive element disappears. It is, therefore, a valuable diagnostic feature indicating a diagnosis of HOCM in an age group where the morphology is usually not the classical asymmetrical form and in which this diagnosis is usually not considered.
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PMID:Pathological features of hypertrophic obstructive cardiomyopathy (HOCM) in the elderly. 116 58

Using digital subtraction coronary angiography (DSA), we evaluated the regional myocardial coronary blood flow reserve (rMFR) in 18 patients with hypertrophic cardiomyopathy (HCM). There were 13 patients with asymmetrical septal hypertrophy (ASH), and 5 with asymmetrical apical hypertrophy (AAH). Eight subjects without apparent cardiac abnormality served as controls. Relations between the rMFR and regional wall thickness as determined by echocardiography were also investigated. Peak contrast density (Cm) and time to Cm (Tm) were measured from digital angiograms at the middle and distal ventricular septum (VS) and at the apical and left ventricular posterior wall (PW). The rMFR of each region of interest was expressed as the ratio of Cm/Tm at the baseline and at peak hyperemic response induced by intracoronary administration of papaverine. The rMFR was significantly lower at the VS and apex in HCM than in controls: middle VS, 1.9 +/- 0.5 vs 3.9 +/- 0.5, p < 0.001; distal VS, 2.0 +/- 0.5 vs 4.4 +/- 0.9, p < 0.001; and the apex, 2.0 +/- 0.7 vs 4.5 +/- 1.6, p < 0.01. However, it did not differ at the PW; 2.6 +/- 0.9 vs 3.0 +/- 0.9 between the 3 groups. The middle VS and apex, where the wall was the thickest, had the lowest rMFR in ASH and AAH. Furthermore, at the VS and apex, a curvilinear relationship was observed between the rMFR and wall thickness (rMFR = -0.88 in WT + 2.39, r = -0.57, p < 0.02).(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:[Regional myocardial coronary blood flow reserve in hypertrophic cardiomyopathy assessed by digital subtraction coronary angiography]. 130 57

The characteristic of myocardial damage in hypertrophic cardiomyopathy (HCM) was evaluated as to whether the damage is limited to the hypertrophied wall or extends throughout the entire wall. The myocardial damage was detected by exercise thallium-201 (Tl-201) scintigraphy and was evaluated using circumferential profile analysis, calculation of initial uptake and washout rate. Eleven patients with asymmetrical hypertrophy (ASH), whose septal and posterior wall thickness ratio exceeded 1.3 on left ventriculography and biventriculography, and 13 age-matched control subjects without heart disease were studied. The mean values of initial uptake in both groups did not differ significantly, but the washout rate for the entire heart was significantly decreased only in the HCM group (p < 0.05). All of the regional washout rates (antero-septal, apical and postero-lateral) were significantly decreased in the HCM group (p < 0.05), without any difference between the hypertrophied wall and the non-thickened free wall being noted. These results demonstrated that the analysis of myocardial damage by exercise Tl-201 scintigraphy using calculation of the washout rate is a very sensitive means of detecting myocardial damage in HCM, and that such myocardial damage is not restricted to the hypertrophied wall, but rather extends to the entire wall, including the free wall which is not thickened.
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PMID:[Distribution of myocardial damage in patients with hypertrophic cardiomyopathy: evaluation by exercise thallium-201 scintigraphy]. 134 29

Radioimmunoassay was used to measure thyroid, somatotropic, parathyroid hormones and cyclic nucleotides in 40 patients with hypertrophic cardiomyopathy and 14 with hypertensive disease concurrent with asymmetrical myocardial hypertrophy. In the patients with hypertrophic cardiomyopathy, the mean blood concentration of thyroid, somatotropic, parathyroid hormones and cyclic nucleotides was generally within the normal ranges and similar to that in hypertensive patients with apparently healthy individuals. The patients with hypertrophic cardiomyopathy concurrent with supraventricular arrhythmias exhibited higher blood levels of total and free thyroxine and thyroxine/thyroxine-bound globulin ration than did patients without arrhythmias. The patients with hypertrophic cardiomyopathy concurrent with arrhythmias displayed increased blood levels of cyclic nucleotides. The findings suggest that thyroid hormones and cyclic nucleotides are likely to make contribution to the pathogenesis of arrhythmias in hypertrophic cardiomyopathy.
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PMID:[Hormonal aspects of the pathogenesis of cardiac arrhythmias in patients with hypertrophic cardiomyopathy]. 140 73

We report a study, assessing involvement of the heart in 33 familial cases of Becker muscular dystrophy (BMD), 31 familiar cases of facioscapulohumeral (FSH) dystrophy, and 27 familial cases of Bethlem myopathy. In the patients with BMD, correlations of myocardial involvement with age and extent of musculoskeletal involvement were made. We performed physical examination, chest x-ray, electrocardiographic (EKG), and echocardiographic examination on all patients, and continuous EKG Holter-monitoring in the patients with FSH dystrophy. Thirteen patients with BMD (45%) showed EKG changes similar to those found in Duchenne muscular dystrophy. Only 1 of the 13 individuals with cardiac involvement was wheelchair-bound. We found no evidence of cardiac changes in the patients with FSH dystrophy. In Bethlem myopathy, only 1 patient had a form of hypertrophic cardiomyopathy (asymmetrical septal hypertrophy).
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PMID:The heart in Becker muscular dystrophy, facioscapulohumeral dystrophy, and Bethlem myopathy. 158 51


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