Gene/Protein Disease Symptom Drug Enzyme Compound
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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Equatorial and longitudinal left ventricular wall stress were calculated at end-diastole in a group of 66 patients in sinus rhythm. Thirty-one patients had volume overload of the left ventricle: six with acute and 21 with chronic aortic incompetence, and four with chronic mitral incompetence. Another six patients had aortic stenosis and 25 had congestive cardiomyopathy. Four patients served as controls. Stress was calculated using a thick-walled ellipsoid model. In patients with volume overload and congestive cardiomyopathy, ventricular dilatation was accompanied by an appropriate increase in wall thickness so that the "stress conversion factor" (the factor relating pressure to stress) was normal and absolute stress depended on end-diastolic pressure. In pressure overload of the left ventricle (aortic stenosis), the increase in wall mass reduced the stress conversion factor so that aboslute fiber stress was normal. These data support the hypothesis that muscle fiber stress may be an important determinant of left ventricular hypertrophy.
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PMID:Cardiac hypertrophy and left ventricular end-diastolic stress. 12 13

The echocardiograms of two patients with sclerodermatous cardiac disease are described. In one patient the pattern was that of a congestive cardiomyopathy with ventricular dilatation and reduced wall motion. In the second patient the pattern was that of an infiltrative cardiomyopathy with thickened walls and reduced wall motion in the absence of ventricular dilatation. Echocardiographic studies are useful in the early detection of pericardial involvement and primary or secondary myocardial involvement by scleroderma and in following the progression of the disease process.
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PMID:Echocardiographic patterns in scleroderma. 13 3

Five uraemic patients who developed progressive cardiac failure with clinical evidence of congestive cardiomyopathy at the start or during haemodialysis treatment were studied. The diagnosis of cardiomyopathy, for which there was no apparent cause, was confirmed by angiocardiographic and haemodynamic studies. These showed a significant increase in left ventricular end-diastolic volume over normal values obtained in 12 patients without uraemia. The mean velocity of myocardial fibre shortening was significantly decreased, as was the index of normalised rigidity. Three of the five patients presented the complete picture of the disease. The other two also had considerable ventricular dilatation and a decreased index of normalised rigidity but normal ejection fraction and only moderately decreased myocardial contractility indices. This suggests that there may be primary involvement of normalised heart muscle rigidity followed by secondary changes in myocardial contractility in uraemic patients with congestive cardiomyopathy.
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PMID:Congestive cardiomyopathy in uraemic patients on long term haemodialysis. 13 69

Echocardiography was used to compare the left ventricular function in 35 cases of congestive cardiomyopathy (COCM), 16 cases of obstructive and 28 cases of non-obstructive asymmetric septal hypertrophy, 43 cases of scleroderma heart disease, 21 cases of ischaemic cardiomyopathy (ICM), 2 cases of restrictive cardiomyopathy, and one case of cardiac amyloidosis. COCM was characterized by left ventricular dilatation, decreased contractility and signs of elevated end-diastolic pressure. In asymmetric septal hypertrophy there was a decreased distensibility of the obstructed left ventricle, both in early and end-diastole, but the pump function remained normal. In scleroderma and amyloid heart disease both the contractility and distensibility of the small, stiff heart were reduced. In restrictive cardiomyopathy the only abnormality was the impaired end-diastolic distensibility. Reduced contractility confined primarily to the interventricular septum and impaired early diastolic distensibility are the characteristic features distinguishing ischaemic cardiomyopathy from COCM. However, echocardiography is not suitable for individual differentiation of ICM and COCM. The COCM can be differentiated from left ventricular aneurysm by M-mode sector scanning technique.
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PMID:Functional differentiation of various types of cardiomyopathies by echocardiography. 15 92

Cross-sectional echocardiography identified two abnormal patterns of mitral valve closure in 14 patients with mitral regurgitation due to papillary muscle dysfunction: (1) in three patients with an akinetic inferior-posterior wall but normal cavity size, papillary muscle fibrosis was associated with late systolic mitral valve prolapse, and (2) in nine patients with ventricular dilatation or ventricular aneurysm, the point of mitral valve coaptation was displaced towards the apex of the left ventricle. In two of these patients both abnormalities were observed. In contrast, abnormal patterns were identified in only four of a group of 40 patients without angiographic evidence of mitral regurgitation (10, normal; 27, coronary artery disease; three, congestive cardiomyopathy). Thus, cross-sectional echocardiography can be useful to identify mitral regurgitation secondary to papillary muscle dysfunction.
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PMID:Cross-sectional echocardiographic spectrum of papillary muscle dysfunction. 42 70

Thirty-four cats with primary myocardial disease were studied. The cats were divided into two groups, depending on the clinical, hemodynamic, angiocardiographic, and pathologic findings. Group A consisted of those cats with hypertrophic cardiomyopathy and Group B consisted of those cats with congestive cardiomyopathy. Similarity in the characteristics of cardiomyopathy in the human cat was found. Both Group A and Group B consisted predominantly of mature adult male cats. The most common presenting signs were dyspnea and/or thromboembolism, systolic murmurs with gallop rhythms on auscultation, cardiomegaly with (Group A) or without (Group B) pulmonary edema, abnormal electrocardiograms, elevated left ventricular end diastolic pressures, and angiocardiographic evidence of mitral regurgitation with left ventricular concentric hypertrophy (Group A) or left ventricular dilatation (Group B). Some cats in Group A also had evidence of left ventricular outflow obstruction. The principal pathologic findings in these cats were left atrial dilatation, symmetric hypertrophy or asymmetric septal hypertrophy of the left ventricle (Group A), and dilatation of the four cardiac chambers (Group B). Aortic thromboembolism was commonly observed in both groups. These clinical and pathologic findings indicate that cardiomyopathy in the cat is similar to the two most common forms of cardiomyopathy in the human (hypertrophic cardiomyopathy, with and without obstruction, and congestive cardiomyopathy).
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PMID:Primary myocardial disease in the cat. A model for human cardiomyopathy. 84 11

The aim of the study was to analyze the relationship between the magnitude of left ventricular (LV) hypertrophy and selected haemodynamic parameters reflecting LV systolic and diastolic function. The "hypertrophy-function" relationship was evaluated in 22 patients with dilated cardiomyopathy (DCM) and in patients with left ventricular dilatation resulting from volume overload due to valve disease (DVOL). The parametres of systolic and diastolic left ventricular function were obtained from right- and left-heart catheterization and quantitative angiocardiography, DCM patients were divided into subgroups depending on the magnitude of hypertrophy and degree of dilatation: Ia- moderate hypertrophy (100 g/m2 < LVMI < 175 g/m2). Ib- massive hypertrophy (LVMI > 175 g/m2); IIa- mass/volume ratio (M/V) < 1.1, and IIb - M/V > 1.1. It was found that the magnitude of myocardial hypertrophy and the M/V ratio do not affect the degree of systolic and diastolic dysfunction in patients with DCM. Myocardial hypertrophy accompanying dilatation due to DCM and DVOL showed very similar progression of impairment of isovolumetric systole and relaxation. Significant differences in EF, LVMDP and LVEDP may result from a different degree of total LV volume stiffness as a consequence of various mechanisms of hypertrophy in DCM and DVOL.
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PMID:The magnitude of left ventricular myocardial hypertrophy related to the degree of its dysfunction in patients with dilated cardiomyopathy (DCM). 130 17

Incessant, rapid, supraventricular tachycardia may be complicated by cardiac failure with ventricular dilatation and hypokinetic wall motion on echocardiography: so-called tachycardia-induced cardiomyopathy. The diagnosis is simple when the cardiac rhythm is not sinus rhythm. The authors report the cases of 4 children aged 7 months to 12 years, referred for diagnosis and treatment of apparently primary cardiomyopathy. The findings of spontaneous or vagally-induced atrioventricular conduction defects, a permanently rapid atrial rhythm though influenced by 24 hour variations, or periodic abnormal rate increases, suggested myocardial dysfunction due to an ectopic atrial tachycardia. This was an essential step in management as the control of the tachycardia by amiodarone or betablocker therapy resulted in regression of symptoms and normalisation of left ventricular function. However, some atrial tachycardias are very resistant to medical treatment and, in such cases, there should be no hesitation in using more radical approaches, surgery or ablation, even and especially in patients with severe cardiac failure. In conclusion, apparently primary dilated cardiomyopathy in children may be due to chronic atrial arrhythmia and it is essential to perform at least Holter monitoring in order not to miss this diagnosis.
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PMID:[Rhythmogenic cardiomyopathies of atrial origin in children. Myth or reality?]. 135 26

Deletions and point mutations of mitochondrial DNA (mtDNA) of patients with dilated or hypertrophic cardiomyopathy were analyzed using the polymerase chain reaction and fluorescence-based direct sequencing. The patients included are with hypertrophic cardiomyopathy associated with left ventricular dilatation, a patient with mitochondrial myopathy, encephalopathy, lactic acidosis, and stroke-like episodes (MELAS), and a patient with fatal infantile cardiomyopathy. Deletions were frequently seen in mtDNA in patients with dilated cardiomyopathy. The mtDNA was sequenced and the direct repeat at each edge of deletion was identified as (5'-CATCAACAACCG-3') which was located in the ATPase6 gene and in the D-loop region. In a patient with hypertrophic cardiomyopathy associated with left ventricular dilatation, another mutant mtDNA was found not to have directly repeated sequence, and was revealed to jump from nucleotide position 8,992 to position 16,072 of mtDNA resulting in a 7,079 bp deletion. This patient had unique point mutation in the tRNA genes. A G-to-A transition in the tRNA(Cys) gene (nucleotide position 5,821) at the aminoacyl acceptor stem and an A-to-G transition in the tRNA(Thr) gene (nucleotide position 15,951) were identified. In a patient with MELAS, an A-to-G transition in the tRNA(Leu)(UUR) gene (nucleotide position 3,243) was observed. This mutation was located at the 5' end of the dihydrouridine loop of this tRNA molecule, and would disturb its function. In a patient with hypertrophic cardiomyopathy associated with lactic acidosis, mutations of mtDNA should be suspected.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Mitochondrial DNA mutations in cardiomyopathy. 143 21

We describe a simple, non-invasive and practical method to determine the peak velocity of tricuspid regurgitant flow (and hence derive systolic pulmonary artery pressure) from examination of the dynamics of retrograde tricuspid flow on Doppler. Based on a previously described relationship between right ventricular systolic pressure and the time interval between pulmonary valve closure and tricuspid valve opening, our technique does not require the peak tricuspid regurgitant velocity to be recorded; nor, as in previous studies does it rely upon recording the jugular venous pulse, right ventricular apexcardiogram or invasive pressure measurements. We have studied 65 patients with right ventricular disease (53 with pulmonary hypertension), and 24 with dilated cardiomyopathy, with M-mode, two-dimensional echocardiography, Doppler, and phonocardiography. The peak tricuspid regurgitant velocity could be predicted from the interval between pulmonary closure and the end of the tricuspid regurgitant signal on Doppler in patients with pulmonary hypertension and those with right ventricular disease with normal pulmonary artery pressure, but not in patients with dilated cardiomyopathy. In patients with pulmonary hypertension or right ventricular dilatation, this may be a useful alternative method in estimating pulmonary artery pressure from Doppler, in cases where it is not possible to record the peak tricuspid regurgitant velocity.
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PMID:Assessment of the peak tricuspid regurgitant velocity from the dynamics of retrograde flow. 156 51


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