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Query: UMLS:C0264733 (ventricular dilatation)
 2,163 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

The case of a girl who presented with gastrointestinal upsets with nausea, vomiting and occasional hypoglycaemic attacks during childhood is reported. At about 5 years of age generalised muscular weakness with severe amyotrophy, cardiomegaly with a cardiothoracic ratio of 0,63, left ventricular hypertrophy on electrocardiography and left ventricular dilatation with hypokinesis on echocardiography were observed. A few weeks later she developed severe cardiac failure. Muscle biopsy showed muscular dystrophy with lipid infiltration due to carnitine deficiency )serum carnitine 9 nmoles/ml, normal values: 46 +/- 6,9 nmoles/ml; muscle carnitine 0,27 nmoles/mg, normal values: 3,0 +/- 0,79 nmoles/mg fresh frozen weight). She improved rapidly with carnitine chlorhydrate and a diet low in lipids and high in medium chain triglycerides. Regression of muscular symptoms and cardiac failure was observed. After 13 months follow-up with no tonicardiac therapy she is much improved; the signs of heart failure have disappeared, the cardiothoracic ratio is now 0,55 and the electrocardiogramme and echocardiogramme are normal.
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PMID:[Lipidic myopathy with severe cardiomyopathy caused by a generalized carnitine deficiency. Favourable course during carnitine hydrochloride treatment]. 11 7

In forty-one patients with various heart diseases including 29 with LVH, the vectorcardiograms of Frank system and angiocardiographic findings correlated minutely. Based on the left ventricular wall thickness in end-diastole, left ventricular end-diastolic volume, and the length of the long axis of the left ventricle obtained in angiocardiograms, typical left ventricular hypertrophy was classified into types 1a, 1b, 2a, 2b anatomically. The vectorcardiograms in these 4 types represented different patterns with regard to the QRS and T loops respectively. The QRS voltage in the left ventricular hypertrophy closely correlated to the left ventricular wall thickness in end-diastole, the left ventricular end-diastolic volume, and the left ventricular mass. Marked ST and T changes in the left ventricular concentric hypertrophy characterized by increase in wall thickness without definite chamber enlargement may be closely related to the abnormal muscle state with the increased left ventricular wall thickness, the probably due to relative hypoxia in origin. The Q loop of patients with severe left ventricular concentric hypertrophy was definitely differentiated from that of most patients with the pure left ventricular eccentric hypertrophy which was characterized by chamber enlargement with usually slight thickening of the wall. A possible mechanism regarding inconspicuous or prominent Q loops in both concentric and eccentric LVH was presented. An important factor of the delay of the time of occurrence of the spatial R vector in the left ventricular eccentric hypertrophy is the greater distance of the intraventricular conducting pathways caused by the left ventricular dilatation. By means of assessing the vectorcardiogram of the left ventricular hypertrophy, relatively exact anatomy of the left ventricular hypertrophy can be determined.
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PMID:Vectorcardiographic findings in concentric and eccentric left ventricular hypertrophy as determined by angiocardiograms. 1. Preliminary report. 12 81

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

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

Echocardiograms (ECHO) and Frank vectorcardiograms (VCGs) were obtained in three groups of patients: Group I (n = 16), concentric left ventricular hypertrophy (LVH) with increased interventricular septal (IVS) and left ventricular posterior wall (LVPW) thickness in the presence of a normal left ventricular internal dimension (LVID); Group II (n = 17), left ventricular dilatation (LVD) with an enlarged LVID, normal IVS and LVPW thickness, and Group III (n = 22), no catheterization evidence of heart disease with normal IVS, LVPW and LVID. VCGs were analyzed with respect to magnitude of the QRS maximal deflection vector (MDV) and +/- 10 msec QRS vectors, horizontal plane (HP) maximal posterior force, time of HP MDV inscription, distal and proximal HP loop areas and HP loop configuration utlizing criteria of Varriale et al. The results indicate that: 1) HP QRS vector magnitude cannot reliably differentiate concentric LVH from isolated LVD and 2) proximal-distal loop area relationships and pattern of the HP QRS loop, when reviewed together, are superior to other criteria for distinguishing whether ECHO determined LVH or LVD is the primary correlate of an enlarged left ventricle.
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PMID:Hypertrophy or dilatation? A vectorial analysis of echocardiographically determined left ventricular enlargement. 14 78

Diastolic wall stress and compliance were determined in 74 patients with essential hypertension during diagnostic cardiac catheterization. Ventricular compliance was normal in compensated essential hypertension without coronary artery disease even at severe left ventricular hypertrophy. In contrast, additional coronary stenosis and ventricular dilatation due to cardiac decompensation was asscociated with considerable decrease in ventricular compliance. Thus, left ventricular hypertrophy in essential hypertension does not imply per se a change in ventricular compliance. A decrease in ventricular compliance was followed by a decrease of forward pump function of the left ventricle. whereas ventricular work index (as estimated as the product out of systolic wall stress and the stroke volume) increased. This disproportion between external and internal ventricular work increased with increasing ventricular dilatation and was greatest in decompensated essential hypertension. Accordingly, decompensated essential hypertension had largest ventricular work load and lowest forward pump function in comparison to all other patient groups with essential hypertension. The mass to volume ratio may be considered an important determinant of the degree of left ventricular hypertrophy in essential hypertension. The relationship between the mass to volume ratio and the systolic wall stress may provide a diagnostic and prognostic evaluation of the left ventricle in essential hypertension on the basis of dynamic ventricular geometry.
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PMID:[The heart in hypertension. III. Determinants of left ventricular hypertrophy and diastolic left ventricular compliance (author's transl)]. 15 7

To evaluate possible differences in the cardiac effects of different types of running training, 22 competing male runners--10 sprinters and 12 endurance runners--were studied with a physical examination, electrocardiography, chest X-ray film and echocardiography. Thirteen sedentary men served as control subjects. There were no differences between the athletic groups in physical findings. However, left ventricular hypertrophy in the electrocardiogram was more apparent in the endurance runners (P less than 0.05), whose relative heart size on chest X-ray examination was also greater than in the sprinters (P less than 0.02). On echocardiography the left ventricular end-diastolic volume was equally greater than normal in both groups of athletes (P less than 0.005), but in the endurance runners the percent chance of the minor axis diameter in systole was greater than in the sprinters or control subjects (P less than 0.02). Values for left ventricular wall thickness and mass were greater than normal in both groups of athletes but were higher in the endurance runners than in the sprinters (P less than 0.001). The left atrial diameter was apparently greater in the endurance runners than in the sprinters or control subjects (P less than 0.001), whereas that of the sprinters did not differ from normal. Thus, intensive sprinter training seems to dilate the left ventricle but causes less increase in wall thickness and mass than training for endurance running and no change in left ventricular function or left atrial size. Endurance running causes left ventricular dilatation equal to that of sprinter training, greater wall hypertrophy and improved systolic emptying of the left ventricle, and it also dilates the left atrium perhaps because of decreased left ventricular compliance.
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PMID:Noninvasive evaluation of the athletic heart: sprinters versus endurance runners. 15 93

The basic criteria for the vectorcardiographic diagnosis of right ventricular enlargement are discussed, in context with the course of myocardial activation. Right ventricular dilatation, secondary to isolated diastolic overloading (atrial septal defect) shows basically different degrees of dextrorotation. The ventricular curve starts to the left on the frontal and horizontal planes, and forward on the last one. Cases with right ventricular hypertrophy, produced by sustained systolic overload, are also evaluated. When the hypertrophy is generalized (pulmonary valvular stenosis), there is an increase in the manifestation of all the resulting vectors of activation of this ventricle: IIs, IIr, and IIIr. As a resultant of these changes, the ventricular curve presents a clockwise rotation in the three planes, and is oriented to the right and forward, with its terminal portions generally located above the E point. When the right ventricular hypertrophy is of the segmentary type, there is an increase of the manifestation of only some of the resulting vectors of the activation of this ventricle. For example, the vector IIr will be increased in cases of tetralogy of Fallot, while the IIIr will be increased in some cases of obstructive chronic pulmonary hypertensive cardiopathy. The T loop, of secondary type, generally opposes the vector IIr on the horizontal plane, and the IIIr on the frontal plane. When an important right ventricular dilatation is associated to a right bundle branch block of intermediate degree, owing to their proximity, the manifestation of the electromotive parietal forces is increased at the expense of the septal ones. This phenomenon produces a characteristic appearance of the SH loop, narrow and with a clockwise rotation.
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PMID:[Vectorcardiographic manifestations of right ventricular enlargement]. 16 77

The basic criteria for the vectorcardiographic diagnosis of left ventricular and biventricular enlargements are discussed on the basis of the myocardial activation sequence. Left ventricular dilatation, secondary to isolated diastolic overloading, increases the manifestation of all the vectors resulting of the activation of this ventricle. These changes reflect the proximity of the left ventricular walls to the exploring electrodes. The vectors above mentioned project themselves as wide ventricular curves with counterclockwise rotation on the three planes. The T loop, of secondary type, is concordant in its orientation with the R loop. Cases with left ventricular hypertrophy, produced by a sustained systolic overloading, are also described. In the presence of global left ventricular hypertrophy without LBBB, the manifestation of all the vectors resulting from the depolarization of this ventricle (I, IIl, IIIl), is increased. This is due to a prolonged duration of the corresponding activation fronts. These vectors are projected on the different segments of the ventricular curves and they show a counterclockwise rotation on the three planes. When LBBB is also present, the first septal vector is not evident. The T loop, of secondary type, opposes the R loop on the frontal and horizontal planes. The presence of left ventricular hypertrophy of the segmentary type, generally increases the manifestation of the vector I, and sometimes, also that of the vector IIIl. When both ventricles are hypertrophied, the electromotive forces of the chamber more severely affected predominate in the vectorcardiographic records.
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PMID:[Vectorcardiographic manifestations of left ventricular and biventricular enlargement]. 16 78

The impact of aging on pulmonary hemodynamics was investigated in 322 patients who underwent right- and left-sided cardiac catheterization and echocardiographic examination, and were free of coronary disease, impaired left ventricular systolic function and left ventricular dilatation. Most of the patients were black (83%) and hypertensive (78%). Mean pulmonary artery pressures increased progressively with age: 16.7 +/- 4.6, 17.9 +/- 6.4 and 20.6 +/- 8.0 mm Hg for those aged less than 45 (n = 50), 45 to 64 (n = 238) and greater than or equal to 65 years (n = 34), respectively (p = 0.020). Pulmonary vascular resistance was 99 +/- 42, 116 +/- 62 and 160 +/- 68 dynes s cm-5, and the ratio of pulmonary to systemic vascular resistance was 78, 80 and 105%, respectively, for the 3 age groups (p less than 0.001). Along with these changes, a decrease in cardiac output and an increase in systolic blood pressure and systemic vascular resistance with age were noted. The effect of age on mean pulmonary artery pressure and pulmonary vascular resistance was statistically significant after adjustment for gender, smoking status, body weight, left ventricular hypertrophy, systolic blood pressure and systemic vascular resistance. Consideration should be given to age-related changes in the pulmonary circulation when defining physiologically normal values.
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PMID:Changes in pulmonary hemodynamics with aging in a predominantly hypertensive population. 163 5


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