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Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

In order to study factors influencing posterior wall thickness during diastole, echocardiograms showing the septum, mitral valve and posterior wall endocardium and epicardium in 15 normal subjects and 49 patients with heart disease were digitized. Maximum wall thickness, minimum cavity dimension and the onset of mitral valve opening are normally synchronous, and an early period of rapid wall thinning, at a peak rate of 10.7 +/- 1.7 cm/sec corresponds closely to rapid filling. In patients with ischaemic heart disease the peak rate and duration of rapid thinning were normal, but thinning preceded mitral valve opening (mean 50 msec). In 11 of 17 patients with hypertrophic cardiomyopathy the peak rate of thinning was reduced and in 2 it was increased. There was a close correlation between the peak thinning rate in this group and the peak rate of increase in dimension. In mitral stenosis peak thinning rate was frequently reduced but in some patients was normal, with the reduced rate of increase in cavity dimension maintained by reversal of septal movement. We conclude that rapid thinning is an intrinsic property of the ventricular wall which is normally associated with rapid filling, but which may be dissociated from filling by asynchronous relaxation or inflow obstruction, or may be modified by myocardial disease.
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PMID:Diastolic changes in left ventricular wall thickness studied by echocardiography. 41 5

Computer analysis of the M-mode echocardiogram in 50 normal newborns provided measurements of wall thicknesses and chamber size and, in addition, assessment of right and left ventricular wall, septal, and cavity dynamics throughout the cardiac cycle. Data obtained with this new technique indicated that (1) right and left ventricular cavity functions are similar in the normal newborn, (2) right and left ventricular cavity filling and emptying vary directly with peak rates of septal and ventricular wall thinning and thickening, respectively, and (3) there is a close time relationship among maximum left atrial dimension, minimum left ventricular dimension, and mitral valve opening. This analysis, which is the first complete analysis of the echocardiogram in the newborn, provides a normal range of septal and ventricular wall dynamics as well as right and left ventricular and left atrial function and has clinical implications in that it may allow early recognition of both congenital and perinatal myocardial disease.
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PMID:Cardiac function in the normal newborn: additional information by computer analysis of the M-mode echocardiogram. 63 44

Seven inbred mouse strains were examined for the presence of chronic Chagas' cardiomyopathy in postacute Trypanosoma cruzi infection. DBA/1, DBA/2, BALB/c, B10.T (6R), B10.Q, B10.D2, and B6 mice were infected for 100 days with the Brazil strain of T. cruzi. Standard histologic examination of cardiac tissue from these mice revealed the following relationship among the different strains based on the severity of observed inflammation (myocarditis): BALB/c, DBA/1, and DBA/2 were the most inflamed; B10.T (6R) and B10.Q were intermediate; and B6 and B10.D2 showed the least inflammation. Examination of these tissues for characteristics of myocardiopathy such as cell swelling, edema, vacuolization, necrosis, myocytolysis, connective tissue infiltration, and thinning of the right ventricular wall indicated a relative relationship among the different strains relative to the severity of cardiomyopathy as follows: BALB/c, DBA/2, and DBA/1 showed the most cardiopathy (pathopermissive); B10.T (6R) and B10.Q showed intermediate pathology; and B6 and B10.D2 showed the least involvement (pathoresistant). Anti-heart antibody present in the sera of all these mice showed specific reactivity in western blots to a 43-kDa glycoprotein from normal heart tissue. Also, anti-heart antibody enzyme-linked immunosorbent assay titers for all mouse strains were similar and showed no correlation with the severity of tissue damage. The fact that different inbred strains show various degrees of myocarditis and cardiomyopathy may be useful in the study of pathogenesis of chronic Chagas' disease. Results from this limited list of inbred strains suggest that background genes, rather than the major histocompatibility complex, play the major role in the expression of cardiac pathogenesis.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Differential cardiac histopathology in inbred mouse strains chronically infected with Trypanosoma cruzi. 149 Dec 99

Four cases of hypertrophic obstructive cardiomyopathy diagnosed on clinical, phonomechanographic, echocardiographic and haemodynamic criteria progressing to dilated cardiomyopathy are reported. This evolution was observed over a number of years (up to 20 years) and was accompanied by a clinical aggravation in all cases with 2 deaths and atrial fibrillation in 3 of the 4 cases. The signs of intraventricular obstruction [systolic murmur, bulge on the carotid pulse tracing, systolic anterior motion of the mitral valve (SAM) and intraventricular pressure gradient] disappeared as the left heart chambers dilated with a reduction in ventricular wall motion and parietal thinning but no change in myocardial mass.
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PMID:[Progression from hypertrophic obstructive cardiomyopathy to dilated cardiomyopathy. Apropos of 4 cases]. 211 75

We report a case of sudden death from hemopericardium consequent to spontaneous rupture of the right ventricle in a 49-year-old chronic chagasic woman. To our knowledge, this is the third reported case of spontaneous cardiac rupture with chagasic cardiomyopathy. In our case we believe that the thinning of the anterior right ventricular wall, its large ray curvature and the increased ventricular pressure were factors favoring the rupture. There was no infarction and the chronic cardiopathy was significant. It caused the thinning of the rupture region through chronic myocarditis.
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PMID:[Sudden death caused by the spontaneous rupture of the right ventricle in a woman with chronic Chagas disease]. 213 89

Isoproterenol treatment leads to endomyocardial fibrosis with muscle fibers encircled by fibrillar collagen. This study was undertaken in the rat to determine if muscle encased in collagen would subsequently become either necrotic or atrophic. For this purpose, we monitored the fibrillar nature of myocardial collagen, its alignment with muscle, and the morphology of the endomyocardium, together with the response in diastolic and systolic myocardial stiffness, immediately on completion (10 days) and 30 days after a course of subcutaneous isoproterenol (500 micrograms/kg/day). We found 1) left ventricular hypertrophy at 10 and 30 days with an increase in collagen volume fraction (p less than 0.01) that consisted of a meshwork of thick and thin collagen fibers that encircled endomyocardial muscle, 2) a variable reduction in endocardial muscle fiber diameter at 30 days with the greatest thinning seen in muscle encircled by fibrous tissue, and 3) an elevation (p less than 0.01) in the slope of the diastolic stress-strain relation at 10 and 30 days. The developed systolic stress-strain relation, which was elevated at 10 days (p less than 0.01), declined (p less than 0.05) with the reduction in endomyocardial muscle mass. Thus, endomyocardial muscle, encircled by fibrillar collagen, will atrophy over time, and this leads to a reduction in active stiffness. These findings may, in part, explain why progressive ventricular dysfunction accompanies chronic myocardial disease with endomyocardial fibrosis.
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PMID:Fibrosis-induced reduction of endomyocardium in the rat after isoproterenol treatment. 252 93

Gated magnetic resonance imaging (MRI) provides excellent anatomic evaluation of the heart, but its capability for assessing cardiac physiology is less clear. Accordingly, regional left ventricular (LV) wall thickening was evaluated by multiphasic transverse images in 37 patients with a variety of myocardial diseases and in 9 normal subjects. Angiography and 2-dimensional echocardiography (2-D echo) were used for comparison. End-diastolic and end-systolic wall thickness, absolute systolic wall thickening and percent systolic wall thickening were determined in 7 regions. Mean systolic wall thickening in normal subjects was not significantly different among the regions. However, there was considerable individual variation in wall thickening, ranging from 18 to 100%. Patients with LV hypertrophy (n = 4), amyloid cardiomyopathy (n = 1), constrictive pericarditis (n = 5), and hypertrophic cardiomyopathy (n = 3) had absolute and percent systolic wall thickening within normal limits. Infarcted segments in patients with ischemic heart disease (n = 17) had reduced absolute and percent systolic wall thickening, often combined with diastolic wall thinning, whereas mean percent systolic wall thickening in adjacent normal myocardial regions was higher than in normal volunteers (p less than 0.001). In patients with coronary artery disease, MRI had a sensitivity and specificity of 93% in detecting regional wall motion abnormalities. Because sagittal images were not acquired, inferior wall motion abnormalities were not assessed by MRI due to parallel wall sectioning in transverse images.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Regional left ventricular wall thickening by magnetic resonance imaging: evaluation in normal persons and patients with global and regional dysfunction. 294 75

Right ventricular arrhythmogenic dysplasia is a rare cardiomyopathy which involves the right ventricle either totally or partially. Up to now diagnoses have been based on Ecg, hemodynamics, angiography and echocardiography. This paper deals with the first 7 patients examined also by means of Computed Tomography. The CT picture is well defined and rather accurate. The most important elements are: total (6/7) or partial (1/7) enlargement of the right ventricle; thinning of right ventricular myocardium (6/7); marked increase in subepicardial fat limited to the right ventricular wall (7/7); right ventricle hypokinesia (7/7). A good correlation exists between CT, echographic and traditional methodologies findings. Because of its densitometric evaluation, CT is much more precise in the demonstration of fatty degeneration. Moreover, it can be very useful in differentiating intracardiac thrombi from hypertrophic papillary muscles and trabeculae.
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PMID:[Arrhythmogenic dysplasia of the right ventricle. Evaluation of 7 cases using computerized tomography]. 296 79

A 20-year-old woman whose echocardiograms showed a rare evolution from hypertrophic to dilated cardiomyopathy during a nine year observation period is described. This patient was initially diagnosed as having hypertrophic obstructive cardiomyopathy (HOCM) at the age of 12 years. Her echocardiogram showed marked thickening of the interventricular septum (IVS) and left ventricular posterior wall (LVPW), asymmetric septal hypertrophy (ASH) and systolic anterior motion of the mitral valve (SAM). Chest radiography revealed a prominent left ventricular border and a cardiothoracic ratio of 0.52. At 18 years of age she experienced onset of palpitation during the 16th week of pregnancy. Her echocardiogram recorded in June 1980 revealed a thickened IVS and LVPW with resolution of the SAM and of the narrow cavity. At 20 years of age she became pregnant again and was admitted to our hospital for the third time at 24 weeks gestation. On admission her blood pressure was 122/60 and her pulse was 56, and moist rales were audible over both lung fields. Peripheral edema was noted. Chest radiography revealed moderate cardiomegaly, a cardiothoracic ratio of 0.66, and congestion of the pulmonary vasculature. An echocardiogram showed thinning of the IVS and LVPW with hypokinesis and dilatation of the cavity compatible with dilated cardiomyopathy (DCM). She delivered a boy on July 15th 1982 at 32 weeks gestation following which she developed marked congestive heart failure. She expired one month later. A chest radiograph made one day before death revealed marked cardiomegaly, a cardiothoracic ratio of 0.76, prominent pulmonary vasculature and a pleural effusion. Autopsy was refused; therefore the terminal DCM-like features were not clarified pathologically. However, the slow progression from HOCM to HCM during eight years and then rapid progression from HCM to DCM during four months was most impressive.
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PMID:[Evolution of dilated cardiomyopathy from hypertrophic obstructive cardiomyopathy: a case report]. 344 76

From January 1982 through December 1985, 11 newborn artiodactyls died with clinical and/or pathologic evidence of cardiomyopathy. Clinical signs were inability to rise, depression, failure to nurse, hypothermia, and shivering. Macroscopically, the animals had mild to marked dilatation and thinning of the interventricular septum and left ventricular free wall. Histologic findings included thinning and waviness of myofibers and acute myodegeneration and myocytolysis.
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PMID:Congestive cardiomyopathy in neonatal artiodactyls. 350 27


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