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

Ten patients with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who had severe symptoms of cardiac failure are described. During a mean follow-up period of 7 years, 6 of these 10 patients showed a substantial increase in left ventricular internal dimension (6 to 15 mm, mean 10) as assessed with M-mode echocardiography, although absolute left ventricular cavity size remained within normal limits in 5 of the 6. Four patients demonstrated substantial septal thinning (5 to 14 mm, mean 8). Left ventricular diastolic function, assessed by radionuclide angiography in nine patients, was impaired in eight who showed decreased peak filling rate (less than 2.5 end-diastolic volumes/s) and prolonged time to peak rate of filling (greater than or equal to 180 ms). Furthermore, left ventricular systolic function, usually supernormal in patients with hypertrophic cardiomyopathy, was depressed (ejection fraction less than or equal to 45%) in six patients. Hence, a subset of patients was identified with nonobstructive hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy who experienced severe cardiac symptoms. The majority of these patients showed both systolic and diastolic left ventricular dysfunction in the presence of a progressive increase in left ventricular internal dimension (but without absolute left ventricular dilation) or ventricular septal thinning or both. Such patients may represent an important component of the natural history of hypertrophic cardiomyopathy which has not been previously fully appreciated.
J Am Coll Cardiol 1986 Sep
PMID:Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy. 294 85

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)
Am J Cardiol 1987 Jan 01
PMID:Regional left ventricular wall thickening by magnetic resonance imaging: evaluation in normal persons and patients with global and regional dysfunction. 294 75

Quantitative cineventriculographic measurements (ventricular volumes, ejection fraction, and myocardial mass) were obtained in 15 neonates with pulmonary atresia and intact ventricular septum. There was a wide dimensional range for the right ventricle, from a reduced through normal to enlarged. A restrictive tricuspid valve (less than 12 mm) was associated with a small or diminutive right ventricle. A normal function of the right ventricle was present only in those cases with normal-sized chambers. The left ventricular end-diastolic volume was always greater than normal. The ejection fraction was normal only if a normal myocardial mass was present. Additional abnormalities were frequent in the myocardium of both ventricles, such as extreme thinning of the wall of the right ventricle and hypoplasia or fibroelastosis of the left ventricle. All these factors can lead to a poor surgical prognosis despite good anatomical correction.
Pediatr Cardiol 1986
PMID:Pulmonary atresia with intact ventricular septum: a quantitative cineventriculographic study of the right and left ventricular function. 295 Mar 81

Development or progression of left ventricular hypertrophy has recently been described in children with hypertrophic cardiomyopathy. To determine whether similar changes in magnitude and distribution of left ventricular hypertrophy may also occur in adult patients with this disease, serial assessment of left ventricular wall thickness was obtained with M-mode and two-dimensional echocardiography in 65 patients with hypertrophic cardiomyopathy who were 23 to 50 years of age. The follow-up period was 3 to 6 years (mean 4). None of the 65 patients showed a substantial increase (greater than or equal to 5 mm) in left ventricular wall thickness; however, 9 (14%) demonstrated a substantial decrease (5 to 9 mm). Wall thinning most commonly involved the anterior ventricular septum (seven patients), but was also identified in the posterior septum (six patients), lateral free wall (two patients) and posterior free wall (one patient). In the nine patients with wall thinning, left ventricular end-diastolic diameter increased significantly (from 44 +/- 6 to 51 +/- 6 mm; p less than 0.001); however, in seven of the nine, absolute cavity size remained within normal limits (less than or equal to 52 mm) at the most recent evaluation. Eight of the nine patients with left ventricular wall thinning and relative cavity enlargement were severely symptomatic and one was mildly symptomatic. In conclusion, substantial progression of left ventricular hypertrophy was not identified in any of the study patients. Hence, if such progression occurs in adults with hypertrophic cardiomyopathy, it is probably rare. Conversely, an important minority of adult patients with hypertrophic cardiomyopathy may show progressive left ventricular wall thinning and relative cavity enlargement, which are usually associated with severe cardiac symptoms.
J Am Coll Cardiol 1987 May
PMID:Absence of progression of left ventricular hypertrophy in adult patients with hypertrophic cardiomyopathy. 295

After acute transmural myocardial infarction, the heart may undergo major remodeling characterized by thinning and dilation of the infarct zone and overall enlargement of the heart. The effect of increased left ventricular pressure on infarct expansion and the extent to which it alters postinfarction remodeling were studied in a rat model. Rats with either aortic banding or a sham operation and a survival period of 3 weeks were further randomized to sham thoracotomy or left coronary ligation. Surviving rats were killed 7 days later and the hearts were fixed in diastole for morphologic analysis. Hearts with aortic banding had a mean peak to peak gradient of 20.7 +/- 4.9 mm Hg across the aortic band at death and a significantly thicker heart than that of the comparison group without an aortic band. Infarct size, as a percent of total left ventricular mass, at the time of death was less in the group with aortic banding, yet infarct expansion was more marked. However, when original infarct size was estimated taking into account the effects of aortic banding, scar formation, infarct expansion and infarct-induced hypertrophy, it was found to be similar in both infarct groups (45.50 +/- 4.2 versus 47.90 +/- 3.1%). Infarct expansion, as measured by cavity dilation and infarct thinning, occurred in both infarct groups but was greater in the group with aortic banding.(ABSTRACT TRUNCATED AT 250 WORDS)
J Am Coll Cardiol 1988 Nov
PMID:Increased afterload aggravates infarct expansion after acute myocardial infarction. 297 4

We investigated the natural course of 59 patients with hypertrophic cardiomyopathy (HCM) in follow-up periods of one to 13 years and analyzed the clinical, hemodynamic and echocardiographic parameters to determine the factors influencing the prognosis. Among these patients, 44 (75%) remained stable in a compensated condition with or without medications. Five patients died suddenly and two died of congestive heart failure. Heart failure developed in another eight. At the initial evaluation, these 15 patients had high left ventricular end-diastolic pressure (mean: 22 +/- 8 mmHg) significantly higher than that of 44 compensated patients (mean: 13 +/- 6 mmHg, p less than 0.001). There were no differences in age at the initial evaluation between compensated and end stage groups. Atrial fibrillation occurred persistently in three and transiently in two among ten patients with heart failure during follow-up periods. Ventricular dimensions and systolic function did not statistically differ between the two groups. However, six patients with heart failure had cavity dilatation and deteriolated ventricular contractile function at the initial evaluation. Four of them did not show any change in left ventricular hypertrophy, but the regional thinning of the wall was observed in the remaining two. There were no characteristic features to predict sudden death in the clinical, hemodynamic or echocardiographic parameters. Thus, increased left ventricular end-diastolic pressure, atrial fibrillation, left ventricular dilatation and the regional thinning of the left ventricular wall are useful predictive markers for poor prognosis in HCM.
J Cardiol Suppl 1987
PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74

The potential of magnetic resonance imaging (MRI) to detect and localize acute myocardial infarction (AMI) in 27 patients a mean interval of 15 days after AMI was evaluated. Eighteen asymptomatic volunteers were also studied to determine the specificity of the observations. The diagnosis of AMI was established by conventional criteria; the infarct was localized by electrocardiography in all patients, technetium pyrophosphate scintigraphy in 19 and necropsy in 1 patient. MRI detected increased myocardial signal intensity in 88%, cavitary signal in 74% and regional wall thinning in 67% of the patients. At least 1 of these 3 features was seen in the area of the infarct in each patient. The sensitivity of these MRI observations was not influenced by location of the infarct or presence of Q waves. Asymptomatic volunteers also had increased myocardial signal in 83%, cavitary signal in 94% and wall thinning in 11% of cases. Some patients had these findings in myocardial segments not suspected of being involved by recent or remote AMI. It is concluded that AMI can be detected by MRI performed an average of 15 days after infarction. However, the hearts of normal volunteers and apparently normal myocardial segments of patients with AMI may have the MRI findings previously associated with AMI. Of these findings, wall thinning was the most predictive of and specific for AMI.
Am J Cardiol 1986 Aug 01
PMID:Detection and localization of recent myocardial infarction by magnetic resonance imaging. 301 85

Hypertrophic cardiomyopathy is a diverse clinical and pathophysiologic disorder of unknown cause that principally involves the left ventricle and is manifested as asymmetric or concentric hypertrophy. If asymmetric, the hypertrophy is usually greatest in the ventricular septum, but variations occur in which the hypertrophy may be maximal at the mid-ventricular level, at the apex, or rarely, in the free wall of the left ventricle. Right ventricular involvement is usually less evident. The principal abnormality in systole is the obstruction to left ventricular outflow caused by systolic anterior motion (SAM) of the anterior or posterior mitral leaflet(s) with mitral leaflet-septal contact. SAM occurs as the result of the Venturi forces created by the rapid ejection of blood through an outflow tract that is narrowed by upper septal hypertrophy, drawing the mitral leaflet(s) anteriorly. The time of onset and duration of mitral leaflet-septal contact determine the magnitude of the pressure gradient. Mitral regurgitation invariably accompanies the obstruction to outflow. Ventriculomyectomy surgery, by thinning the septum and widening the outflow tract, abolishes the abnormal mitral leaflet motion and, consequently, the obstruction to outflow and the mitral regurgitation. In symptomatic patients with resting obstruction this form of surgery more dramatically relieves the systolic abnormalities and the accompanying symptoms than any form of medical therapy currently available. The extent of hypertrophy is believed to be the principal determinant of impaired left ventricular relaxation and increased chamber stiffness that characterize diastole in hypertrophic cardiomyopathy. Diastolic dysfunction is common to most such patients irrespective of the presence or absence of outflow obstruction. Calcium entry blockers may improve the left ventricular relaxation process and relieve symptoms in patients with hypertrophic cardiomyopathy, particularly the subgroup with no obstruction to outflow. Atrial and ventricular arrhythmias are responsible for a significant proportion of the morbidity and mortality, and their prevalence appears to depend on the presence of obstruction and the extent of hypertrophy. Thus, the major manifestations of hypertrophic cardiomyopathy in systole and diastole, as well as the disturbances in rhythm, appear to be related to the site and/or extent of the hypertrophic process. We have learned much about hypertrophic cardiomyopathy in the 30 years since its modern description. The vast majority of symptomatic patients can now be improved with specific medical or surgical therapy.(ABSTRACT TRUNCATED AT 400 WORDS)
Cardiol Clin 1988 May
PMID:Hypertrophic cardiomyopathy. 306 84

Pressure overload hypertrophy of the left ventricle is associated with abnormal left ventricular early diastolic filling. The roles of the extent of cardiac hypertrophy, depressed left ventricular systolic function and aging in the pathogenesis of left ventricular diastolic dysfunction have not, however, been fully defined. To determine the relative importance of these factors in the pathogenesis of diastolic dysfunction in pressure overload hypertrophy, 16 children and 25 adults with aortic stenosis were compared with 48 normal children and adults, using rates of left ventricular early diastolic filling and wall thinning derived from M-mode echocardiography. Left ventricular early diastolic filling and wall thinning rates were significantly depressed in both children and adults with aortic stenosis as compared with values in normal subjects. Filling and thinning rates correlated negatively with age, left ventricular peak systolic pressure and wall thickness in all subjects. Furthermore, the effect of age on diastolic function appeared to be mediated by age-related increases in systolic pressure and wall thickness. In adults with aortic stenosis, early diastolic filling and wall thinning rates were depressed to a similar extent in subjects with normal and abnormal systolic function; thus, diastolic dysfunction does not appear to be a manifestation of abnormal systolic loading and ejection performance. These results suggest that extent of hypertrophy itself plays a dominant role in the mechanism of impaired left ventricular early diastolic filling in pressure overload due to aortic stenosis.
J Am Coll Cardiol 1985 May
PMID:Early diastolic left ventricular function in children and adults with aortic stenosis. 315 35

Infarct expansion, regional dilation and thinning of the infarct zone, occurs within 1 day after myocardial infarction. Whether the early change in regional shape of infarct expansion affects the architecture of remote normal regions is unknown. To study this question, 45 rats with a transmural infarct were killed at 1, 2 and 3 days after infarction and their hearts were examined for infarct size and extent of expansion. Wall thickness and radius of curvature were measured within, adjacent to and remote from the infarct zone. Equivalent regions were analyzed in eight control hearts. The extent of disproportionate wall thinning and increased radius of curvature within the infarct zone of hearts with expansion was not dependent on infarct size. Significant wall thinning and increased regional radius of curvature were also seen in adjacent and remote regions of the hearts with expansion (p less than 0.001). These structural changes outside of the infarct occurred independent of infarct age and size, and were not seen in hearts without infarct expansion. Thus, when disproportionate thinning and dilation occur in the infarct region, they are accompanied by a distortion in shape of the entire heart including remote normal myocardium. This remote remodeling of noninfarcted myocardium correlates with extent of expansion, but not with age or size of the infarct.
J Am Coll Cardiol 1985 Jun
PMID:Global cardiac remodeling after acute myocardial infarction: a study in the rat model. 315 87


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