Gene/Protein Disease Symptom Drug Enzyme Compound
Pivot Concepts:   Target Concepts:
Query: UMLS:C0851184 (thinning)
 11,252 document(s) hit in 31,850,051 MEDLINE articles (0.00 seconds)

Coronary artery narrowing, ranging from 19% to 61%, was induced in rats and ventricular performance, myocardial damage, and myocyte hypertrophy were examined 1 mo later. Animals were separated into two groups, exhibiting ventricular dysfunction and failure, respectively. Dysfunction consisted of a 2.4-fold increase in left ventricular end diastolic pressure (LVEDP), 15% decrease in left ventricular peak systolic pressure (LVPSP), 24% reduction in developed pressure (DP), and a 16% depression in-dP/dt. Failure was defined on the basis of a 4.7-fold elevation in LVEDP, and a 26%, 47%, 45%, and 41% decrease in LVPSP, DP, +dP/dt, and -dP/dt. Moreover, in this group, right ventricular end diastolic and systolic pressures increased 5.5- and 1.2-fold. Left and right ventricular weights expanded 23% and 51% with dysfunction and 30% and 56% with failure. Left ventricular hypertrophy was characterized by ventricular dilation and wall thinning which were more severe in the failing animals. Foci of damage were found in both groups but tissue injury was more prominent in the endomyocardium and in failing rats. Finally, myocyte loss in the ventricle was 10% and 20% with dysfunction and failure whereas the corresponding enlargements of the unaffected myocytes were 34% and 53%. Thus, coronary narrowing led to abnormalities in cardiac dynamics with an increase in diastolic wall stress and extensive ventricular remodeling in spite of a moderate loss of myocytes and compensatory reactive hypertrophy of the viable cells.
 ...
PMID:Chronic coronary artery constriction leads to moderate myocyte loss and left ventricular dysfunction and failure in rats. 153 47

To examine the relations among hypertrophy, fibrosis and diastolic performance in early experimental hypertension, 18 control dogs and 12 dogs with experimental left ventricular hypertrophy were studied. Diastolic function was impaired in dogs with left ventricular hypertrophy, with decreased Doppler early to atrial inflow velocity ratio (E/A) (1.35 versus 1.72), increased atrial filling fraction (35% versus 29%), decreased sonomicrometric peak rates of wall thinning (-2.01 versus -3.37 liters/s) and filling (4.33 versus 6.64 liters/s) and prolonged time constant of isovolumetric relaxation (tau; 34.3 versus 28.1 ms). Neither chamber stiffness (k; P = AekV) nor passive elastic stiffness (E; E = k sigma, where sigma = stress) was increased. At postmortem examination, the hypertensive left ventricle weighed significantly more than normal (116 versus 80 g; p less than 0.01) and had greater muscle fiber diameter at endocardial and epicardial sampling sites in the apical free wall, basal free wall and septum (mean diameter 50 +/- 8 microns in hypertensive dogs, 37 +/- 8 microns in normal dogs; p less than 0.01). In contrast, neither percent fibrosis (1.2 +/- 0.8 versus 0.9 +/- 0.6 in normal dogs) nor fibrotic volume (1.21 +/- 0.63 versus 0.72 +/- 0.42%/g in normal dogs) was significantly increased. Peak volumetric filling rate was inversely related to fiber diameter (r = -0.74, p less than 0.001), although no variable of left ventricular function was significantly related to percent or volume fibrosis (all r less than 0.60, all p greater than 0.05). Thus, diastolic dysfunction may exist in the setting of hypertrophy without significant fibrosis. Increased myocyte size was associated with early diastolic filling abnormalities characteristic of the hypertensive left ventricle. Fibrosis appears to be a less important determinant of diastolic performance.
 ...
PMID:Hypertrophy, fibrosis and diastolic dysfunction in early canine experimental hypertension. 182 98

An important antecedent to the development of late congestive heart failure is left ventricular dilatation and remodeling following myocardial infarction, which occurs in 30-40% of acute anterior transmural infarcts. Dilatation and remodeling commence within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and uninfarcted regions of the myocardium are equally involved in the process. The remodeling process comprises left ventricular wall thinning (mainly due to cell slippage), chamber dilatation, and compensatory hypertrophy of the uninfarcted segment of the myocardium. The hypertrophy may initially be physiologic but may ultimately become a pathologic process, and thereby contribute to pump dysfunction. The possible reasons why the ventricular hypertrophy may ultimately be dysfunctional include alterations in local architecture and their sequelae alone or in concert with local changes in the beta-adrenergic, alpha-adrenergic, or renin angiotensin systems. At the present time, there are encouraging data to suggest that nitroglycerin, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process.
 ...
PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

To examine the time course of the functional consequences of progressive left ventricular hypertrophy, diastolic left ventricular inflow and wall thinning variables were analyzed in 13 dogs before and 2, 4, 8 and 12 weeks after creation of perinephritic hypertension. Left ventricular echocardiograms were digitized for dimensions, mass and peak rates of wall thinning (-dh/dt/h) and cavity enlargement (dD/dt/D). Doppler recordings of left ventricular inflow were analyzed for peak early (E) and late (A) diastolic inflow velocities, their ratio and atrial filling fraction. At 2 weeks, systolic blood pressure increased from 151 to 233 mm Hg, wall stress from 52 to 80 kdynes/cm2 and posterior wall thickness from 0.68 to 0.84 cm (all p less than 0.05). Left ventricular mass increased from 90 to 115 g over 12 weeks (p less than 0.05). Heart rate, cavity size and systolic shortening were unchanged at all data points. Diastolic abnormalities accompanied the developing hypertrophy and included impairment of early function, as demonstrated by a peak rate of wall thinning, from -13.4 to -8.9 l/s at 2 weeks (p less than 0.05), increased dependence on atrial systolic filling, a decrease in E/A from 1.68 to 1.29 at 4 weeks (p less than 0.05) and an increase in atrial filling fraction from 30% to 43% at 8 weeks (p = NS). Thus, diastolic dysfunction is an early consequence of experimental left ventricular hypertrophy. Different aspects of diastolic impairment are sensitively reflected by echocardiographic Doppler recordings, suggesting that these methods should be useful for the detection of diastolic dysfunction in human patients.
 ...
PMID:Alterations in diastolic function in response to progressive left ventricular hypertrophy. 252 6

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.
 ...
PMID:Fibrosis-induced reduction of endomyocardium in the rat after isoproterenol treatment. 252 93

To assess the possible role of restoring forces underlying left ventricular wall motion during rapid filling, the time relations between left ventricular dimensions and filling velocity were studied by digitised M-mode and Doppler echocardiography in 23 normal children and 43 patients: 11 with mild and 17 with severe mitral regurgitation, and 15 with left ventricular hypertrophy due to aortic stenosis. In normal children, peak mitral flow velocity characteristically lagged peak rate of dimension increase by 50 +/- 15 msec, and peak rate of posterior wall thinning by 35 +/- 15 msec, (P less than 0.01 for both). Towards the apex, and along the long axis of the ventricle, these phase differences between dimension and flow velocity were not apparent. The characteristic time relations between flow velocity and transverse dimension were also present in patients with left ventricular hypertrophy or mild mitral regurgitation, but when mitral regurgitation was severe they were lost and there was no significant difference in timing between peak flow velocity and peak rate of dimension change (-2 +/- 30 msec) or wall thinning (-4 +/- 25 msec). We conclude that phase differences between left ventricular wall motion and mitral inflow velocity are present in the normal ventricles of children. They cannot be explained on the basis of simple shape changes or passive filling of the relaxing ventricle, but strongly suggest the additional presence of ventricular restoring forces. They persist in patients with left ventricular hypertrophy or mild mitral regurgitation, but are lost when the regurgitation is severe, the filling pattern reverting to that predicted for passive distension of the ventricular cavity by a high left atrial pressure.
 ...
PMID:Phase differences between left ventricular wall motion and transmitral flow in man: evidence for involvement of ventricular restoring forces in normal rapid filling. 252 30

To explore relationship between hypertrophy of left ventricle and its shape, blood supply and calcium turnover, the study enrolled 105 male patients with ischemic heart disease or those suspected of its presence. All patients underwent contrast coronary ventriculography, M-mode echocardiography and sectorial scanning. Moderately limited myocardial blood supply was found to be a factor, stimulating its local hypertrophy. In the event of severely impaired blood supply, no substantial myocardial hypertrophy is detectable in corresponding regions, while dynamic observation not infrequently reveals thinning of the wall. Patients with intact coronary arteries, and having more elongated shape of left ventricular cavity, demonstrate larger thickness of walls along the long axis, that is probably due to dependence of intramyocardial tension on the radius of the wall curvature. While performing ventriculography in the patients with hypertrophic myocardium, disclosed elevated level of calcium in the blood and enhanced calcium uptake by cardiac muscle versus patients without left ventricular hypertrophy.
 ...
PMID:Significance of left ventricular shape, its blood supply and calcium turnover for evolving myocardial hypertrophy. 252 3

Infarct expansion and infarct extension are events early in the course of myocardial infarction with serious short- and long-term consequences. Infarct expansion, disproportionate thinning, and dilatation of the infarct segment probably begin within hours of acute infarction and usually reach peak extent within seven to 14 days. Clinical data suggest that infarct expansion occurs in approximately 35% to 45% of anterior transmural myocardial infarctions and to a lesser extent in infarctions at other sites. Although expansion usually develops in large infarcts, the extent of transmural necrosis rather than absolute infarct size predicts its occurrence. Expansion has an adverse effect on infarct structure and function for several reasons. Functional infarct size is increased because of infarct segment lengthening, and expansion results in over-all ventricular dilatation. Thus, patients with expansion of an infarct have poorer exercise tolerance, more congestive heart failure symptoms, and greater early and late mortality than those without expansion. Infarct rupture and late aneurysm formation are two additional structural consequences of infarct expansion. Experimental and clinical data suggest that the incidence and severity of expansion can be modified by interventions. Increased ventricular loading conditions and steroidal and nonsteroidal antiinflammatory agents make expansion more severe. Reperfusion of the infarct segment and pharmacologic interventions that decrease ventricular afterload lessen the severity of expansion. Previous myocardial infarction and preexisting ventricular hypertrophy may also limit the development of infarct expansion. Infarct extension is defined clinically as early in-hospital reinfarction after a myocardial infarction. The pathologic finding of infarct extension is necrotic and healing myocardium of several different recent ages within the same vascular territory. Although this pathologic criterion usually cannot be verified, studies employing invasive and noninvasive assessment of patients with early reinfarction provide evidence that the new myocardial injury is usually in the same vascular risk region as the original infarction. A variety of different criteria have been applied in the clinical diagnosis of infarct extension, and this has resulted in a large range of estimated frequencies from under 10% to as high as 86%. High estimates are found in studies using one or two nonspecific criteria such as ST segment shift or reelevation of total CK. The lowest rates have been found when combinations of criteria are used.(ABSTRACT TRUNCATED AT 400 WORDS)
 ...
PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

The relation between ventricular function and electrocardiographic evidence of hypertrophy (by voltage criteria, "strain", and U wave inversion) was examined by means of M mode echocardiography and apex cardiography in 73 patients with diseases associated with left ventricular hypertrophy and 10 normal volunteers. In patients with disease, left ventricular cavity dimension and fractional shortening were unrelated to electrocardiographic findings, but left ventricular posterior wall thickness was greater in those with strain or U wave inversion. Without U wave inversion, hypertrophy and strain were weakly related to diastolic abnormalities, but the addition of U wave inversion was strongly associated with a reduced rate of early diastolic posterior wall thinning, prolonged isovolumic relaxation time, delayed mitral valve opening after minimum cavity dimension, and a pronounced increase in transverse dimension during the isovolumic period suggesting incoordinate relaxation. It is concluded that, whereas a negative U wave frequently occurs in association with the pattern of left ventricular hypertrophy or strain, it alone is strongly related to abnormalities of isovolumic relaxation. The close relation between incoordinate relaxation and U wave inversion, events which occur virtually simultaneously during the isovolumic period, suggests a mechanical influence on U wave genesis.
 ...
PMID:U waves in ventricular hypertrophy: possible demonstration of mechano-electrical feedback. 293 60

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.
 ...
PMID:Severe functional limitation in patients with hypertrophic cardiomyopathy and only mild localized left ventricular hypertrophy. 294 85


1 2 3 4 5 Next >>