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)

Echocardiographic findings in patients with ischemic heart disease are described; their correlations with clinical, hemodynamic and angiographic data are presented and discussed. Regional abnormalities of left ventricular wall motion and/or thickening during systole are detected in 84 per cent of patients with acute myocardial infarction and in a high percentage of patients with larger than or equal to 75 per cent narrowing of a major coronary artery. These abnormalities may occur with stress and may be reversible. Left ventricular wall thinning during systole indicates acute ischemia or infarction and thin, dense myocardial echoes indicate scar. Echocardiographic evidence of left ventricular dysfunction is useful in predicting heart failure and mortality in patients with acute myocardial infarction and in predicting surgical mortality for patients undergoing aneurysmectomy and/or coronary artery bypass surgery. Echocardiography has not proved useful in determining graft patency following coronary artery bypass surgery. Technical difficulties and limitations of echocardiography in patients with coronary artery disease are discussed.
 ...
PMID:Echocardiography in ischemic heart disease. 32 1

Early in the acute phase of myocardial infarction the phenomenon of expansion may occur, with regional thinning and dilatation of necrotic region. This complication may be detected by echocardiography since the first hours of infarction. During the two subsequent weeks, an additional increase of left ventricular volume may occur, due to an increase of length of the infarcted segments and, as well, of the contractile segments which suffer a "volume overload hypertrophy". This is the phenomenon of remodeling. Finally during the first year post infarction, a progressive left ventricular dilatation may develop. This late dilatation seems to be due to an increase of perimeter of the contractile regions only. By the time this topographic changes have occurred, the left ventricle assumes a more spheric configuration. Left ventricular dilatation affects adversely cardiac function, with higher incidences of heart failure and death. Experimental and clinical studies show that, in selected patients, remodeling and ventricular dilatation may be attenuated by the administration of angiotensin-converting-enzyme inhibitors, with better indices of left ventricular function. Final results of several on-going multicenter studies are awaited for; they will allow a better definition of the role of ACE inhibitors on prevention and treatment of left ventricular dysfunction after myocardial infarction.
 ...
PMID:[Expansion of infarction, dilatation and ventricular remodelling. Therapeutic potential of angiotensin-converting enzyme inhibitors]. 161 Jun 13

LV enlargement is an important determinant of survival after AMI. Pathophysiologic mechanisms leading to LV dilatation after an AMI include early thinning and stretching of the infarcted segment (e.g., infarct expansion) and hypertrophy of the noninfarcted myocardium. Such LV dilatation may adversely affect subsequent cardiac function, leading to heart failure and death. Experimental data in animals and preliminary studies in humans have demonstrated that early administration of captopril, an angiotensin-converting enzyme inhibitor, may limit infarct expansion and will attenuate progressive LV dilatation. This article discussed the clinical importance of the dilated left ventricle and reviewed advances and ongoing research in the use of angiotensin-converting enzyme inhibitors in the chronic phase after AMI.
 ...
PMID:Left ventricular remodeling after acute myocardial infarction: clinical course and beneficial effects of angiotensin-converting enzyme inhibition. 182 84

An abnormal elevation in collagen concentration or myocardial fibrosis occurs in the hypertrophied left ventricle of the rat with renovascular hypertension (RHT). The structural nature and functional consequences of this fibrosis and the mechanisms involved in its appearance were reviewed for various phases of hypertrophy. Within days after the onset of renal ischemia, type I collagen messenger ribonucleic acid is expressed. An interstitial fibrosis follows, characterized by an increased dimension of existing perimysial fibers and the appearance of fibrillar collagen in spaces previously devoid of collagen, together with a perivascular fibrosis of intramyocardial coronary arteries. These expressions of myocardial fibrosis are associated with an increase in diastolic and systolic myocardial stiffness. Endomyocardial fibrosis serves to further increase diastolic stiffness while myocytes encircled by fibrillar collagen become atrophic. Each of these consequences of myocardial fibrosis reduce myocyte length-dependent force generation. At 32 weeks of RHT there is an obvious diastolic and systolic dysfunction of the ventricle together with heart failure that includes ventricular dilatation, wall thinning and reduced ejection fraction. The mechanisms involved in mediating fibrosis in RHT appear to be multiple. Myocyte necrosis and fibroblast proliferation have been associated with elevated circulating angiotensin II. Necrosis in RHT was not seen with captopril pretreatment or in the hypertension and hypertrophy that accompanied infrarenal aorta banding. An alteration in coronary artery permeability may be responsible for the perivascular fibrosis that is not seen with captopril pretreatment. Thus in RHT, the hemodynamic status of the ventricle determines myocyte hypertrophy while the elevation in circulating angiotensin II is responsible for the remodeling of nonmyocyte compartments, including the appearance of myocardial fibrosis.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Myocardial fibrosis and pathologic hypertrophy in the rat with renovascular hypertension. 213 51

Intracoronary administration of anticardiac cytotoxic serum increased the sarcolemma passive permeability for Ca2+ ions and reduced the activity of Na+-Ca2+ and Na+,K+-ATPase exchange in dogs. Electronic microscopy revealed thinning of glycocalix, destabilizing of the sarcolemma phospholipid bilayer, and development of intracellular oedema. Disturbances of the sarcolemma structure and function seem to be able to cause the development of cardiac insufficiency of immune origin.
 ...
PMID:[Disordered ion-transport processes in the cardiomyocyte membranes in the immune action on the heart]. 245 77

The left ventricular dimension and posterior wall dynamics were studied by computer assisted analysis of M mode echocardiography in 25 normal children (group 1) and 32 transfusion dependent children with beta thalassaemia major who had no evidence of heart failure (group 2). Twenty seven of those in group 2 remained well but five died of cardiac decompensation within 12 months. Compared with group 1, the left ventricular fractional shortening and ejection fraction were normal in those in group 2 who survived but diminished in those who died. Evaluation of left ventricular dimension and posterior wall dynamics during systole (peak shortening rate, peak velocity of circumferential fibre shortening, and peak posterior wall thickening rate) showed similar findings in that only the group who died had abnormal values. The left ventricular dimension and posterior wall diastolic dynamics (peak relaxation rate, normalised peak relaxation, peak wall thinning, and normalised peak wall thinning rate), however, showed progressively slower rates in all the children in group 2. The findings suggest that left ventricular diastolic dysfunction occurs early in myocardial impairment in patients with beta thalassaemia major. When there are abnormalities in both diastole and systole, the myocardial impairment is advanced and the prognosis is poor.
 ...
PMID:Left ventricular function in beta thalassaemia major. 262 27

This study describes the long-term outcome of 33 patients with hypertrophic cardiomyopathy who experienced a cardiac arrest but were successfully resuscitated. Cardiac arrest occurred at ages 9 to 62 years (mean 32); five patients survived multiple (two or three) arrests. A variety of treatments were administered; 18 patients with left ventricular outflow tract obstruction underwent ventricular septal myotomy-myectomy or mitral valve replacement and also received drug therapy; 15 patients received medical therapy alone. To date, 22 (67%) of the 33 patients have survived after the initial cardiac arrest for periods of 17 months to 22 years (mean 7 years); 12 patients have survived for greater than or equal to 5 and 6 for greater than or equal to 10 years. Of the 22 survivors, 16 have remained asymptomatic or only mildly symptomatic over the period of follow-up; 6 others have become severely symptomatic with heart failure, including 3 with evidence of left ventricular wall thinning and cavity enlargement. Eight patients ultimately died of natural cardiac causes (suddenly or of progressive heart failure) 7 months to 8.4 years (mean 4 years) after their initial cardiac arrest. Actuarial patient survival was 97 +/- 3%, 74 +/- 9% and 61 +/- 11% after 1, 5 and 10 years, respectively. Event-free rate (defined as actuarial survival without recurrent cardiac arrest of death) was 83 +/- 7%, 65 +/- 9% and 53 +/- 11%, respectively. For this group of patients with hypertrophic cardiomyopathy who were treated in a nonsystematic fashion with a variety of therapeutic strategies, the long-term outcome after surviving a cardiac arrest was variable.(ABSTRACT TRUNCATED AT 250 WORDS)
 ...
PMID:Long-term outcome of patients with hypertrophic cardiomyopathy successfully resuscitated after cardiac arrest. 270 10

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

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.
 ...
PMID:[Natural course of hypertrophic cardiomyopathy: clinical, hemodynamic and echocardiographic features in the end stage]. 297 74

Thirty-seven children receiving chemotherapy including adriamycin were studied with echocardiography. Abnormal left ventricular function assessed by systolic time intervals (STI) and/or left ventricular shortening fraction (delta LVID) was present in 30%, and dilated left ventricle was in 45% of the case, often accompanied by thinning the left ventricular wall. Three patients developed congestive heart failure, one with fatal outcome. Two of these patients had received chest irradiation along with the chemotherapeutic treatment. These three patients with overt heart failure had gross abnormalities in several echocardiographic variables of which delta LVID seemed most specific.
 ...
PMID:Echocardiographic findings in children treated for malignancy with chemotherapy including adriamycin. 315 66


1 2 3 4 5 6 7 8 9 10 Next >>