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

Nine children with endocardial fibroelastosis were followed from the time of admission with congestive heart failure until either death or discharge. Review of multiple clinical features showed that only the electrocardiographic pattern could be correlated with death or survival. The presence of a delayed transition zone with anterior force loss on the initial electrocardiogram ('infarct pattern') was noted in all the children who died. Progression of these changes with a pattern of anterolateral 'infarct' in two and inferior wall 'infarct' in two occurred before death. Necropsy on three of the four children confirmed the diagnosis of endocardial fibroelastosis. There was extensive fibrosis and thinning of the left ventricular myocardium as well as involvement of the mitral valve structures. Review of published cases supports the view that an 'infarct' pattern in a child with endocardial fibroelastosis is usually associated with death and that this pattern is a negative prognostic sign for survival.
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PMID:Prognostic value of the electrocardiogram in endocardial fibroelastosis. 13 69

We reviewed 201Tl images of a 32 year old man with dilated hypertrophic cardiomyopathy (DHCM). At 22 years of age, when he was diagnosed as having nonobstructive hypertrophic cardiomyopathy (HCM)IVST; 20mm, Dd; 44mm, EF; 62%), 201Tl images showed only a small defect in the anteroseptal segment. At 27 years of age, when he had the first cardiac symptom as palpitation on exertion, his perfusion defect of 201Tl became wider. At 32 years age, he was hospitalized because of deterioration of congestive heart failure. Echocardiography revealed left ventricular wall thinning(IVST; 6mm), left ventricular cavity enlargement (Dd; 63mm) with a large mural thrombus and reduced left ventricular ejection fraction (EF; 32%). Thus 201Tl images may provide useful information on the process of DHCM from HCM.
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PMID:[A case of hypertrophic cardiomyopathy with progressive cavity dilatation--a review of serial 201Tl myocardial imaging]. 192 7

Two cases of Japanese girls with congenital cutis laxa associated with cardiovascular abnormalities are described. Case 1: A 12-year-old girl has been under our observation from the age of 6 months. Cardioangiogram revealed dilatation of the ascending aorta, meandering of the descending aorta and the coronary arteries, coiling of the carotid and innominate (brachiocephalic) arteries, and hypoplasia of the pulmonary arteries. Case 2: A 2.8/12-year-old girl died after our follow-up from the age of 3 months. The cause of death was congestive heart failure secondary to peripheral stenosis of the pulmonary arteries. In both cases, skin biopsy revealed a decreased number of elastic fibers and an increased amount of acidic mucopolysaccharides. The same histological features were observed in the pulmonary arteries and other arteries as well. Electron microscopic findings were diffuse thinning of elastic fibers and reduced elastic content. The high blood level of elastase (167.8 micrograms/l) in case 1 may cast a light on the unknown etiology of the disease.
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PMID:Vascular abnormalities in congenital cutis laxa--report of two cases. 211 64

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.
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PMID:Left ventricular dilatation and failure post-myocardial infarction: pathophysiology and possible pharmacologic interventions. 214 59

Left ventricular dilation and remodelling occur in 35-40% of anterior transmural myocardial infarcts and these events are important antecedents to the development of late congestive heart failure. This process commences within the first 24 hours following myocardial infarction and may be steadily progressive over months to years. Both the infarcted and the uninfarcted regions of myocardium are equally involved in the process. Thinning of the left ventricular wall occurs mainly as a result of cell slippage. In addition, compensatory hypertrophy occurs in the uninfarcted segment of the myocardium. While this hypertrophy may initially be physiological, it ultimately appears to become a pathological process and thereby contributes to pump dysfunction. At the present time there are encouraging data to suggest that nitroglycerin, administered in the setting of the acute infarction, or the angiotensin converting enzyme inhibitor captopril, may ameliorate this process. Whether a patent infarct related artery further limits dilation is uncertain and is currently under investigation.
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PMID:The prevention of congestive heart failure: left ventricular dilation and its management. 215 39

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.
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PMID:Left ventricular function in beta thalassaemia major. 262 27

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)
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PMID:Myocardial infarct expansion, infarct extension, and reinfarction: pathophysiologic concepts. 288 58

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.
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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.
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PMID:Echocardiographic findings in children treated for malignancy with chemotherapy including adriamycin. 315 66

Serial two-dimensional echocardiographic and thallium-201 scintigraphic findings are described in a patient with acute myocarditis diagnosed by endomyocardial biopsy. On the 4th day of illness, just before the onset of congestive heart failure, the echocardiogram showed asymmetric septal hypertrophy (IVS/PW = 16 mm/10 mm = 1.6) and thallium-201 scintigram showed the ventricular septal thickening. On the 8th day of illness, when severe congestive heart failure was seen, asymmetric septal hypertrophy disappeared (IVS/PW = 8 mm/8 mm = 1.0), the left ventricle dilated markedly (LVDd = 63 mm), and the wall motion became poor (EF = 0.24). After one month, when congestive heart failure and clinical inflammatory findings disappeared, the contractility somewhat improved (EF = 0.43), although marked left ventricular dilatation remained. Thallium-201 scintigram showed some scattered persistent perfusion defects, thinning of the ventricular septal thickening, and dilatation of the left ventricle. The right ventricular endomyocardial biopsy revealed the histologic findings of the late stage of acute myocarditis. It is concluded that transient thickening of the ventricular wall may represent early changes in acute myocarditis.
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PMID:Reversible asymmetric septal hypertrophy in acute myocarditis. Serial findings of two-dimensional echocardiogram and thallium-201 scintigram. 316 41


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