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

Systolic wall thickening abnormalities are sensitive indicators of ischemia and infarction. One purpose of this investigation was to assess the relation between coronary risk area, infarct size and wall thickening abnormalities (dyskinesia) using 2-dimensional echocardiography (2-D echo) in a closed-chest conscious dog model of acute myocardial infarction. The second purpose was to study the effects of systemic hypertension (SH) and left ventricular (LV) hypertrophy on these relations. Our hypothesis was that the infarct size and the extent of 2D echocardiographic dyskinesia would be quantitatively different in SH-LV hypertrophy, a condition in which coronary vascular reserve is diminished. Permanent circumflex coronary occlusion was performed in 15 conscious normal dogs and in 14 dogs with LV hypertrophy secondary to renal hypertension. Two-dimensional echocardiograms were obtained before, 20 minutes after and 2 days after coronary occlusion. The systolic wall thickening along 12 equidistant radii was analyzed in short-axis images. Percent dyskinesia on 2-D echo was defined as the percentage of radii showing systolic thinning. Infarct size was determined pathologically and risk area was determined angiographically. For a given risk area, coronary occlusion resulted in a larger infarction in dogs with SH-LV hypertrophy than in normal dogs (p less than 0.05). Two-dimensional echocardiographic dyskinesia correlated well with infarct size both at 20 minutes (r = 0.92) and 2 days (r = 0.94); dyskinesia modestly overestimated the infarct size and underestimated the risk area. The relations were similar in both normal and SH-LV hypertrophy groups.(ABSTRACT TRUNCATED AT 250 WORDS)
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PMID:Relations between 2-dimensional echocardiographic wall thickening abnormalities, myocardial infarct size and coronary risk area in normal and hypertrophied myocardium in dogs. 622 35

Digitised M mode echocardiography was used to determine the relation between the degree of left ventricular hypertrophy and abnormalities of isovolumic relaxation and diastolic function. Fifty six patients with varying severity of non-malignant systemic hypertension without evidence of ischaemic heart disease, left ventricular dilation, or clinical heart failure were studied. In addition, 10 athletes with hypertrophy and 20 normal subjects were studied. Athletes and patients with moderate (systolic blood pressure 175 to 200 mm Hg) and severe hypertension (greater than 200 mm Hg) had a significant increase in left ventricular mass. Cavity dimensions were normal in hypertensive patients and increased in athletes. Systolic function was normal in all groups. Regardless of the degree of hypertrophy patients with hypertension had a prolonged isovolumic relaxation period and delayed mitral valve opening. Patients with hypertrophy also had a reduced rate and prolonged duration of rapid early diastolic dimension increase and posterior wall thinning. Athletes, however, who had an equivalent degree of hypertrophy to patients with moderate or severe hypertension had entirely normal function. Measurements of diastolic function were significantly correlated with wall thickness and left ventricular mass. These indices of hypertrophy, particularly posterior wall thickness and the sum of posterior wall and septal thickness, were positively correlated with the duration of isovolumic relaxation and delay in mitral opening and negatively with the peak rate of early diastolic dimension increase and wall thinning. Thus in hypertensive patients with non-dilated left ventricular hypertrophy there appears to be a relation between the degree of wall thickening and abnormalities of diastolic function.
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PMID:Left ventricular hypertrophy. Relation of structure to diastolic function in hypertension. 623 10

The blood perfusion of different parts of the brain tissue was examined by means of microspheres 15 and 50 micron in diameter, in normotensive control rats and in animals with experimental renovascular hypertension. The microspheres were labelled with fluorescein isothiocyanate and their numbers in the tissue were determined in consecutive histological sections by UV microscopy. In the control rats, the incidence of wedged microspheres per 1 mm3 tissue was high in the cerebellum, cerebral cortex, subcortical tissue and pons Varolii, but low in the thalamic and hypothalamic regions, indicating that these parts were relatively poorly perfused with blood. The significantly greater accumulation of microspheres in the cortex and subcortical tissue of hypertensive rats seems to have been due to hypertensive narrowing of the arterioles. Conversely, the diminished incidence of microspheres in the thalamus and hypothalamus may have been due partly to microsphere trapping in the narrowed upstream blood vessels and partly to thinning of the capillary network. Total microsphere recovery in the brains of the control and the hypertensive rats was almost identical, implying that only the distribution of brain blood perfusion is altered in experimental hypertension.
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PMID:Distribution of microspheres in the brain of hypertensive rats. 647 42

The effects of variations in transmural pressure over a range of 0 to 200 mmHg on transendothelial transport of macromolecules were studied in the canine common carotid artery. The uptake of 125I-albumin per unit artery weight increased with rising pressure. There was no significant difference in albumin permeability per unit luminal surface area between 0 and 100 mmHg, but permeability nearly doubled when pressure was raised to 200 mmHg. The contribution of an increased rate of transendothelial vesicle diffusion, as evaluated from the experimental determination of the ratio of attached-to-free vesicles and theoretical modeling, was found to be negligible. The reduction in transendothelial vesicle diffusion distance due to pressure-induced thinning of the peripheral zone contributes to a 25% increase in permeability. With the use of colloidal Ag and Au of various sizes, vesicle loading of particles with diameters greater than or equal to 15 nm was found to be severely restricted at transmural pressure less than or equal to 100 mmHg, but it was significantly enhanced at 200 mmHg, when particles as large as 25 nm became detectable in endothelial vesicles and subendothelial space. This hypertension-induced increase in macromolecular transport across the endothelium may cause an overloading of the arterial wall with low-density lipoproteins and play a significant role in atherogenesis.
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PMID:Effects of arterial pressure on endothelial transport of macromolecules. 648 72

Six hundred and twenty-five patients with diabetes mellitus were studied by standardised clinical methods, resting and exercise electrocardiography (ECG) and digitised echocardiography to determine the prevalence of coronary and non-coronary heart disease. Clinical evidence of coronary artery disease (angina and infarction) was present in 110 (18 per cent) normotensive patients. Hypertension (blood pressure greater than 165/95 mmHg) was present in 172 (27 per cent) of whom 32 had cardiac symptoms. Heart failure or left ventricular dilatation was seen in 18 of whom 11 had either hypertension or coronary artery disease and six asymptomatic patients had unexplained ventricular hypertrophy. Echocardiograms in 245 of 290 asymptomatic patients with normal ECG showed that relaxation was prolonged (p less than 0.001) and mitral valve opening delayed (p less than 0.001) from normal especially in those with severe microangiopathy (proliferative retinopathy and/or heavy proteinuria). The peak rates of cavity dimension increase and posterior wall thinning were reduced from normal (both p less than 0.001) and patients with severe microangiopathy had the most marked changes. Redivision of these 245 diabetics by abnormalities of left ventricular function showed that 147 had normal function in whom only one of 23 (random 15 per cent sample) had a positive exercise ECG. Prolonged relaxation or delayed mitral valve opening alone (a nonspecific abnormality) was present in 41 and only three of 28 had a positive exercise ECG. Thirty-one had delayed mitral valve opening with inco-ordinate relaxation (abnormalities very suggestive of coronary artery disease) of whom 20 of 29 had a positive exercise ECG. Twenty-six had delayed mitral valve opening with slow cavity dimension increase or wall thinning (without hypertrophy) of whom 21 of 25 had a negative exercise ECG. This is a relatively specific abnormality similar to that found in left ventricular hypertrophy. Coronary artery disease is common in symptomatic and asymptomatic forms in diabetes mellitus. Non-coronary left ventricular diseases, such as dilation and hypertrophy, are probably no more common in diabetics than non-diabetics. A small number of diabetics with severe microangiopathy had abnormal relaxation and reduced peak rate of dimension increase or wall thinning which may represent left ventricular disease due to microangiopathy.
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PMID:A prospective study of heart disease in diabetes mellitus. 670 23

Previous reviews of hematuria in children and adolescents have included patients with proteinuria and other renal functional abnormalities such as hypertension and reduced GFR. We report the clinico-pathological correlations in 76 pediatric patients, aged 3 to 19 years, who underwent a renal biopsy because of isolated hematuria during the 10-year period, 1972 to 1981. All specimens were examined by light and electron microscopy and immunofluorescence techniques. The overall prevalence of abnormal renal histology was 56%. The vast majority (41 of 43) of the abnormal biopsy specimens could be classified into four distinct histological categories: (1) Alport syndrome (N = 9); (2) IgA nephropathy (N = 8); (3) thinning of the glomerular basement membrane (N = 17); (4) vascular C3 staining (N = 7). The children were divided into three clinical subgroups (1) isolated microscopic hematuria ( IMH ), N = 42; (2) IMH plus a family history of hematuria in a first degree relative, N = 15; and (3) IMH plus at least one episode of gross hematuria, N = 19. A significant graded increase in the likelihood of obtaining an abnormal renal biopsy was demonstrated (X2 = 10, P less than 0.007) from groups one to three. Sex, age at onset, or duration of hematuria were not associated with an increased proportion of histopathologic abnormalities. These findings indicate that the yield of a renal biopsy in children with isolated hematuria can be predicted accurately from specific clinical characteristics.
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PMID:Isolated hematuria in children: indications for a renal biopsy. 672 31

Hypertension and atherosclerotic coronary arterial obstruction frequently coexist in patients. However, the effect of increased aortic pressure on ischemic segmental dysfunction is not well understood. We studied the effects of aortic pressure increases on segmental left ventricular function during myocardial ischemia. Eighty-two dogs instrumented with three to six pairs of pulse-transit piezoelectric crystals were studied in an awake, unsedated state to measure segmental wall thickness. A pneumatic balloon occluder was positioned around the proximal left anterior descending artery (LAD). Thirty-three dogs underwent LAD occlusion and served as normotensive controls (group A). Group B dogs (n = 23) received a 6-hour infusion of phenylephrine (PE) beginning 5 minutes after LAD occlusion to increase aortic diastolic arterial pressure to 120-130 mm Hg; aortic pressure was then allowed to return to normal for the subsequent 18 hours. The eight dogs in group C received a 6-hour infusion of PE, but no coronary arterial occlusion was produced. In group D (n = 12), distal constriction of the thoracic aorta was maintained for 24 hours after LAD occlusion. Regional myocardial blood flow (RMBF) was measured with radioactive microspheres in six conscious dogs and both RMBF and intramyocardial PCO2 were measured in seven open-chest dogs to assess alterations in regional myocardial oxygen supply and demand. Segments of myocardium were arbitrarily grouped according to the amount of net systolic thickening (NET) present 5 minutes after LAD occlusion and before increasing aortic pressure: group 1 retained 67-100+% of control NET, group 2 0-67%, and group 3 less than 0% (paradoxic motion). In dogs receiving PE plus LAD occlusion and in dogs with aortic constriction and LAD occlusion, NET was transiently depressed in groups 1 and 2 compared with the normotensive cohort; 24 hours after occlusion, NET in groups 1, 2 and 3 did not differ significantly from that in the normotensive dogs. Systemic hypertension resulted in a significant increase in endocardial and midwall RMBF and, in seven open-chest dogs, decreased the intramyocardial accumulation of carbon dioxide after LAD occlusion. Increased aortic pressure in dogs without coronary occlusion produced reversible decreases in end-diastolic wall thickness, NET and LV dP/dt. Thus, the production of systemic hypertension with diastolic pressures of 110-120 mm Hg acutely or for 6 hours during evolving canine myocardial infarction does not appear to exert an important deleterious effect on myocardial oxygen supply and demand. However, 24 hours of mildly increased aortic pressure accentuates end-diastolic wall thinning in segments with paradoxic systolic motion and results in a failure of their return to control values at this period.
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PMID:Effects of systemic hypertension on ischemic and nonischemic regional left ventricular function in awake, unsedated dogs after experimental coronary occlusion. 679 86

Pathological and hemodynamic concepts regarding the origin, growth, and rupture of intracranial saccular aneurysms are reviewed. Aneurysms form as a result of an interplay between hemodynamic factors, such as axial stream impingement and the water hammer effect, and structural weaknesses at apices of arterial bifurcations, such as congenital and acquired medial defects, funnel-shaped dilatations, and areas of thinning. Hypertension and time aid the formation of aneurysms. Unknown factors in women and in some families also play a role. Enlargement of aneurysms results from an interplay between mechanical factors, such as self-excitation and resonance, that produce structural fatigue and pathological processes of repair of the aneurysmal wall. Rupture of aneurysms is caused by the same hemodynamic factors that effect growth and is also influenced by extramural pressure. Pathologically, a major rupture may be preceded by fibrinous and leukocytic infiltration of the wall, bleb formation, and a minor hemorrhage. Such minor leaks can be followed by healing and growth. Aneurysms that escape major hemorrhage or heal successfully after a hemorrhage can grow to giant proportions, but remain susceptible to rupture despite their size, unless they become completely thrombosed. Intramural thrombosis may be stimulated by minor leaks and is dependent upon the physical characteristics of aneurysms. Experimental, angiographic, and clinical studies that pertain to the origin, growth, and rupture of aneurysms are also reviewed.
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PMID:Origin, growth, and rupture of saccular aneurysms: a review. 701 Feb 5

Renal disease, although not a cardinal feature of the Laurence-Moon-Biedl-Bardet syndrome (LMBBS), occurs in more than 70% of patients and is an important cause of morbidity and mortality. Renal ultrastructural changes have not been well delineated. We have studied glomeruli from three patients with LMBBS and have found similar ultrastructural changes in glomerular basement membrane (GBM). Two patients had decreased renal function, hypertension, and markedly abnormal intravenous urograms with reduced concentration of dye and abnormal pelvicalyceal systems; one patient had normal renal function and minimal distortion of the pelvicalyceal system of one kidney. Ligh microscopy revealed varying degrees of increase in mesangial cellularity and matrix. These changes involved almost all glomeruli and were segmental. The abnormalities ranged from mild mesangial cell proliferation to complete sclerosis of the glomerular tuft. Ultrastructural study revealed marked alterations of the glomerular basement membrane: effacement of the trilaminar architecture, segmental and irregular thickening alternating with thinning and rarefaction, accumulation of granular and fibrillary material within the inner third of the GBM. These ultrastructural changes may be the earliest and primary glomerular abnormality seen in LMBBS because they were seen in a patient who had minimal changes on light microscopy.
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PMID:Ultrastructural changes in the glomerular basement membrane of patients with Laurence-Moon-Biedl-Bardet syndrome. 731 62

Long-term study of 21 PNH patients revealed an unexpectedly high incidence of functional and anatomic renal abnormalities. Most patients demonstrated varying degrees of hematuria and proteinuria distinct from hemoglobinuria. Evaluation of renal function revealed hyposthenuria, abnormal tubular function, and declining creatinine clearance. Radiologically these patients had enlarged kidneys, cortical infarcts, cortical thinning, and papillary necrosis which were confirmed by autopsy studies. Hypertension developed in eight patients. Urinary tract infection was uncommon. The renal findings bear striking similarity to those of sickle cell anemia. Contrary to the usual opinion, out studies clearly showed evidence of widespread renal pathology in PNH most likely due to repeated microvascular thrombosis similar to the venous thrombosis involving other organs in this disorder.
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PMID:The kidneys in paroxysmal nocturnal hemoglobinuria. 744 17


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