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

Manufacturing factors have seldom been implicated as a direct cause of structural deterioration of valvular bioprostheses; this phenomenon has generally been considered to be of a host-dependent origin. We analyzed the clinical and pathologic data from 12 Carpentier-Edwards mitral bioprostheses removed from 12 patients because of severe dysfunction and showing detachment of the porcine aortic wall from the stent in one commissure or more. These 12 prostheses were part of a group of 92 such valves that were explanted and displayed structural deterioration. They belong to a population of 405 Carpentier-Edwards bioprostheses implanted in the mitral position in our institution between May 1978 and November 1988. The patients included three men and nine women with a mean age of 54 +/- 13 years. One patient had a history of chronic renal failure, and two had systemic hypertension. Prosthesis sizes were 29, 31, and 33 mm (n = 4 for each size). The models of the valves were 6625 (n = 8) and 6650 (n = 4). Mean duration of implantation of the prostheses was 99 +/- 27 months (52 to 136 months) and did not differ depending on the model. There was no significant clustering of commissural detachments depending on valve size, year of implantation, or gender of the patient. No similar phenomenon was observed among 76 explanted aortic Carpentier-Edwards bioprostheses with structural deterioration from a population of 441 valves implanted during the same time frame. Native porcine aortic roots (n = 5) and aortic Carpentier-Edwards bioprostheses explanted because of structural deterioration (n = 4) were used as controls for comparison. Macroscopic examination showed single commissural dehiscence in 10 patients and double in two. Radiology disclosed no or mild mineralization in eight valves and no calcium in the area of aortic wall dehiscence, except for heavily calcified valves. Light microscopy evidenced a significant thinning of the aortic wall at the paracommissural level of mitral bioprostheses (351 +/- 68 microns) compared with either aortic bioprostheses (526 +/- 59 microns; p < 0.01) or control native porcine aortic roots (419 +/- 50 microns; p < 0.01). No difference was found in terms of aortic wall thickness between detached (322 +/- 42 microns) and intact (366 +/- 74 microns) commissures in mitral bioprostheses.(ABSTRACT TRUNCATED AT 400 WORDS)
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PMID:Commissural dehiscence of Carpentier-Edwards mitral bioprostheses. Explant analysis and pathogenesis. 756 35

Using digitized M-mode echocardiograms, we evaluated left ventricular (LV) anatomy and function at rest and during handgrip in 24 normotensive young adults with both parents hypertensive (HP+), each matched for age, sex, body weight, and body surface area with one normotensive adult with both parents normotensive (HP-). LV parameters were within the normal range in all HP+ and HP-. At rest, HP+ as compared to HP- had higher systolic and diastolic blood pressure (BP), septal and posterior wall thickness, and LV mass; LV diastolic diameter and end-systolic wall stress were similar in the two groups. Modified midwall fractional shortening, peak shortening rate of LV diameter and peak thickening rate of LV posterior wall, indices of LV systolic function, and peak lengthening rate of LV diameter and peak thinning rate of LV posterior wall, indices of ventricular relaxation, were significantly higher in HP+. Handgrip induced significant (P < .001) and percent-comparable increases of systolic and diastolic BP, heart rate, and cardiac output in HP+ and HP-; peak shortening and lengthening rates of LV diameter and peak thickening and thinning rates of LV posterior wall increased significantly in HP-, whereas in HP+ the value of the four parameters, higher at rest as compared to HP-, did not show any further increase. In conclusion, normotensive young adults with high genetic risk for hypertension have higher BP and thicker and overactive LV as compared to subjects with normotensive parents. Handgrip stimulates LV function in offspring of normotensives, but not the already hyperkinetic LV of hypertensive offspring.
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PMID:Left ventricular anatomy and function in normotensive young adults with hypertensive parents. Study at rest and during handgrip. 775 43

The purpose of this prospective study was to determine the prevalence of renal abnormalities in 88 older asymptomatic siblings of the children with vesicoureteral reflux (VUR), using ultrasound (US) as a diagnostic method. The age of the siblings ranged from 5 to 15 years, the median age being 8.33 years. A midstream urine sample was taken for standard urinalysis and urine culture, and blood pressure was measured in all children. US examination did not reveal chronic inflammatory changes of the kidneys such as a small shrunken kidney, noticeable parenchymal thinning or parenchymal echogenicity changes; nor did it reveal a small kidney due to growth retardation or any dilatation of the renal tract to indicate reflux. No hypertension was found. The study failed to prove the benefit of US screening of older asymptomatic siblings. The results of the present study are discussed in relation to other techniques and investigations/screening for VUR.
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PMID:Ultrasound screening of older asymptomatic siblings of children with vesicoureteral reflux: is it beneficial? 800 86

A case of Ask-Upmark kidney is presented. An 18-year-old male patient referred to this facility presented with symptoms of hypertension, microscopic hematuria and proteinuria. A hormonal study revealed a high plasma renin activity level. Intravenous pyelography and abdominal computed tomography revealed thinning of the cortex with calyceal dilatation. Arteriography revealed a deep cortical groove in the middle portion of the kidney without renal arterial stenosis. Plasma renin activity of the left renal vein was significantly higher than that of the right renal vein. A left simple nephrectomy was performed under the diagnosis of Ask-Upmark kidney. Postoperatively, plasma renin activity returned to the normal range and a decrease in blood pressure was noted. Recent reports have suggested Ask-Upmark kidney to be a consequence of vesicoureteral reflux rather than a true congenital malformation. Our case indicated no evidence of vesicoureteral reflux and suggests that the lesion was congenital rather than acquired.
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PMID:[Ask-Upmark kidney: a case report]. 807 59

Arterial hypertension leads to left ventricular hypertrophy. In proportion to increased left ventricular systolic pressure, left ventricular hypertrophy is considered to be of adaptive nature from the point of view of wall stress regulation. In the beginning, left ventricular function is normal, whereas diastolic filling is already compromised by the process of hypertrophy and altered ventricular geometry. In case of ventricular dilation and wall thinning, wall stress increases and leads to an increment in myocardial oxygen demand and a decrease of left ventricular ejection fraction. This is followed by a further decline in intrinsic myocardial contractility and a decrease in the elastic material properties of the myocardium. The structure of the myocardium is characterized by myocyte hypertrophy, a process of reactive and reparative fibrosis and alterations of the coronary microcirculation. Coronary vasodilator reserve is markedly impaired and is likely to initiate a process of malperfusion and malnutrition under increased metabolic demands. Particularly, the combined involvement of myocytes, interstitium, and intramyocardial vasculature appears to predispose to late heart failure after prolonged exposure to chronic pressure overload in arterial hypertension.
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PMID:Heart failure on the basis of hypertension. 848 35

The authors present 2 cases of tumours of third ventricle with intracranial hypertension and cerebrospinal fluid rhinorrhea. The cause of the CSF rhinorrhea most often was thinning of lamina ethmoidalis and dura mater and rarely intussusception of arachnoidea into the intrasellar space in patients with oval orifice for the stalk of pituitary body due to prolonged intracranial hypertension. Efficacious treatment of CSF rhinorrhea comprises not only removing of the tumor but also introducing the valve and in some cases tightening of the base of the anterior and middle fossa.
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PMID:[Two cases of colloid cysts of the third ventricle with nasal rhinorrhea]. 850 51

Left ventricular hypertrophy is an adaptive response to long standing hypertension. However, the influence of left ventricular hypertrophy with hypertension on extent of infarct expansion has not been studied. We compared the effects of left ventricular hypertrophy with hypertension on infarct expansion in spontaneously hypertensive rats (SHR, n = 76), Wistar-Kyoto rats (WKY; n = 46) and spontaneously hypertensive rats treated with delapril, an angiotensin converting enzyme (ACE) inhibitor (SHRD; n = 39). The survival rates at 7 days after myocardial infarction were 41%, 24%, and 46% for WKY, SHR, and SHRD. The survival rate of SHR was significantly lower than those of both SHRD and WKY (P < .05). In the surviving rats (18 SHR, 19 WKY, 18 SHRD), both left ventricular cavity area (LCVA) and the infarct segment length per the noninfarct segment length (FW/IVS), measured as indices of left ventricular dilation, were significantly less in SHR and SHRD than in WKY, and the thickness of the left ventricular free wall (Wth), used as an index of left ventricular thinning, was significantly higher in both SHR and SHRD than in WKY (P < .01). However, there was no significant difference in FW/IVS, LCVA, and Wth between SHR and SHRD. Hemodynamic findings 1 week after coronary occlusion demonstrated that all rats were in heart failure, and there were no significant differences in hemodynamics among the three groups. In conclusion, our findings showed that hypertrophy with hypertension reduced infarct expansion, but that reduction of blood pressure by ACE inhibitor did not reduce infarct expansion more than hypertrophy did. However, this finding suggest that an ACE inhibitor may improve the rate of survival of patients with left ventricular hypertrophy with hypertension.
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PMID:Effects of chronic hypertension and left ventricular hypertrophy on the extent of infarct expansion in rats. 886 21

Using digitized M-mode echocardiography, we evaluated the acute effect of nifedipine on left ventricular (LV) diastolic dysfunction in 30 untreated hypertensives, evaluated at rest and during handgrip, both before and 30' after nifedipine (20 mg sublingually). At rest, after nifedipine blood pressure and end-systolic wall stress significantly decreased and peak lengthening rate of LV diameter, peak thinning rate of LV posterior wall and Doppler E/A ratio increased. Before and after nifedipine handgrip induced significant increases of blood pressure, heart rate and end-systolic wall stress; diastolic parameters significantly decreased during basal handgrip and did not change during handgrip after nifedipine. Nifedipine induced an acute improvement of LV diastolic dysfunction, that persisted when afterload increased during handgrip. Therefore nifedipine seems to improve LV diastolic function not only by reducing afterload, but also through a direct action on the myocardium. Besides, these results demonstrate that LV diastolic abnormalities in hypertension are partly dynamic and reversible.
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PMID:Effect of sublingual nifedipine on left ventricular diastolic dysfunction in hypertensives: echo-Doppler study at rest and during handgrip. 912 21

Thin glomerular basement membrane (GBM) nephropathy, also called familial benign hematuria, is characterized by chronic hematuria and uniform thinning of the lamina densa of the glomerular basement membrane. It generally holds an excellent renal prognosis. Alport syndrome in early stages can also show attenuation of the GBM; conversely, renal insufficiency has been reported in familial benign hematuria. To discern early Alport syndrome from thin GBM nephropathy, we carried out a prospective epidemiological study in which 19 normotensive and non-azotemic adult patients with chronic microscopic (18 of 19) and macroscopic (1 of 19) hematuria and biopsy-proven thin GBM nephropathy were followed for a median of 12 years (range 9 to 15 years). Renal biopsies of thin GBM patients at entry showed an increased incidence of focal global glomerulosclerosis when compared to disease controls as IgA nephropathy (P = 0.047) and normal renal tissue (P = 0.0075). All renal biopsies showed the presence of the Goodpasture antigen when tested immunohistochemically. Presence of Alport syndrome was excluded clinically as none of the patients had complaints of hearing loss or abnormalities by audiography and ophthalmology. At the end of follow-up, the incidence of hypertension in thin GBM nephropathy (35%) exceeded that of healthy clinical controls (P = 0.048), and one hypertensive patient developed mild renal failure. In the normotensive patients, the glomerular filtration rate at follow-up as measured by inulin clearance was reduced in three out of seven; these were over 50 years of age. Although no family members were known to have renal disease at inclusion, within four families six elderly first degree relatives had developed unexplained renal insufficiency at the end of follow-up. Thus, thin GBM nephropathy predisposes to premature glomerular obsolescence, leading in time to increased incidences of hypertension and late onset renal insufficiency.
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PMID:Thin GBM nephropathy: premature glomerular obsolescence is associated with hypertension and late onset renal failure. 915 Apr 78

The potential role of transient sarcolemmal membrane wounding as a signal transduction event for cardiomyocyte hypertrophy was evaluated in rats with short-term pressure overload caused by banding of the proximal aorta. This procedure resulted in significant increases in left ventricular systolic (1.5-fold) and end-diastolic (2.6-fold) pressures and wall stresses that were associated with significant wall thinning and cavitary enlargement. Quantitative image analysis of frozen sections of the stressed ventricles obtained 60 minutes after banding demonstrated a 6- to 10-fold increase in cytosolic staining with a horseradish peroxidase-labeled anti-albumin antibody compared with sham-operated controls, indicating that an increase in transient sarcolemmal membrane permeability (wounding) is an early response to an abrupt increase in hemodynamic load in vivo. We conclude that an intense hemodynamic stress in vivo can result in histologically detectable cardiomyocyte wounding.
Hypertension 1997 Nov
PMID:Cardiac myocyte membrane wounding in the abruptly pressure-overloaded rat heart under high wall stress. 936 53


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