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PubMed1997

Thyroid hormone improves function and Ca2+ handling in pressure overload hypertrophy. Association with increased sarcoplasmic reticulum Ca2+-ATPase and alpha-myosin heavy chain in rat hearts.

We asked whether thyroid hormone (T4) would improve heart function in left ventricular hypertrophy (LVH) induced by pressure overload (aortic banding). After banding for 10-22 wk, rats were treated with T4 or saline for 10-14 d. Isovolumic LV pressure and cytosolic [Ca2+] (indo-1) were assessed in perfused hearts. Sarcoplasmic reticulum Ca2+-ATPase (SERCA), phospholamban, and alpha- and beta-myosin heavy chain (MHC) proteins were assayed in homogenates of myocytes isolated from the same hearts. Of 14 banded hearts treated with saline, 8 had compensated LVH with normal function (LVHcomp), whereas 6 had abnormal contraction, relaxation, and calcium handling (LVHdecomp). In contrast, banded animals treated with T4 had no myocardial dysfunction; these hearts had increased contractility, and faster relaxation and cytosolic [Ca2+] decline compared with LVHcomp and LVHdecomp. Myocytes from banded hearts treated with T4 were hypertrophied but had increased concentrations of alpha-MHC and SERCA proteins, similar to physiological hypertrophy induced by exercise. Thus thyroid hormone improves LV function and calcium handling in pressure overload hypertrophy, and these beneficial effects are related to changes in myocyte gene expression. Induction of physiological hypertrophy by thyroid hormone-like signaling might be a therapeutic strategy for treating cardiac dysfunction in pathological hypertrophy and heart failure.

Animals↗
PubMed2004

Losartan but not enalaprilat acutely reduces reperfusion ventricular tachyarrhythmias in hypertrophied rat hearts after low-flow ischaemia.

Based on clinical and experimental studies, angiotensin II receptor blockers and angiotensin converting enzyme inhibitors have been proposed to exert acute anti-arrhythmic effects in heart failure patients. Therefore, the goal of this study was to assess acute anti-arrhythmic effects of losartan and enalaprilat in hypertrophied rat hearts during low-flow ischaemia and reperfusion. In dose-finding experiments in non-hypertrophied isolated perfused hearts, we performed dose-response curves of losartan and enalaprilat studying monophasic action potential duration at 90% repolarisation (MAPD(90%)) and ventricular fibrillation (VF) threshold. Subsequently, we determined the effects of losartan and enalaprilat (in therapeutically relevant concentrations) on ventricular tachyarrhythmias induced by low-flow ischaemia/reperfusion in hearts demonstrating left ventricular (LV) hypertrophy 70 days after aortic banding. We found that neither drug significantly affected MAPD(90%) (1 nM-1 mM) or VF threshold (1 microM losartan and 10 microM enalaprilat) in non-hypertrophied hearts. Similarly in hypertrophied hearts, neither drug significantly affected the incidence or the duration of ventricular tachyarrhythmias (ventricular tachycardia and VF) during low-flow ischaemia. However, 1 microM losartan significantly reduced the duration of ventricular tachyarrhythmias during reperfusion. In conclusion, neither losartan nor enalaprilat is acutely anti-arrhythmic in hypertrophied rat hearts during low-flow ischaemia. During reperfusion, however, losartan but not enalaprilat exerts acute anti-arrhythmic effects.

Action Potentials↗
PubMed1998

Relationship between electrocardiographic voltage and geometric patterns of left ventricular hypertrophy in patients with essential hypertension.

To assess whether we could predict left ventricular (LV) geometric patterns on echocardiography from voltages in standard electrocardiograms (ECG) in patients with essential hypertension, standard 12-lead ECG and echocardiograms were recorded in 106 consecutive, untreated patients (50+/-11 yr old) with essential hypertension. Subjects were assigned to the following four groups based on relative wall thickness (RWT) and LV mass index (LVMI) as determined by echocardiography: a normal geometry group (n = 44), a concentric remodeling group (increased RWT and normal LVMI, n = 10), an eccentric hypertrophy group (increased LVMI and normal RWT, n = 23), and a concentric hypertrophy group (increased RWT and LVMI, n = 29). The following ECG variables were determined: Sokolow-Lyon voltage (SV1 = RV5: SL), Cornell voltage (RaVL + SV3: CN), sum of 12-lead QRS voltage (12-lead sum), and RV6/RV5 ratio (RV6/V5). LVMI correlated with SL, CN, and 12-lead sum, but not with RV6/V5 in the study group as a whole. The concentric hypertrophy group showed increased voltages for all ECG variables except RV6/V5. The concentric remodeling group showed increased voltages for SL and 12-lead sum, but a decreased RV6/V5 ratio. In contrast, the eccentric hypertrophy group had increased voltage only for the 12-lead sum. The combination of SL, RV6/V5, and CN showed modest sensitivity and specificity in the diagnosis of concentric remodeling, concentric hypertrophy, and normal geometry, but not in the diagnosis of eccentric hypertrophy. Conventional ECG criteria can predict LVMI, but not LV geometry in the patients with essential hypertension. The combination of SL, CN, and RV6/V5 is useful in differentiating the four LV geometric patterns seen in essential hypertension.

Adult↗
PubMed1999

Left ventricular hypertrophy in hypertension: stimuli, patterns, and consequences.

Left ventricular (LV) size in childhood closely parallels body size, whereas in adulthood LV mass is increasingly affected by effects of obesity, hypertension, the level of cardiac volume load, and the level of LV myocardial contractility. Recently, additional independent associations of diabetes, arterial structure and function and as yet unknown genes with higher LV mass have been defined; angiotensin II and insulin have also been suggested to be additive stimuli to LV hypertrophy. Consideration of the level of LV mass and of the LV wall thickness/chamber radius ratio (relative wall thickness) has identified four different geometric patterns of LV adaptation to hypertension, including concentric LV hypertrophy (increased mass and wall thickness), eccentric hypertrophy (increased mass, normal relative wall thickness), concentric remodeling (increased relative wall thickness with normal mass) and normal LV geometry. Concentric hypertrophy is associated with especially high arterial pressure while eccentric hypertrophy is associated with obesity and elevated volume load. Numerous studies show that increased LV mass predicts cardiovascular events and death independently of all conventional risk factors; initial studies have also identified adverse implications of low LV midwall function and high relative wall thickness. Pioneer studies strongly suggest that reversal of LV hypertrophy is associated with an improved prognosis.

Blood Pressure↗
PubMed2005

Induction and analysis of cardiac hypertrophy in transgenic animal models.

Myocardial hypertrophy is an adaptational process of the heart to increased workload caused by mechanical stress, growth factors, cytokines, catecholamines, or primary genetic abnormalities. Chronic induction of hypertrophy leads to the gradual deterioration of ventricular function and is an independent risk factor for cardiac-related morbidity and mortality in patients with hypertension and ventricular arrythmias. Transgenic animals are very useful models to study the factors involved in the pathogenesis of cardiac hypertrophy. To achieve this goal, rodents lacking or overexpressing a specific gene are subjected to banding of the abdominal aorta, an experimental model of cardiac hypertrophy that leads to pressure overload on the heart. After periods between 3 and 21 d, parameters such as cardiac hemodynamics, morphologic alterations, and expression of marker genes (e.g., the gene for atrial natriuretic peptide) are analyzed in genetically modified animals and compared with controls elucidating a possible implication of the modified gene in the pathogenic process leading to myocardial hypertrophy. This article summarizes the techniques necessary to induce left ventricular hypertrophy by aortic banding and to analyze the effects of this experimental model on hemodynamics, cardiac morphology, and gene expression of transgenic and control animals.

Animals↗
PubMed2006

Electrocardiography in the diagnosis of right ventricular hypertrophy in children.

OBJECTIVE: Although the electrocardiogram is commonly obtained in the evaluation of patients with pulmonary hypertension, its value as a screening test for right ventricular hypertrophy or pulmonary hypertension is unclear. Therefore, we sought to determine the value of an electrocardiogram in the diagnosis of right ventricular hypertrophy using echocardiography as the gold standard. METHODS: We identified children without congenital heart disease who underwent evaluation for suspected pulmonary hypertension that included both an electrocardiogram and echocardiography within a specified time frame. RESULTS: A total of 76 echocardiography-electrocardiogram pairs for pulmonary hypertension were identified. Although there was a significant relationship between electrocardiogram and echocardiography evidence of right ventricular hypertrophy, the sensitivity of an electrocardiogram in diagnosing echocardiography-documented right ventricular hypertrophy was only 69%, and the positive predictive value was 67%. There was no relationship between electrocardiogram changes and Doppler tricuspid regurgitation gradient. CONCLUSION: Despite a statistically significant relationship between an electrocardiogram and echocardiography in the diagnosis of right ventricular hypertrophy, an electrocardiogram has limited value as a screening tool for right ventricular hypertrophy because of its relatively low sensitivity and positive predictive value.

Adolescent↗
PubMed2000

Reactive oxygen species stimulate p44/42 mitogen-activated protein kinase and induce p27(Kip1): role in angiotensin II-mediated hypertrophy of proximal tubular cells.

Angiotensin II (AngII) induces G(1) phase arrest and hypertrophy of cultured renal proximal tubular cells. In previous studies, it was shown that these effects depend on oxygen radical-mediated induction of p27(Kip1), an inhibitor of cyclin-dependent kinases. The present study was undertaken to investigate whether mitogen-activated protein (MAP) kinases serve as signaling intermediates between AngII-induced oxidative stress and induction of p27(Kip1). AngII (10(-7) M) induces a biphasic phosphorylation pattern of p44/42 MAP kinase with an early phosphorylation after 2 min and a later, second phosphorylation peak after prolong incubation (12 h) in cultured proximal tubular cells from two different species (MCT and LLC-PK(1) cells). Total protein expression of MAP kinase was not changed by AngII. These phosphorylation patterns of p44/42 MAP kinase caused activation of the enzyme, as detected by phosphorylated MAP substrate Elk-1 after immuno-precipitation of MAP kinase. Exogenous H(2)O(2) also stimulates a biphasic phosphorylation of p44/42 MAP kinase. The flavoprotein inhibitor diphenylene iodinium, as well as the antioxidant N-acetylcysteine, prevented AngII-induced p44/42 MAP kinase phosphorylation, indicating involvement of reactive oxygen species generated by membrane-bound NAD(P)H oxidase. The MAP kinase kinase inhibitor PD98059 completely inhibits AngII-induced p27(Kip1) expression and (3)[H]leucine incorporation into proteins as a previously established marker of cell hypertrophy. PD98059 did not attenuate AngII-stimulated intracellular synthesis of oxygen radicals. Transient transfection with p44/42 MAP kinase antisense, but not sense, phosphorothioate-modified oligonucleotides also prevented AngII-induced MAP kinase phosphorylation, p27(Kip1) expression, and cell hypertrophy. Furthermore, induction of p27(Kip1) by H(2)O(2) was also abolished in the presence of PD98059. Although AngII induces phosphorylation of the stress-activated p38 MAP kinase, inhibition of this enzyme with SB203580 failed to attenuate induced p27(Kip1) expression and hypertrophy. These data provide evidence that AngII- mediated oxygen stress leads to the phosphorylation of p44/42 MAP kinase in proximal tubular cells. Activation of this enzyme is essential for p27(Kip1) expression, G(1) phase arrest, and hypertrophy of proximal tubular cells. These findings may lead to new concepts concerning interference of the development of proximal tubular hypertrophy, which may eventually turn into a maladaptive process in vivo leading ultimately to tubular atrophy and tubulointerstitial fibrosis.

Angiotensin II↗
PubMed1996

Focal glomerulosclerosis and maximal glomerular hypertrophy in human nephronopenia.

This study examines the relationship of the degree of glomerular hypertrophy in nephronopenia to the development of focal segmental glomerulosclerosis (FGS) in humans. To this end, group mean glomerular diameters in a variety of acquired and congenital nephronopenic states in native kidneys and long-surviving renal allografts with and without FGS were analyzed and compared. The results indicate that all groups of native nephronopenic kidneys without FGS develop significant and equivalent glomerular hypertrophy. By contrast, long-surviving renal allografts without FGS do not undergo glomerular hypertrophy. For groups with FGS, long-surviving renal homografts had a significantly smaller mean glomerular diameter when compared with any other group of native nephronopenic kidneys. There was no significant difference among group mean glomerular diameters of native nephronopenic kidneys with FGS. Pairwise comparisons in each category of nephronopenia indicated that, except in the groups with uninephrectomy, the mean glomerular diameters were significantly larger in those with FGS than without. These observations are interpreted to indicate that nephronopenic individuals with native kidneys, by undergoing glomerular hypertrophy, consume much or all their capacity for glomerular enlargement. This brings them closer to their maximal diameters at which FGS develops. Finally, long-surviving renal allografts without nephronopenic FGS do not undergo glomerular hypertrophy. However, when FGS develops in long-surviving allografts, it does so at glomerular diameters significantly smaller than in native nephronopenic kidneys, reflecting their decreased capacity to undergo glomerular hypertrophy, acquiring maximal diameters at a smaller dimension than native nephronopenic kidneys.

Adolescent↗
PubMed1996

Role of lysosomal cathepsin activities in cell hypertrophy induced by NH4Cl in cultured renal proximal tubule cells.

An increase of renal ammoniagenesis has been implicated in renal hypertrophy associated with various clinical disorders such as metabolic acidosis, diabetic nephropathy, and renal insufficiency. In vivo and in vitro studies have shown that ammonia promotes hypertrophy in tubular epithelial cells. To elucidate its role on protein turnover, the effects of NH4Cl on the activities of cathepsins B, H, and L+B, as well as on protein synthesis and degradation in LLC-PK1 cells, were investigated. The results show that NH4Cl (20 mM) induced cell hypertrophy, as defined by an increase in both cell protein content and cell volume (+25.5 +/- 1.3 and +10.4 +/- 0.1% after 48 h). This hypertrophy was associated with the suppression of the activities of cathepsins B and L+B (-57.0 +/- 0.9 and -54.5 +/- 1.5% after 48 h) and a reduction of protein degradation rate (-59.7 +/- 4.1% after 48 h), but without enhanced protein synthesis. The findings were further supported with an additional experiment, showing that the protein synthesis inhibitor cycloheximide (10 microM) did not blunt NH4Cl-induced cell hypertrophy. Moreover, NH4Cl (20 mM) resulted in a persistent elevation of the lysosomal pH, whereas the rise in the cytosolic pH was only transient. This alkalinization in lysosomes may be causatively involved in the impairment of the activities of cathepsins B and L+B. In conclusion, the suppression of the activities of cathepsins B and L+B and the subsequent reduction of protein breakdown due to intralysosomal alkalinization contribute to NH4Cl-induced hypertrophy in LLC-PK1 cells.

Ammonium Chloride↗
PubMed2005

Hypertrophy of ligamentum flavum in lumbar spinal stenosis associated with increased proteinase inhibitor concentration.

BACKGROUND: It is well known that age-related fibrosis, or decreases in the elastin-to-collagen ratio of the ligamentum flavum, along with hypertrophy of the ligamentum flavum, are associated with lumbar spinal stenosis. However, the molecular mechanism by which this fibrosis and hypertrophy develop is unknown. Tissue inhibitors of matrix metalloproteinase (TIMPs) are proteinase inhibitors that suppress extracellular matrix degradation. Elevated TIMP-1 and TIMP-2 expression has been implicated in various fibrotic diseases of the liver, kidney, lung, and heart. These TIMPs can also induce cellular proliferation and inhibit apoptosis in a wide range of cell types. These findings led us to postulate that TIMP-1 and TIMP-2 might also be associated with hypertrophy and fibrosis of the ligamentum flavum in lumbar spinal stenosis. METHODS: We quantified and localized TIMP expression in ligamentum flavum tissues that had been obtained during surgery from thirty patients with spinal stenosis and from thirty gender-matched control patients with disc herniation. The thickness of the ligamentum flavum at the level of the facet joint was measured on axial T1-weighted magnetic resonance images. In addition, we examined ligamentum flavum tissues for the expression of markers of cellular proliferation and apoptosis. RESULTS: The ligamentum flavum was significantly thicker in the patients with spinal stenosis (mean, 5.68 mm) than in the patients with disc herniation (mean, 2.70 mm) (p < 0.001). The concentration of TIMP-2 in the ligamentum flavum was significantly higher in the patients with spinal stenosis (mean, 12.62 ng/mL) than in those with disc herniation (mean, 8.85 ng/mL) (p = 0.028). TIMP-1 and TIMP-2 were detected in the cytoplasm of ligamentum flavum fibroblasts. TIMP-1 and TIMP-2 concentrations were associated with hypertrophy of the ligamentum flavum (p = 0.015 and p = 0.003, respectively). None of the samples from the patients with stenosis had evidence of proliferation of ligamentum flavum fibroblasts. The expression of markers for apoptosis was significantly higher in the patients with spinal stenosis (58.8%) than in those with disc herniation (26.6%) (p < 0.001). CONCLUSIONS: Increased TIMP expression has been implicated in fibrosis and hypertrophy of the extracellular matrix of several organs. Our results suggest that increased expression of TIMP-2 in ligamentum flavum fibroblasts is associated with fibrosis and hypertrophy of the ligamentum flavum in patients with spinal stenosis.

Aged↗
PubMed2005

Intracardiac basic fibroblast growth factor and transforming growth factor-beta 1 mRNA and their proteins expression level in patients with pressure or volume-overload right or left ventricular hypertrophy.

OBJECTIVES: The aim of the study was to investigate the pathogenic role of intracardiac basic fibroblast growth factor (bFGF) and transforming growth factor beta-1 (TGF beta-1) mRNA and their protein expression level in patients with ventricular volume or pressure-overload. BACKGROUND: Myocardial hypertrophy is responsiveness of cardiomyocytes and interstitial cells to ventricular stress produced by ventricular preload or/and afterload and a series of growth factors. However, the molecular mechanism by which the changes of bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload lead to distinct forms of cardiac hypertrophy is unclear. METHODS: 32 patients were divided into two groups: 16 patients with cardiac volume overload leading to left ventricular hypertrophy (VG) and 16 patients with pressure overload leading to right ventricular hypertrophy (PG), respectively, as compared with 5 unexpected deaths of noncardiac disease (CG), which is determinated by echocardiography and/or pathologic examination following operation; intracardiac bFGF and TGF beta-1 mRNA and their protein expression level were determined by immunohistochemistry and in situ hybridization as well as image analysis; cardiomyocytes and fibril collagen of type I and III were examined by haemotoxylin and eosin (HE) staining or sirius-red staining. RESULTS: Cardiocyte transverse diameter and fibril collagen of extracellular matrix, intracardiac bFGF and TGF beta-1 mRNA and their protein expression level in patients with volume or pressure-overload were significantly increased in both VG and PG, as compared with CG. CONCLUSION: This is the first paper to suggest that intracardiac bFGF and TGF beta-1 play a pivotal role in patients with pressure or volume-overload leading to right or left ventricular hypertrophy, composed of cardiomyocyte hypertrophy and extracellular matrix proliferation.

Adolescent↗
PubMed1992

Does a reduction in left ventricular hypertrophy reduce cardiovascular morbidity and mortality?

Left ventricular hypertrophy is an important risk factor for sudden death and other cardiovascular morbidity and mortality irrespective of the level of arterial blood pressure. Left ventricular hypertrophy, i.e. an increase in wall thickness at the expense of left ventricular volume, is an adaptive mechanism observed in patients with long standing arterial hypertension. Severe left ventricular hypertrophy is associated with a reduction in left ventricular compliance, impaired coronary reserve, ventricular ectopy, and impaired contractile function. Left ventricular hypertrophy can be reduced by antihypertensive therapy; however, not all antihypertensive agents have the same effect on left ventricular hypertrophy despite their similar effects on arterial blood pressure. Angiotensin converting enzyme (ACE) inhibitors appear to be the most powerful agents for reducing left ventricular hypertrophy, followed by the nondihydropyridine calcium antagonists. In addition to reducing left ventricular mass and arterial blood pressure, certain calcium antagonists also improve left ventricular filling, suppress ventricular ectopy, and maintain or enhance contractile function. However, despite these beneficial effects, it is not known whether the risk of cardiovascular morbidity and mortality can be prevented or reduced by specific antihypertensive agents.

Cardiovascular Diseases↗
PubMed2002

Resistance training and cardiac hypertrophy: unravelling the training effect.

Resistance training (RT) is a popular method of conditioning to enhance sport performance as well as an effective form of exercise to attenuate the age-mediated decline in muscle strength and mass. Although the benefits of RT on skeletal muscle morphology and function are well established, its effect on left ventricular (LV) morphology remains equivocal. Some investigations have found that RT is associated with an obligatory increase in LV wall thickness and mass with minimal alteration in LV internal cavity dimension, an effect called concentric hypertrophy. However, others report that short- (<5 years) to long-term (>18 years) RT does not alter LV morphology, arguing that concentric hypertrophy is not an obligatory adaptation secondary to this form of exertion. This disparity between studies on whether RT consistently results in cardiac hypertrophy could be caused by: (i) acute cardiopulmonary mechanisms that minimise the increase in transmural pressure (i.e. ventricular pressure minus intrathoracic pressure) and LV wall stress during exercise; (ii) the underlying use of anabolic steroids by the athletes; or (iii) the specific type of RT performed. We propose that when LV geometry is altered after RT, the pattern is usually concentric hypertrophy in Olympic weightlifters. However, the pattern of eccentric hypertrophy (increased LV mass secondary to an increase in diastolic internal cavity dimension and wall thickness) is not uncommon in bodybuilders. Of particular interest, nearly 40% of all RT athletes have normal LV geometry, and these athletes are typically powerlifters. RT athletes who use anabolic steroids have been shown to have significantly higher LV mass compared with drug-free sport-matched athletes. This brief review will sort out some of the factors that may affect the acute and chronic outcome of RT on LV morphology. In addition, a conceptual framework is offered to help explain why cardiac hypertrophy is not always found in RT athletes.

Adaptation, Physiological↗
PubMedDate not supplied

The relationship of blood pressure to cardiac hypertrophy: experimental studies in rats.

Cardiac hypertrophy is an independent predictor of morbidity and mortality. The exact relationship between blood pressure, hormones and cardiac hypertrophy is unclear. This study was undertaken to determine if intermittent elevation of blood pressure could cause left ventricular hypertrophy. Blood pressure was elevated intermittently by intraperitoneal injections of angiotensin II, noradrenalin and methoxamine. Blood pressure was acutely elevated by 60 mmHg or more for periods lasting up to 1 hour on up to 4 occasions each day. Cardiac index was measured 2 and 4 weeks after the experiment started. The cardiac index was increased by all procedures. The results were complicated by a retardation of growth in some experimental groups, meaning that the cardiac weight did not increase though the index did. In a study looking at the interaction of sodium and angiotensin II high sodium intake caused left ventricular hypertrophy and injections of angiotensin II caused further left ventricular hypertrophy. This study indicated that acute intermittent elevation of blood pressure could cause left ventricular hypertrophy and suggests that wall stress rather than 24 hour workload is the important triggering mechanism.

Angiotensin II↗
PubMed1999

Insulin-like growth factor (IGF-I) induces myotube hypertrophy associated with an increase in anaerobic glycolysis in a clonal skeletal-muscle cell model.

Insulin-like growth factor-I (IGF-I) is an important autocrine/paracrine mediator of skeletal-muscle growth and development. To develop a definitive cultured cell model of skeletal-muscle hypertrophy, C2C12 cells were stably transfected with IGF-I and clonal lines developed and evaluated. Quantitative morphometric analysis showed that IGF-I-transfected myotubes had a larger area (2381+/-60 micrometer2 versus 1429+/-39 micrometer2; P<0.0001) and a greater maximum width (21.4+/-0.6 micrometer versus 13.9+/-0.3 micrometer; P<0.0001) than control C2C12 myotubes, independent of the number of cell nuclei per myotube. IGF-I-transfected myotubes had higher levels of protein synthesis but no difference in DNA synthesis when compared with control myotubes, indicating the development of hypertrophy rather than hyperplasia. Both lactate dehydrogenase and alanine aminotransferase activities were increased (3- and 5-fold respectively), and total lactate levels were higher (2.3-fold) in IGF-I-transfected compared with control myotubes, indicating an increase in anaerobic glycolysis in the hypertrophied myotubes. However, expression of genes involved in skeletal-muscle growth or hypertrophy in vivo, e.g. myocyte nuclear factor and myostatin, was not altered in the IGF-I myotubes. Finally, myotube hypertrophy could also be induced by treatment of C2C12 cells with recombinant IGF-I or by growing C2C12 cells in conditioned media from IGF-I-transfected cells. This quantitative model should be uniquely useful for elucidating the molecular mechanisms of skeletal-muscle hypertrophy.

Animals↗
PubMed1999

Papillary hypertrophy of the upper tarsal conjunctiva during contact lens wear: a 4-month study with ethyl-6-O-decanoyl-glucoside.

PURPOSE: We studied the potential effect of ethyl-6-O-decanoyl-glucoside (EDG) on papillary hypertrophy in contact lens wearers who were recruited on the basis of papillary hypertrophy and a long history of contact lens wear. The contact lens care solutions were 0.00025% chlorhexidine acetate (CHX) with or without 0.005% EDG. METHODS: Nineteen subjects wearing both ionic and non-ionic contact lenses for 6-18 hours used either CHX or CHX+EDG as a cleaning and disinfecting agent. CHX and CHX+EDG was used simultaneously by each subject but in different eyes during two consecutive periods of 8 weeks. Symptoms and signs were recorded at three examinations during the study. The protein content of contact lenses and tryptase activity of tear fluids were measured. RESULTS: The degree of papillary hypertrophy did not decrease in either the CHX or CHX+EDG groups. Also, there were no differences in protein content of lenses nor tryptase activity of tear fluids in either group. There was a significant correlation between papillary hypertrophy and tryptase activity during the study. CONCLUSIONS: Despite the earlier finding that EDG prevents development of papillary hypertrophy in contact lens wearers, EDG still cannot reverse established signs of papillary hypertrophy.

Adult↗
PubMed2000

Treatment with lansoprazole also induces hypertrophy of the parietal cells of the stomach.

The aim of the present study was to investigate whether not only omeprazole but also lansoprazole leads to hypertrophy of the parietal cells of the gastric mucosa. We investigated the gastric mucosa of 295 patients with gastro-esophageal reflux disease prior to therapy, after 8 weeks of treatment with 30 mg lansoprazole/day, and after 6 and 12 months of long-term treatment with 15 or 30 mg lansoprazole, or 20 mg omeprazole/day. In a small group of 48 patients, a follow-up examination was carried out 3 months after termination of the study. Following acute treatment with 30 mg lansoprazole/day, 84% of the patients revealed parietal cell hypertrophy, while under long-term treatment this figure rose to 89%. The grade of the parietal cell hypertrophy increased continuously under long-term treatment. With regard to the incidence and grading of parietal cell hypertrophy, no significant differences were found among the three groups receiving long-term treatment. Three months after termination of treatment with these proton-pump inhibitors, the hypertrophy of the parietal cells had largely disappeared again. This study shows that hypertrophy of the parietal cells in the gastric mucosa occurs not only under treatment with omeprazole, but also under therapy with lansoprazole, and is reversible when the proton pump inhibitors are discontinued.

2-Pyridinylmethylsulfinylbenzimidazoles↗
PubMed2000

Comparison of electrocardiographic criteria for diagnosis of left ventricular hypertrophy in hypertension: the MAVI study.

BACKGROUND: Standard electrocardiography (ECG) is a specific, but poorly sensitive tool for diagnosis of left ventricular (LV) hypertrophy. In a large population of subjects with hypertension we tested some standard ECG criteria in their sensitivity and specificity for LV hypertrophy. LV mass at echocardiography was the reference standard. METHODS: In the setting of the MAVI (MAssa Ventricolare sinistra nel soggetto Iperteso) study, the ECG and echocardiographic tracings of 947 hypertensive subjects were read blindly in a central office. RESULTS: Prevalence of LV hypertrophy at ECG was 0.6, 3.0, 4.8, 7.1, 11.1, 11.9 and 18.4%, respectively, using the following criteria: Wilson, typical strain, Romhilt-Estes score > or = 5 points, Gubner-Ungerleider, Sokolow-Lyon, Cornell voltage (S(V3)+R(avL) > 2.8 mV in men or 2.0 mV in women) and Perugia score (positivity of at least one of the following: S(V3)+R(aVL) > 2.4 mV in men or > 2.0 mV in women, a typical strain pattern, or a Romhilt-Estes point score >or = 5). Prevalence of LV hypertrophy at echocardiography ranged from 27.2% (LV mass > 125 g/m2) to 49.9% (LV mass > 51.0 g/m2.7). Using the latter gold standard, sensitivity and specificity of the above ECG criteria were 0.8 and 99.6% (Wilson), 3.8 and 97.9% (strain), 5.9 and 96.4% (Romhilt-Estes), 9.7 and 95.6% (Gubner-Ungerleider), 11.2 and 91.1% (Sokolow-Lyon), 15.2 and 91.4% (Cornell), and 22.2 and 85.4% (Perugia score). CONCLUSIONS: Sensitivity of traditional ECG criteria for LV hypertrophy in subjects with hypertension is poor. However, the combination of three highly specific criteria (Romhilt-Estes, LV strain and Cornell) in a cumulative score produces a rise in sensitivity without excessive deterioration of specificity, with a prevalence of LV hypertrophy at ECG of 18.4%. Traditional interpretation of ECG is valuable and should be reconsidered in the clinical work-up of subjects with hypertension.

Aged↗