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Wall Stress (wall + stress)

Distribution by Scientific Domains
Medical Sciences90%

Kinds of Wall Stress

  • circumferential wall stress
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    Selected Abstracts

    Effects of Wall Stress on the Dynamics of Ventricular Fibrillation: A Simulation Study Using a Dynamic Mechanoelectric Model of Ventricular Tissue

    JOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008
    SATOKO HIRABAYASHI master of environment
    Introduction: To investigate the mechanisms underlying the increased prevalence of ventricular fibrillation (VF) in the mechanically compromised heart, we developed a fully coupled electromechanical model of the human ventricular myocardium. Methods and Results: The model formulated the biophysics of specific ionic currents, excitation,contraction coupling, anisotropic nonlinear deformation of the myocardium, and mechanoelectric feedback (MEF) through stretch-activated channels. Our model suggests that sustained stretches shorten the action potential duration (APD) and flatten the electrical restitution curve, whereas stretches applied at the wavefront prolong the APD. Using this model, we examined the effects of mechanical stresses on the dynamics of spiral reentry. The strain distribution during spiral reentry was complex, and a high strain-gradient region was located in the core of the spiral wave. The wavefront around the core was highly stretched, even at lower pressures, resulting in prolongation of the APD and extension of the refractory area in the wavetail. As the left ventricular pressure increased, the stretched area became wider and the refractory area was further extended. The extended refractory area in the wavetail facilitated the wave breakup and meandering of tips through interactions between the wavefront and wavetail. Conclusions: This simulation study indicates that mechanical loading promotes meandering and wave breaks of spiral reentry through MEF. Mechanical loading under pathological conditions may contribute to the maintenance of VF through these mechanisms. [source]

    An Echocardiographic Analysis of the Long-Term Effects of Carvedilol on Left Ventricular Remodeling, Systolic Performance, and Ventricular Filling Patterns in Dilated Cardiomyopathy

    ECHOCARDIOGRAPHY, Issue 7 2005
    Peter S. Rahko M.D.
    Background: The long-term clinical benefit of beta blockade is well recognized, but data quantifying long-term effects of beta blockade on remodeling of the left ventricle (LV) is limited. Methods: This consecutive series evaluates the long-term response of the LV to the addition of carvedilol to conventional therapy for dilated cardiomyopathy. There were 33 patients who had a LV ejection fraction <45%, LV enlargement and symptomatic heart failure. Quantitative Doppler echocardiography was performed at baseline 6, 12, 24, and 36 months after initiation of carvedilol to evaluate LV ejection fraction, LV volume, wall stress, mass, regional function, and diastolic performance. Results: Compared to baseline there was a significant and sustained reduction in end-systolic volume and end-systolic wall stress with a corresponding improvement in LV ejection fraction. The LV mass did not decline but relative wall thickness increased toward normal. An analysis of regional wall motion responses showed an improvement in all areas, particularly the apical, septal, and lateral walls that was significantly more frequent in patients with a nonischemic etiology. Filling patterns of the LV remained abnormal throughout the study but changed with therapy suggesting a decline in filling pressures. These changes were sustained for 3 years. Conclusion: (1) The addition of carvedilol to conventional therapy for a dilated cardiomyopathy significantly improves LV ejection fraction and reduces LV end-systolic volume and wall stress for at least 3 years, (2) the response to 6 months of treatment predicts the long-term response, (3) the typical response is partial improvement of the LV, complete return to normal size, and function is uncommon, and (4) abnormalities of LV filling persist in virtually all patients throughout the course of treatment. [source]

    Acute Cardiac Effects of Nicotine in Healthy Young Adults

    ECHOCARDIOGRAPHY, Issue 6 2002
    Catherine D. Jolma M.D.
    Background: Nicotine is known to have many physiologic effects. The influence of nicotine delivered in chewing gum upon cardiac hemodynamics and conduction has not been well-characterized. Methods: We studied the effects of nicotine in nonsmoking adults (6 male, 5 female; ages 23,36 years) using a double-blind, randomized, cross-over study. Subjects chewed nicotine gum (4 mg) or placebo. After 20 minutes (approximate time to peak nicotine levels), echocardiograms and signal-averaged electrocardiograms (SAECG) were obtained. After 40 minutes, subjects were again given nicotine gum or placebo in cross-over fashion. Standard echocardiographic measurements were made from two-dimensional images. We then calculated end-systolic wall stress (ESWS), shortening fraction (SF), systemic vascular resistance (SVR), velocity for circumferential fiber shortening corrected for heart rate (Vcfc), stroke volume, and cardiac output. P wave and QRS duration were measured from SAECG. Results: Significant differences (P < 0.05) from control or placebo were found for ESWS, mean blood pressure, cardiac output, SVR, heart rate, and P wave duration. No significant changes were seen in left ventricular ejection time (LVET), LV dimensions, SF, contractility (Vcfc), or QRS duration. Conclusions: These results suggest that nicotine chewing gum increases afterload and cardiac output. Cardiac contractility does not change acutely in response to nicotine gum. Heart rate and P wave duration are increased by chewing nicotine gum. [source]

    Cardiovascular risk factors and collateral artery formation

    EUROPEAN JOURNAL OF CLINICAL INVESTIGATION, Issue 12 2009
    D. De Groot
    Abstract Arterial lumen narrowing and vascular occlusion is the actual cause of morbidity and mortality in atherosclerotic disease. Collateral artery formation (arteriogenesis) refers to an active remodelling of non-functional vascular anastomoses to functional collateral arteries, capable to bypass the site of obstruction and preserve the tissue that is jeopardized by ischaemia. Hemodynamic forces such as shear stress and wall stress play a pivotal role in collateral artery formation, accompanied by the expression of various cytokines and invasion of circulating leucocytes. Arteriogenesis hence represents an important compensatory mechanism for atherosclerotic vessel occlusion. As arteriogenesis mostly occurs when lumen narrowing by atherosclerotic plaques takes place, presence of cardiovascular risk factors (e.g. hypertension, hypercholesterolaemia and diabetes) is highly likely. Risk factors for atherosclerotic disease affect collateral artery growth directly and indirectly by altering hemodynamic forces or influencing cellular function and proliferation. Adequate collateralization varies significantly among atherosclerotic patients, some profit from the presence of extensive collateral networks, whereas others do not. Cardiovascular risk factors could increase the risk of adverse cardiovascular events in certain patients because of the reduced protection through an alternative vascular network. Likewise, drugs primarily thought to control cardiovascular risk factors might contribute or counteract collateral artery growth. This review summarizes current knowledge on the influence of cardiovascular risk factors and the effects of cardiovascular medication on the development of collateral vessels in experimental and clinical studies. [source]

    Three-dimensional MRI assessment of regional wall stress after acute myocardial infarction predicts postdischarge cardiac events

    JOURNAL OF MAGNETIC RESONANCE IMAGING, Issue 3 2008
    Fabrice Prunier MD
    Abstract Purpose To determine the prognostic significance of systolic wall stress (SWS) after reperfused acute myocardial infarction (AMI) using MRI. Materials and Methods A total of 105 patients underwent MRI 7.8 ± 4.2 days after AMI reperfusion. SWS was calculated by using a three-dimensional (3D) MRI approach to left ventricular (LV) wall thickness and to the radius of curvature. Between hospital discharge and the end of follow-up, an average of 4.1 ± 1.7 years after AMI, 19 patients experienced a major cardiac event, including cardiac death, nonfatal reinfarction or heart failure (18.3%). Results The results were mainly driven by heart failure outcome. In univariate analysis the following factors were predictive of postdischarge major adverse cardiac events: 1) at the time of AMI: higher heart rate, previous calcium antagonist treatment, in-hospital congestive heart failure, proximal left anterior descending artery (LAD) occlusion, a lower ejection fraction, higher maximal ST segment elevation before reperfusion, and ST segment reduction lower than 50% after reperfusion; 2) MRI parameters: higher LV end-systolic volume, lower ejection fraction, higher global SWS, higher SWS in the infarcted area (SWS MI) and higher SWS in the remote myocardium (SWS remote). In the final multivariate model, only SWS MI (odds ratio [OR]: 1.62; 95% confidence interval [CI]: 1.01,2.60; P = 0.046) and SWS remote (OR: 2.17; 95% CI: 1.02,4.65; P = 0.046) were independent predictors. Conclusion Regional SWS assessed by means of MRI a few days after AMI appears to be strong predictor of postdischarge cardiac events, identifying a subset of at risk patients who could qualify for more aggressive management. J. Magn. Reson. Imaging 2008. © 2008 Wiley-Liss, Inc. [source]

    A Theoretical Model for the Myogenic Response Based on the Length,Tension Characteristics of Vascular Smooth Muscle

    MICROCIRCULATION, Issue 4 2005
    BRIAN E. CARLSON
    ABSTRACT Objective: A theoretical model is developed to describe the myogenic response of resistance vessels to changes in intravascular pressure, based on a consideration of the active and passive length,tension characteristics of vascular smooth muscle (VSM). The dependence of model parameters on vessel diameter is examined. Methods: The vessel wall is represented mechanically as a nonlinear passive component in parallel with an active contractile component. The level of VSM tone is assumed to have a sigmoidal dependence on circumferential wall tension or stress. Model parameters are optimized for each of 18 independent experimental data sets previously obtained using pressure or wire myograph systems. Results: Close fits between model predictions and experimental data are found in each case. An alternative formulation in which VSM tone depends on circumferential wall stress is found also to be consistent with available data. Significant trends in model parameters as a function of diameter are found. Conclusions: The results support the hypothesis that circumferential tension or stress in the wall provides the signal for myogenic responses. The model provides a basis for simulating steady-state myogenic responses in vascular networks containing a range of vessel diameters. [source]

    Effects of intra-abdominal CO2 -insufflation on normal and impaired myocardial function: an experimental study

    ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 6 2003
    C. A. Greim
    Background:, Intra-abdominal pressure (IAP) elevation during CO2 -pneumoperitoneum increases cardiac afterload and may enhance dysfunction of the already compromized heart. This study focused on the effects of acute IAP increases on left and right ventricular loadings and contractility in the heart with impaired global function. Methods:, Impairment of myocardial function (IMF) was pharmacologically induced in 16 pigs by administration of halothane and propranolol, while baseline arterial pressure was maintained by intravenous phenylephrine. Intra-abdominal pressure was gradually increased by 10 mmHg up to 30 mmHg in the supine position (IMF group 1, n = 8) or in a head-down tilted position (IMF group 2, n = 8). In two control groups with normal myocardial function, IAP was also increased in the supine position or the head-down tilted position. Cardiac function in all groups was assessed by epicardial echocardiography, intraventricular pressure measurements and pulmonary artery catheterization. Results:, The increase in IAP was accompanied by a transient rise in LV end-systolic wall stress and reduced cardiac output significantly by 16,24% in all groups. In the IMF groups, LV end-diastolic transmural pressure increased by 34,60% to peak values of 24 mmHg, while cross-sectional LV end-diastolic areas remained unchanged. Increases in right ventricular end-diastolic volume and decreases in right ventricular ejection fraction as well as in cardiac output were most pronounced at IAP 20 mmHg and significantly stronger in both IMF groups than in the control groups (P < 0.001). Conclusion:, Following the acute elevation of IAP, the right ventricular volume load shifted more extensively in the IMF groups than in the animals with normal myocardial function. Myocardial function in the impaired heart may worsen during IAP elevation due to right ventricular load alterations rather than a LV afterload increase. [source]

    Antibiotics that inhibit cell wall biosynthesis induce expression of the Bacillus subtilis,W and ,M regulons

    MOLECULAR MICROBIOLOGY, Issue 5 2002
    Min Cao
    Summary Bacillus subtilis encodes seven extracytoplasmic function (ECF) sigma factors. The ,W regulon includes functions involved in detoxification and protection against antimicrobials, whereas ,M is essential for growth at high salt concentrations. We now report that antibiotics that inhibit cell wall biosynthesis induce both ,W and ,M regulons as monitored using DNA microarrays. Induction of selected ,W -dependent genes was confirmed using lacZ reporter fusions and Northern blot analysis. The ability of vancomycin to induce the ,W regulon is dependent on both ,W and the cognate anti- , , RsiW, but is independent of the transition state regulator AbrB. These results suggest that the membrane-localized RsiW anti- ,W factor mediates the transcriptional response to cell wall stress. Our findings are consistent with the idea that one function of ECF , factors is to coordinate antibiosis stress responses and cell envelope homeostasis. [source]

    B-type natriuretic peptide as a marker for cardiac dysfunction in anthracycline-treated children

    PEDIATRIC BLOOD & CANCER, Issue 6 2007
    Sanjeev Aggarwal MD
    Abstract Background Anthracyclines (AC) are useful antineoplastic agents, whose utility is limited by progressive cardiotoxicity. Our purpose was to evaluate plasma B-type natriuretic peptide (BNP), as a screening test for detecting late cardiac dysfunction in AC-treated children and to determine the prevalence of late cardiac dysfunction at low cumulative AC doses. Materials and Methods This was a prospective study in which patients who had completed AC therapy at least 1 year earlier, underwent a detailed echocardiogram and a simultaneous BNP level. Cardiac dysfunction was defined as any one of the following: shortening fraction (FS) <29%, rate corrected velocity of circumferential fiber shortening (VCFc) <0.9 c·sec,1, end systolic wall stress (ESWS) >60 g·cm,2, abnormal VCFc: ESWS ratio or decreased mitral inflow velocity (E/A) ratios, compared to age-specific norms. Results The cohort (n,=,63) included 37 males with a median age of 13.1 years (range, 6.5,26.5 years). Cardiac dysfunction was found in 26 (41%) patients and in 40% of patients who received cumulative doses <150 mg·m,2. ESWS was the most common abnormality. Mean BNP levels in the subset with abnormal function were significantly higher than the normal group (23.4,±,25.3 vs. 14.2,±,8.9 pg·ml,1, P,=,0.02). Conclusions Plasma BNP was significantly elevated in AC-treated patients with late cardiac dysfunction, although there was considerable overlap of levels between groups with and without cardiac dysfunction. BNP may need further evaluation as a serial index of cardiac function in this population. Cardiac dysfunction was observed in a significant proportion of patients, even at low cumulative AC doses. Pediatr Blood Cancer 2007;49:812,816. © 2006 Wiley-Liss, Inc. [source]

    Operative contractility: A functional concept of the inotropic state

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 10 2005
    Roberto Curiel
    SUMMARY 1.,Initial unsuccessful attempts to evaluate ventricular function in terms of the ,heart as a pump' led to focusing on the ,heart as a muscle' and to the concept of myocardial contractility. However, no clinically ideal index exists to assess the contractile state. The aim of the present study was to develop a mathematical model to assess cardiac contractility. 2.,A tri-axial system was conceived for preload (PL), afterload (AL) and contractility, where stroke volume (SV) was represented as the volume of the tetrahedron. Based on this model, ,operative' contractility (,OperCon') was calculated from the readily measured values of PL, AL and SV. The model was tested retrospectively under a variety of different experimental and clinical conditions, in 71 studies in humans and 29 studies in dogs. A prospective echocardiographic study was performed in 143 consecutive subjects to evaluate the ability of the model to assess contractility when SV and PL were measured volumetrically (mL) or dimensionally (cm). 3.,With inotropic interventions, OperCon changes were comparable to those of ejection fraction (EF), velocity of shortening (Vcf) and dP/dt-max. Only with positive inotropic interventions did elastance (Ees) show significantly larger changes. With load manipulations, OperCon showed significantly smaller changes than EF and Ees and comparable changes to Vcf and dP/dt-max. Values of OperCon were similar when AL was represented by systolic blood pressure or wall stress and when volumetric or dimensional values were used. 4.,Operative contractility is a reliable, simple and versatile method to assess cardiac contractility. [source]

    COMPARISON OF ANGIOTENSIN II-INDUCED BLOOD PRESSURE AND STRUCTURAL CHANGES IN FISCHER 344 AND WISTAR KYOTO RATS

    CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2004
    Jocelyne Blanc
    SUMMARY 1.,The purpose of the present study was to evaluate the blood pressure (BP) response, the BP and heart rate (HR) components of the startle reaction and the structure of the carotid artery and the aorta during chronic infusion of angiotensin (Ang) II in Fischer 344 (F344) compared with Wistar Kyoto (WKY) rats, two in-bred normotensive contrasted strains. 2.,Osmotic mini-pumps filled with saline vehicle or AngII (120 ng/kg per min) were implanted subcutaneously in 8-week-old normotensive rats and infused for 4 weeks in F344 rats (saline, n = 10; AngII, n = 10) and WKY rats (saline, n = 10; AngII, n = 9). Basal BP, HR and the responses to an acoustic startle stimulus (duration 0.7 s, 115 dB) were recorded in conscious rats. The structure of the carotid artery and aorta was determined in 4% formaldehyde-fixed arteries. 3.,Compared with WKY rats, vehicle-treated F344 rats had lower bodyweight (BW; 266 ± 7 vs 299 ± 9 g; P < 0.05) and heart weight (0.80 ± 0.02 vs 0.98 ± 0.04 g; P < 0.05) and higher aortic systolic BP (SBP; 131 ± 1 vs 123 ± 5 mmHg; P < 0.001) and diastolic BP (98 ± 3 vs 89 ± 2 mmHg; P < 0.001). In F344 rats, compared with the WKY rats, the wall thickness/BW ratio was increased in the carotid artery (156 ± 9 vs 131 ± 6 nm/g; P < 0.05) and abdominal aorta (264 ± 13 vs 217 ± 12 nm/g; P < 0.05) and decreased in the thoracic aorta (246 ± 13 vs 275 ± 8 nm/g; P < 0.05). There was no difference in elastin and collagen density. Angiotensin II differentially enhanced BP in both strains: (SBP: 163 ± 5 and 132 ± 4 mmHg in F344 and WKY rats, respectively; Pstrain × treatment < 0.05). Circumferential wall stress was increased in the aorta of F344 rats compared with WKY rats (1176 ± 39 vs 956 ± 12 kPa (P < 0.001) and 1107 ± 42 vs 813 ± 12 kPa (P < 0.001) in thoracic and abdominal aortas, respectively). The startle response was amplified in F344 rats, with enhanced increases in SBP and pulse pressure (PP) and bradycardia compared with responses of WKY rats (+44 ± 9 mmHg, +10 ± 2 mmHg and ,40 ± 17 b.p.m., respectively, in F344 rats vs+28 ± 4 mmHg, + 4 ± 2 mmHg and ,19 ± 10 b.p.m. in WKY rats, respectively; Pstrain < 0.05 for BP and PP). The startle response was not affected by AngII. 4.,These results indicate a higher BP producing an increase in wall thickness in F344 rats compared with WKY rats. We propose that an increase in sympathetic nervous activity causes these haemodynamic differences, as suggested by the excessive increase in BP during an acoustic startle stimulus. Angiotensin II increased BP in F344 rats, but did not exaggerate the increase in BP during the startle reaction. [source]

    Phenotyping the Right Ventricle in Patients with Pulmonary Hypertension

    CLINICAL AND TRANSLATIONAL SCIENCE, Issue 4 2009
    M.S., Marc A. Simon M.D.
    Abstract Right ventricular (RV) failure is associated with poor outcomes in pulmonary hypertension (PH). We sought to phenotype the RV in PH patients with compensated and decompensated RV function by quantifying regional and global RV structural and functional changes. Twenty-two patients (age 51 ± 11, 14 females, mean pulmonary artery (PA) pressure range 13,79 mmHg) underwent right heart catheterization, echocardiography, and ECG-gated multislice computed tomography of the chest. Patients were divided into three groups: Normal, PH with hemodynamically compensated, and decompensated RV function (PH-C and PH-D, respectively). RV wall thickness (WT) was measured at end-diastole (ED) and end-systole (ES) in three regions: infundibulum, lateral free wall, and inferior free wall. Globally, RV volumes progressively increased from Normal to PH-C to PH-D and RV ejection fraction decreased. Regionally, WT increased and fractional wall thickening (FWT) decreased in a spatially heterogeneous manner. Infundibular wall stress was elevated and FWT was lower regardless of the status of global RV function. In PH, there are significant phenotypic abnormalities in the RV even in the absence of overt hemodynamic RV decompensation. Regional changes in RV structure and function may be early markers of patients at risk for developing RV failure. [source]

    Growth hormone, acromegaly, and heart failure: an intricate triangulation

    CLINICAL ENDOCRINOLOGY, Issue 6 2003
    Luigi Saccà
    Summary Short-term GH or IGF-I excess provides a model of physiological cardiac growth associated with functional advantage. The physiological nature of cardiac growth is accounted for by the following: (i) the increment in cardiomyocyte size occurs prevalently at expense of the short axis. This is the basis for the concentric pattern of left ventricular (LV) hypertrophy, with consequent fall in LV wall stress and functional improvement; (ii) cardiomyocyte growth is associated with improved contractility and relaxation, and a favourable energetic setting; (iii) the capillary density of the myocardial tissue is not affected; (iv) there is a balanced growth of cardiomyocytes and nonmyocyte elements, which accounts for the lack of interstitial fibrosis; (v) myocardial energetics and mechanics are not perturbed; and (vi) the growth response is not associated with the gene re-programming that characterizes pathologic cardiac hypertrophy and heart failure. Overall, the mechanisms activated by GH or IGF-I appear to be entirely different from those of chronic heart failure. Not to be neglected is also the fact that GH, through its nitric oxide (NO)-releasing action, contributes to the maintenance of normal vascular reactivity and peripheral vascular resistance. This particular kind of interaction of GH with the cardiovascular system accounts for: (i) the lack of cardiac impairment in short-term acromegaly; (ii) the beneficial effects of GH and IGF-I in various models of heart failure; (iii) the protective effect of GH and IGF-I against post-infarction ventricular remodelling; (iv) the reversal of endothelial dysfunction in patients with heart failure treated with GH; and (v) the cardiac abnormalities associated with GH deficiency and their correction after GH therapy. If it is clear that GH and IGF-I exert favourable effects on the heart in the short term, it is equally undeniable that GH excess with time causes pathologic cardiac hypertrophy and, if it is not corrected, eventually leads to cardiac failure. Why then, at one point in time in the natural history of acromegaly, does physiological cardiac growth become maladaptive and translate into heart failure? Before this transition takes places, the acromegalic heart shares very few features with other models of chronic heart failure. None of the mechanisms involved in the progression of heart failure is clearly operative in acromegaly, save for the presence of insulin-resistance and mild alterations of lipoproteins and clot factors. Is this enough to account for the development of heart failure? Probably not. On the other hand, it must be stressed that GH and IGF-I activate several mechanisms that play a protective role against the development of heart failure. These include ventricular unloading, deactivation of neurohormonal components, antiapoptotic effect and enhanced vascular reactivity. Ultimately, all data available concur to hypothesize that acromegalic cardiomyopathy represents a progressive model of cardiac hypertrophy in which the cardiotoxic and pro-remodelling effect is intrinsic to the excessive and unrestrained myocardial growth. [source]

    Relation of serum leptin and insulin-like growth factor-1 levels to intima-media thickness and functions of common carotid artery in children and adolescents with type 1 diabetes

    ACTA PAEDIATRICA, Issue 8 2004
    ME Atabek
    Background and aim: Leptin and insulin-like growth factor-1 (IGF-1) have been suggested to be involved in the pathogenesis of atherosclerosis. The aim of this study was to evaluate the relationship between serum leptin, IGF-1 and intima-media thickness (IMT) and functions of common carotid artery (CCA) in children and adolescent patients with type 1 diabetes. Material and methods: Serum leptin and IGF-1 levels were measured in 45 diabetic patients (23 girls and 22 boys). Age, diabetes duration as well as major cardiovascular risk factors, including anthropometric and metabolic parameters, were matched between girls and boys. The relation of serum leptin and IGF-1 levels to CCA structure and functions were measured by ultrasonography as IMT, cross-sectional compliance (CSC), cross-sectional distensibility (CSD), diastolic wall stress (DWS) and incremental elastic modulus (IEM). Results: Serum leptin levels of diabetic girls were higher than those in the boys (21.8 ± 14.5 ,g/1 vs 8.9 ± 10.6 ,.g/1, p= 0.002). However, the difference for serum IGF-1 levels was not significant between diabetic girls and boys (240.7 ± 96.8 ,g/ml vs 234.7 ± 93.2 ng/ml; p < 0.05). In all subjects, leptin levels were correlated with CSC (p= 0.04), CSD (p= 0.04) and IEM (p= 0.01), and IGF-I levels were only correlated with CSC (p= 0.01). Leptin did not show any correlation with ultrasonographic measurements in both girls and boys separately. IGF-1 was correlated with CSC (p= 0.001), CSD (p= 0.002) and IEM (p > 0.001) in boys but not in girls. In a multivariate regression model, IGF-1 emerged as independent correlates for mean CSD and IEM in boys but not in girls. Conclusion: Serum leptin and IGF-1 levels in children and adolescent patients with type 1 diabetes are associated with functions of common carotid artery, and the association of IGF-1 levels is influenced by sex. [source]

    Assessment of left ventricular systolic function using tissue Doppler imaging in children after successful repair of aortic coarctation

    CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 1 2010
    Tomasz Florianczyk
    Summary Aim:, Assessment of left ventricular systolic function in children after the successful repair of aortic coarctation using tissue Doppler imaging (TDI). Methods:, The study group consisted of 32 patients (mean age 12·0 ± 4·2 years) after the aortic coarctation repair. The TDI parameters and the conventional echocardiographic endocardial and midwall indices of the left ventricular systolic function were analysed and compared with the results obtained from 34 healthy children. Results:, The systolic mitral annulus motion velocity, systolic myocardial velocity of the medial segment of the left ventricular septal wall, left ventricular strain and Strain Rate (SR) in the study group were significantly higher than in the control group, respectively: 6·92 ± 0·75 cm s,1 versus 6·45 ± 0·83 cm s,1; 5·82 ± 1·03 cm s,1 versus 5·08 ± 1·11 cm s,1; ,28·67 ± 6·04% versus ,22·53 ± 6·44% and ,3·20 ± 0·76 s,1 versus ,2·39 ± 0·49 s,1. Except midwall shortening fraction the conventional endocardial and midwall echocardiographic indices in the study group were significantly higher in comparison to the healthy controls. The left ventricular systolic meridional fibre stress and end-systolic circumferential wall stress did not differ between the examined groups. There were no differences of the TDI or conventional parameters between hypertensive and normotensive patients. Conclusions:, Left ventricular systolic performance in children after the surgical repair of aortic coarctation reveals tendency to rise in late follow-up despite a satisfactory result after surgery. Higher systolic strain and SR in children treated due to coarctation of the aorta may suggest the increased preserved left ventricular performance despite normalization of afterload. [source]

    Physiological determinants of the variation in left ventricular mass from early adolescence to late adulthood in healthy subjects

    CLINICAL PHYSIOLOGY AND FUNCTIONAL IMAGING, Issue 4 2007
    Peter A. Cain
    Summary Background:, The physiological determinants of left ventricular mass (LVM) measured by cardiac magnetic resonance (CMR) imaging are not well defined as prior investigators have studied either adults or adolescents in isolation or have not strictly excluded hypertension or accounted for the effects of exercise habits, haemodynamic, demographic, or body shape characteristics. Methods:, Ninety-seven healthy volunteers (11,81 years, 51 males) underwent CMR. All parameters [unstandardized and adjusted for body surface area (BSA)] were analysed according to gender and by adolescence versus adulthood (adolescents <20 years, adults ,20 years). The influence of haemodynamic factors, exercise and demographic factors on LVM were determined with multivariate linear regression. Results:, Left ventricular mass rose during adolescence and declined in adulthood. LVM and LVMBSA were higher in males both in adults (LVM: 188 ± 22 versus 140 ± 21 g, P<0·001; LVMBSA: 94 ± 11 versus 80 ± 11 g m,2, P<0·001) and in adolescents when adjusted for BSA (LVM: 128 ± 29 versus 107 ± 20 g, P = 0·063; LVMBSA: 82 ± 8 versus 71 ± 10 g m,2, P = 0·025). In adults, systolic blood pressure (SBP) and self-reported physical activity increased while meridional and circumferential wall stress were constant with age. Multivariate regression analysis revealed age, gender and BSA as the major determinants of LVM (global R2 = 0·68). Conclusions:, Normal LVM shows variation over a broad age range in both genders with a rise in adolescence and subsequent decline with increasing age in adulthood despite an increase in SBP and physical activity. BSA, age and gender were found to be major contributors to the variation in LVM in healthy adults, while haemodynamic factors, exercise and wall stress were not. [source]

    Protein N-glycosylation determines functionality of the Saccharomyces cerevisiae cell wall integrity sensor Mid2p

    MOLECULAR MICROBIOLOGY, Issue 6 2008
    Franziska Hutzler
    Summary The fungal cell wall is a highly dynamic structure that is essential to maintain cell shape and stability. Hence in yeasts and fungi cell wall integrity is tightly controlled. The Saccharomyces cerevisiae plasma membrane protein Mid2p is a putative mechanosensor that responds to cell wall stresses and morphological changes during pheromone induction. The extracellular domain of Mid2p, which is crucial to sensing, is highly O- and N-glycosylated. We showed that O-mannosylation is determining stability of Mid2p. If and how N-glycosylation is linked to Mid2p function was unknown. Here we demonstrate that Mid2p contains a single high mannose N-linked glycan at position Asn-35. The N -glycan is located close to the N-terminus and is exposed from the plasma membrane towards the cell wall through a highly O-mannosylated domain that is predicted to adopt a rod-like conformation. In contrast to O-mannosylation, lack of the N-linked glycan affects neither, stability of Mid2p nor distribution at the plasma membrane during vegetative and sexual growth. However, non-N-glycosylated Mid2p fails to perceive cell wall challenges. Our data further demonstrate that both the extent of the N-linked glycan and its distance from the plasma membrane affect Mid2p function, suggesting the N -glycan to be directly involved in Mid2p sensing. [source]