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Hypertrophy
Kinds of Hypertrophy Selected AbstractsEPIGALLOCATECHIN-3-GALLATE ATTENUATES CARDIAC HYPERTROPHY IN HYPERTENSIVE RATS IN PART BY MODULATION OF MITOGEN-ACTIVATED PROTEIN KINASE SIGNALSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2009Dan-Dan Chen SUMMARY 1It has been demonstrated that epigallocatechin-3-gallate (EGCG) inhibits cardiac hypertrophy through its antihypertensive and anti-oxidant effects. However, the underlying molecular mechanism is not clear. 2In the present study, we tested the hypothesis that EGCG attenuates transaortic abdominal aortic constriction (TAC)-induced ventricular hypertrophy by regulating mitogen-activated protein kinase (MAPK) signal pathways in hypertensive rats. Four groups of rats were used: (i) a sham-operated control group; (ii) an EGCG-treated (50 mg/kg per day, i.p., for 21 days) sham-operated group; (iii) a TAC group; and (iv) an EGCG-treated TAC group. Histological analysis of whole hearts and biochemical analyses of left ventricular (LV) tissue were used to investigate the effects of EGCG. 3The results showed that the LV myocyte diameter and the expression of atrial natriuretic peptide, brain natriuretic peptide and ,-myocardial heavy chain were significantly decreased in the EGCG-treated (50 mg/kg per day, i.p.) TAC group. Levels of reactive oxygen species and malondialdehyde in the lV were significantly reduced by EGCG in the TAC group. Total superoxide dismutase, catalase and glutathione peroxidase activities were decreased in the TAC group, and this decrease was significantly restored by EGCG treatment. Phosphorylation of extracellular signal-regulated kinase 2, p38 and c-Jun N-terminal kinase 1 was significantly reversed in the LV of EGCG-treated TAC rats (40%, 53% and 52%vs TAC, respectively), accompanied by significant inhibition of nuclear factor-,B and activator protein-1. Transaortic abdominal aortic constriction significantly upregulated LV expression of matrix metalloproteinase-9 from 32 ± 6 to 100 ± 12% and this increase was inhibited by EGCG treatment (from 100 ± 12 to 50 ± 15%). In addition, TAC decreased mitochondrial DNA copy number and the activity of respiratory chain complexes I (from 100 ± 7 to 68 ± 5%), III (from 100 ± 4 to 2 ± 5%) and IV (from 766 ± 2 to 100 ± 5%); this decrease was reversed by EGCG treatment to levels seen in sham-operated rats. 4In conclusion, EGCG attenuates TAC-induced ventricular hypertrophy in hypertensive rats in part by suppression of anti-oxidant enzymes and regulation of MAPK signals. [source] DOPAMINE D2 RECEPTOR STIMULATION INHIBITS ANGIOTENSIN II-INDUCED HYPERTROPHY IN CULTURED NEONATAL RAT VENTRICULAR MYOCYTESCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2009Hong Li SUMMARY 1Myocardial hypertrophy is a common pathological change that accompanies cardiovascular disease. Dopamine D2 receptors have been demonstrated in cardiovascular tissues. However, the pathophysiological involvement of D2 receptors in myocardial hypertrophy is unclear. Therefore, the effects of the D2 receptor agonist bromocriptine and the D2 receptor antagonist haloperidol on angiotensin (Ang) II- or endothelin (ET)-1-induced hypertrophy of cultured neonatal rat ventricular myocytes were investigated in the present study. 2Protein content and protein synthesis, determined by examining [3H]-leucine uptake, were used as estimates of cardiomyocyte hypertrophy. The expression of D2 receptor protein in neonatal rat ventricular myocytes was determined using western blotting. Changes in [Ca2+]i in cardiomyocytes were observed by laser scanning confocal microscopy. 3Angiotensin II and ET-1, both at 10 nmol/L, induced myocyte hypertrophy, as demonstrated by increased protein content and synthesis, [Ca2+]i levels, protein kinase C (PKC) activity and phosphorylation of extracellular signal-regulated kinase, c-Jun N-terminal kinase and mitogen-activated protein kinase (MAPK) p38 (p38). Concomitant treatment of cells with 10 nmol/L AngII plus 10 µmol/L bromocriptine significantly inhibited cardiomyocyte hypertrophy, MAPK phosphorylation and PKC activity in the membrane, as well as [Ca2+]i signalling pathways, compared with the effects of AngII alone. In addition, 10 µmol/L bromocriptine significantly inhibited cardiomyocyte hypertrophy induced by 10 nmol/L ET-1. However, pretreatment with haloperidol (10 µmol/L) had no significant effects on cardiomyocyte hypertrophy induced by either AngII or ET-1. 4In conclusion, D2 receptor stimulation inhibits AngII-induced hypertrophy of cultured neonatal rat ventricular myocytes via inhibition of MAPK, PKC and [Ca2+]i signalling pathways. [source] INVOLVEMENT OF PROLYLCARBOXYPEPTIDASE IN THE EFFECT OF RUTAECARPINE ON THE REGRESSION OF MESENTERIC ARTERY HYPERTROPHY IN RENOVASCULAR HYPERTENSIVE RATSCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 3 2009Xu-Ping Qin SUMMARY 1Previous studies indicate that rutaecarpine blocks increases in blood pressure and inhibits vascular hypertrophy in experimentally hypertensive rats. The aim of the present study was to determine whether the effects of rutaecarpine are related to activation of prolylcarboxypeptidase (PRCP). 2Renovascular hypertensive rats (Goldblatt two-kidney, one-clip (2K1C)) were developed using male Sprague-Dawley rats. Chronic treatment with rutaecarpine (10 or 40 mg/kg per day) or losartan (20 mg/kg per day) for 4 weeks to the hypertensive rats caused a sustained dose-dependent attenuation of increases in blood pressure, increased lumen diameter and decreased media thickness, which was accompanied by a similar reduction in the media cross-sectional area : lumen area ratio in mesenteric arteries compared with untreated hypertensive rats. 3Angiotensin (Ang) II expression was significantly increased in mesenteric arteries of hypertensive rats compared with sham-operated rats. No significant differences in plasma AngII levels were observed between untreated hypertensive and sham-operated rats. Hypertensive rats treated with high-dose rutaecarpine had significantly decreased Ang II levels in both the plasma and mesenteric arteries. 4Expression of PRCP protein or kallikrein mRNA was significantly inhibited in the right kidneys and mesenteric arteries of hypertensive rats. However, expression of PRCP protein and kallikrein mRNA was significantly increased after treatment with rutaecarpine or losartan (20 mg/kg per day). 5The data suggest that the repression of increases in systolic blood pressure and reversal of mesenteric artery remodelling by rutaecarpine may be related to increased expression of PRCP in the circulation and small arteries in 2K1C hypertensive rats. [source] ADENOVIRUS-MEDIATED FKBP12.6 OVEREXPRESSION INDUCES HYPERTROPHY AND APOPTOSIS IN CULTURED NEONATAL CARDIOMYOCYTESCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2009Jian Zhong SUMMARY 1Cardiac ryanodine RyR2 receptors regulate Ca2+ release from the sarcoplasmic reticulum (SR). FK506 binding protein (FKBP) 12.6 prevents aberrant SR Ca2+ leakage during diastole, thereby maintaining the integrity of RyR2 function. Previous studies have focused mainly on FKBP12.6 deficiency and so the pathophysiological consequences of FKBP12.6 overexpression remain unclear. Herein, we investigate the effect of FKBP12.6 overexpression on cardiac hypertrophic and apoptotic signalling. 2Human FKBP12.6 cDNA was cloned into pAdTrack-CMV and the resulting plasmid, along with a control empty plasmid, were transfected into bacteria. The resulting virus, namely Ad-FKBP12.6 containing green fluorescent protein, was propagated and purified. Neonatal rat cardiomyocytes were infected with this virus. Protein and DNA synthesis were measured by [3H]-leucine and [3H]-thymidine incorporation, respectively. Expression of p38 mitogen-activated protein kinase (MAPK), phosphorylated extracellular signal-regulated kinase 1 or 2 (p-ERK1/2) and Bax were examined by western blotting. 3Compared with control cells, cardiomyocytes that overexpressed FKBP12.6 became hypertrophic and hyperplastic, with increased levels of both p38 MAPK and p-ERK1/2. At the same time, overexpression of FKBP12.6 induced apoptosis of cardiomyocytes, as determined by both Bax protein expression and DNA fragmentation. Rapamycin treatment downregulated the expression of p-ERK1/2, p38 MAPK and Bax in stimulated cardiomyocytes, with or without FKBP12.6 overexpression, and enhanced protein synthesis, but had no effect on DNA synthesis in cardiomyocytes. 4In conclusion, FKBP12.6 overexpression may participate in pathophysiological processes through both hypertrophic and apoptotic signalling pathways, leading to cardiomyocyte damage and death. [source] DIFFERENCES BETWEEN PATHOLOGICAL AND PHYSIOLOGICAL CARDIAC HYPERTROPHY: NOVEL THERAPEUTIC STRATEGIES TO TREAT HEART FAILURECLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2007Julie R McMullen SUMMARY 1In general, cardiac hypertrophy (an increase in heart mass) is a poor prognostic sign. Cardiac enlargement is a characteristic of most forms of heart failure. Cardiac hypertrophy that occurs in athletes (physiological hypertrophy) is a notable exception. 2Physiological cardiac hypertrophy in response to exercise training differs in its structural and molecular profile to pathological hypertrophy associated with pressure or volume overload in disease. Physiological hypertrophy is characterized by normal organization of cardiac structure and normal or enhanced cardiac function, whereas pathological hypertrophy is commonly associated with upregulation of fetal genes, fibrosis, cardiac dysfunction and increased mortality. 3It is now clear that several signalling molecules play unique roles in the regulation of pathological and physiological cardiac hypertrophy. 4The present review discusses the possibility of targeting cardioprotective signalling pathways and genes activated in the athlete's heart to treat or prevent heart failure. [source] MOUSE STRAIN-SPECIFIC DIFFERENCES IN CARDIAC METABOLIC ENZYME ACTIVITIES OBSERVED IN A MODEL OF ISOPROTERENOL-INDUCED CARDIAC HYPERTROPHYCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 1-2 2007Michael D Faulx SUMMARY 1Alterations in myocardial energy metabolism accompany pressure overload-induced hypertrophy. We previously described a novel model of catecholamine-induced hypertrophy in which A/J mice exhibit more robust cardiac hypertrophy than B6 mice. Accordingly, we assessed the influence of mouse strain on the activities of key myocardial metabolic enzymes and whether there are strain-related metabolic adaptations to short-term, high-dose isoproterenol (ISO) administration. 2Thirty-nine male mice (19 A/J mice, 20 B6 mice), aged 12,15 weeks, were randomly assigned to receive either ISO (100 mg/kg, s.c.) or vehicle (sterile water) daily for 5 days. On Day 6, all hearts were excised, weighed, freeze clamped and assayed for pyruvate dehydrogenase (PDH), medium chain acyl-CoA dehydrogenase, carnitine palmitoyl transferase I and citrate synthase activities. Plasma fatty acids (FA) were also measured. 3The ISO-treated A/J mice demonstrated greater percentage increases in gravimetric heart weight/bodyweight ratio than ISO-treated B6 mice (24 vs 3%, respectively; P < 0.001). All enzyme activities were significantly greater in vehicle-treated B6 mice than in A/J mice, illustrating a greater capacity for aerobic metabolism in B6 mice. Administration of ISO reduced PDHa (active form) activity in B6 mice by 47% (P < 0.001), with no significant change seen in A/J mice. Free FA levels were not significantly different between groups; thus, the differences in PDHa were not due to changes in FA. 4The basal activity of myocardial metabolic enzymes is greater in B6 mice than in A/J mice and ISO alters myocardial PDH activity in a mouse strain-dependent manner. Compared with A/J mice, B6 mice demonstrate less ISO-induced cardiac hypertrophy, but greater activity of key enzymes regulating FA and carbohydrate oxidation, which may protect against the development of hypertrophy. The metabolic adaptations associated with ISO-induced hypertrophy differ from those reported with pressure overload hypertrophy. [source] DIFFERENTIAL REGULATION OF ANGIOTENSIN II RECEPTORS DURING RENAL INJURY AND COMPENSATORY HYPERTROPHY IN THE RATCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 4 2005Emma Joly SUMMARY 1.,The renin-angiotensin system may be involved in the compensatory adaptations occurring after the reduction of renal mass and during the consecutive changes leading to chronic renal failure. We therefore investigated the regulation of angiotensin II receptors in two models of renal hypertrophy in the rat: hypertrophy following uninephrectomy (UNx) or subtotal nephrectomy (STNx). The level of angiotensin type 1 (AT1A -R and AT1B -R) and type 2 (AT2 -R) receptor mRNA was quantified by competitive reverse transcription-polymerase chain reaction (RT-PCR) in specific renal zones and the intrarenal distribution of angiotensin II receptors was analysed by immunohistochemistry. 2.,In the UNx rats, AT1 -R mRNA expression was not modified in the cortex or in the inner stripe of the outer medulla of the residual kidney at any time after the surgery (1, 4 and 12 weeks). In contrast, AT1 -R mRNA expression was significantly reduced in these zones in STNx rats (,33% and ,40%, respectively). This downregulation was organ-specific, as AT1 -R mRNA levels were not modified in the liver. The proportions of AT1 -R subtype (AT1A and AT1B) mRNA were unchanged by UNx or STNx. Very low levels of AT2 -R mRNA were found in the cortex of all groups. Immunostaining revealed a similar localization of AT1 -R in mesangial cells, proximal tubule, basolateral membrane of thick ascending limb, in both models of hypertrophy. AT1 -R labelling was also detected in the apical membrane of intercalated cells of cortical collecting ducts. 3.,This differential mRNA expression of angiotensin II receptors during compensatory hypertrophy and renal injury suggests that the development of renal hypertrophy is independent of AT1 -R and AT2 -R gene expression levels. [source] Evaluation of Radiofrequency Thermal Ablation Results in Inferior Turbinate Hypertrophies by Magnetic Resonance ImagingTHE LARYNGOSCOPE, Issue 4 2007Tarik Sapci MD Abstract Objectives: Nasal obstruction caused by inferior turbinate hypertrophies is one of the most frequent problems in otolaryngology. Treatment of this disease may involve medical and surgical methods. Thermal ablation with radiofrequency energy has become quite popular in the recent years as one of the surgical methods used when medical therapy is not adequate. Study Design: Prospective, clinical trial. Methods: Thermal ablation with radiofrequency energy was used in this study on the inferior turbinates of 21 patients who had nasal obstruction caused by inferior turbinate hypertrophy only. The results were evaluated subjectively by preoperative and postoperative patient- and physician-assigned visual analogue scales and objectively by magnetic resonance imaging (MRI) investigation. Results: By the end of the postoperative week 10, 64.76% recovery was detected according to the patient evaluation, and 40.75% recovery was detected according to the physician evaluation. Measurement of the average volumes of the inferior turbinates by MRI revealed a 8.70% postoperative reduction. The most significant change was detected in the anterior-posterior length measurement performed in the axial plane. Conclusions: These results suggest that thermal ablation with radiofrequency energy is an easily applied, efficient, and reliable technique in treatment of the inferior turbinate hypertrophy, and that anterior-posterior length measurement in the axial section of the inferior turbinate by MRI, which is thought as an objective evaluation method, could be an efficient diagnostic tool in detecting the efficiency of radiofrequency on inferior turbinate. [source] The Potential of Soluble Epoxide Hydrolase Inhibition in the Treatment of Cardiac HypertrophyCONGESTIVE HEART FAILURE, Issue 4 2008Todd R. Harris PhD First page of article [source] Alterations of M-cadherin, neural cell adhesion molecule and , -catenin expression in satellite cells during overload-induced skeletal muscle hypertrophyACTA PHYSIOLOGICA, Issue 3 2006M. Ishido Abstract Aim:, Neural cell adhesion molecule (NCAM) and M-cadherin are cell adhesion molecules expressed on the surface of skeletal muscle satellite cell (SC). During myogenic morphogenesis, M-cadherin participates in mediating terminal differentiation and fusion of myoblasts by forming a complex with , -catenin and that NCAM contributes to myotube formation by fusion of myoblasts. Hypertrophy and hyperplasia of functionally overloaded skeletal muscle results from the fusion with SCs into the existing myofibres or new myofibre formation by SC,SC fusion. However, the alterations of NCAM, M-cadherin and , -catenin expressions in SCs in response to functional overload have not been investigated. Methods:, Using immunohistochemical approaches, we examined the temporal and spatial expression patterns of these factors expressed in SCs during the functional overload of skeletal muscles. Results:, Myofibres with SCs showing NCAM+/M-cadherin,, NCAM+/M-cadherin+ or NCAM,/M-cadherin+ were detected in overloaded muscles. The percentage changes of myofibres with SCs showing NCAM+/M-cadherin,, NCAM+/M-cadherin+ or NCAM,/M-cadherin+ were elevated in day-3 post-overloaded muscles, and then only the percentage changes of myofibres with SCs showing NCAM,/M-cadherin+ were significantly increased in day-7 post-overload muscles (P < 0.05). Both , -catenin and M-cadherin were co-localized throughout quiescent, proliferation and differentiation stages of SCs. Conclusion:, These results suggested that the expressions of NCAM, M-cadherin and , -catenin in SCs may be controlled by distinct regulatory mechanisms during functional overload, and that interactions among NCAM, M-cadherin and , -catenin in SCs may play important roles to contribute to overload-induced muscle hypertrophy via fusion with each other or into the existing myofibres of SCs. [source] Clinical Value of the Tissue Doppler S Wave to Characterize Left Ventricular Hypertrophy as Defined by EchocardiographyECHOCARDIOGRAPHY, Issue 4 2010Demian Chejtman M.D. Left ventricular hypertrophy (LVH) may be a physiological finding and may also be associated with different disease entities and hence, with different outcomes. Regional myocardial function can be assessed with color Doppler tissue imaging, specifically by the waveform of the isovolumic contraction (IC) period and the regional systolic wave ("s"). Methods and Results: We studied five groups (G): healthy, sedentary young volunteers (G1, n:10); healthy sedentary adult volunteers (G2, n:8); and subjects with LVH (left ventricular mass index >125 g/m2) including: high performance athletes (G3, n:21), subjects with hypertension (G4, n:21), subjects with hypertrophic cardiomyopathy (HCM) (G5, n:18). We measured peak "s" wave velocity (cm/sec) at the basal and mid septum, the IC/s ratio, and basal to mid-septal velocity difference (BMVD) of the "s" wave. Regional "s" wave values (cm/sec) were G1 = 5.6 ± 1; G2 = 5.4 ± 0.8; G3 = 5.7 ± 0.6; G4 = 5.3 ± 1.1; G5 = 4.2 ± 1.1 (P < 0.0001). The IC/s ratio was G1 = 0.28 ± 0.18; G2 = 0.39 ± 0.21; G3 = 0.23 ± 0.10; G4 = 0.42 ± 0.15; G5 = 0.64 ± 0.15 (P < 0.0001). The BMVD (cm/sec) was G1 = 2 ± 0.51; G2 = 1.71 ± 0.29; G3 = 1.78 ± 0.44; G4 = 1.26 ± 0.96; G5 = 0.45 ± 0.4 (P < 0.0001). IC/s < 0.38 discriminated physiological from pathological forms of hypertrophy (sensitivity 90%; specificity 88%). Peak "s" wave velocity discriminated HCM from other causes of hypertrophy, with a cutoff value of 4.46 cm/sec (sensitivity 72%; specificity 90%). BMVD <0.98 cm/sec detected HCM with 89% sensitivity and 86% specificity. Conclusions: Peak "s" wave velocity and two indices: IC/s and BMDV are novel parameters that may allow to discriminate physiological from pathological forms of hypertrophy as well as different subtypes of hypertrophy. (ECHOCARDIOGRAPHY 2010;27:370-377) [source] The Effects of Antihypertensive Treatment on the Doppler-Derived Myocardial Performance Index in Patients with Hypertensive Left Ventricular Hypertrophy: Results from the Swedish Irbesartan in Left Ventricular Hypertrophy Investigation Versus Atenolol (SILVHIA)ECHOCARDIOGRAPHY, Issue 7 2009Stefan Liljedahl M.D. Objectives: To investigate the effects of antihypertensive treatment on the Doppler-derived myocardial performance index (MPI) in patients with hypertensive left ventricular hypertrophy. Methods: The MPI was measured at baseline and after 48 weeks of antihypertensive treatment in 93 participants of the SILVHIA trial, where individuals with primary hypertension and left ventricular hypertrophy were randomized to double blind treatment with either irbesartan or atenolol. Results: Antihypertensive treatment lowered MPI (mean difference ,0.03 ± 0.01, P = 0.04). Changes in MPI by treatment were associated with changes in left ventricular ejection fraction (,-coefficient ,0.35 P = 0.005), stroke volume/pulse pressure (reflecting arterial compliance, ,-coefficient ,0.39 P < 0.001) and peripheral vascular resistance (,-coefficient 0.28 P < 0.04). Furthermore, there was a borderline significant association between changes in MPI and changes in E-wave deceleration time (reflecting diastolic function, ,-coefficient 0.23, P = 0.06). No associations were found between changes in MPI and changes in blood pressure, E/A-ratio, left ventricular mass index, relative wall thickness or heart rate. A stepwise multivariable regression model confirmed the association between changes in MPI and changes in ejection fraction and stroke volume/pulse pressure (all P < 0.05), as well as the trend for E-wave deceleration time (P = 0.08), but not in the case of peripheral vascular resistance. Conclusion: The MPI exhibited a modest decrease after 48 weeks of antihypertensive treatment in patients with hypertensive left ventricular hypertrophy. Changes in MPI were associated with changes in left ventricular function and vascular compliance, rather than with changes in left ventricular remodeling or blood pressure. [source] Disproportionately High Risk of Left Ventricular Hypertrophy in Indo-Asian Women: A Call for More StudiesECHOCARDIOGRAPHY, Issue 8 2008F.A.C.C., Fahim H. Jafary M.D. Objective: Indo-Asians have one of the highest rates of cardiovascular disease worldwide. Estimates and determinants of left ventricular hypertrophy (LVH) in this population are not known. We sought to determine the prevalence of and risk factors for LVH in Karachi, Pakistan.Methods: We conducted a population-based cross-sectional study on 320 randomly selected adults from the general population aged 40 years or above. LVH was defined as increased left ventricular mass index (LVMI) on echocardiogram (>115 g/m2 in men and >95 g/m2 in women) employing the adjusted Devereux equation. Multivariable models were built and logistic regression analysis was done for the primary outcome of LVH.Results: Mean age of subjects was 52.7 (10.4) years, 50% were women. Mean LVMI (SD) was 72.0 (19.2) [median 71.1] g/m2 in men and 75.7 (25.9) [median 72.9] g/m2 in women. The overall prevalence of LVH was 21.9% in women and 2.5% in men (P < 0.001). The factors (odds ratio, 95% CI) independently associated with LVH were women versus men (11.35, 3.79,34.02), systolic blood pressure > versus < 140 mmHg (2.70, 1.23,5.93), waist circumference (1.05, 1.02,1.08 for each cm increase) and illiteracy (2.43, 1.07,5.52).Conclusions: Urban Pakistani women appear to have a disproportionately high risk of LVH compared to men using standard echocardiographic criteria. Further research is needed to verify these results by establishing population-specific reference values for LVH and correlating cut-points for increased LVMI with prognosis. Concerted efforts are needed to reduce the high burden of risk factors in Indo-Asian women. [source] Real Time Three-Dimensional Echocardiography Evaluation of Mitral Annular Characteristics in Patients with Myocardial HypertrophyECHOCARDIOGRAPHY, Issue 4 2008Fatih Yalēin M.D. It has been shown that systolic excursion of the mitral annulus (MA) correlates well with left ventricular (LV) systolic function. Evaluation of the complicated shape and dynamics of the mitral annulus, however, may require rigorous methodology. The aim of this study was to investigate differences in MA motion between hypertrophic cardiomyopathy (HCM) and left ventricular hypertrophy (LVH) patients due to hypertension or aortic stenosis using real time three-dimensional echocardiography (RT3DE). We studied 10 HCM, 10 LVH, and 10 controls. Mean MA area changes between early and late systole were 9.5 ± 4.3% in HCM, 26 ± 15% in LVH and 19 ± 10% in normal controls. MA apicobasal motion was 5.8 ± 4 mm in HCM, 11 ± 4 mm in LVH, and 13.6 ± 6 mm in normal controls. RT3DE with digital reconstruction of MA accurately display complicated MA geometry and dynamics during a cardiac cycle. Annular function in LVH was similar to that of the normal group while annular apicobasal motion and area changes were reduced in HCM. [source] Hypertrophy and physiological death of equine chondrocytes in vitroEQUINE VETERINARY JOURNAL, Issue 6 2007Y. A. Ahmed Summary Reasons for performing study: Equine osteochondrosis results from a failure of endochondral ossification during skeletal growth. Endochondral ossification involves chondrocyte proliferation, hypertrophy and death. Until recently no culture system was available to study these processes in equine chondrocytes. Objective: To optimise an in vitro model in which equine chondrocytes can be induced to undergo hypertrophy and physiological death as seen in vivo. Methods: Chondrocytes isolated from fetal or older (neonatal, growing and mature) horses were cultured as pellets in 10% fetal calf serum (FCS) or 10% horse serum (HS). The pellets were examined by light and electron microscopy. Total RNA was extracted from the pellets, and quantitative PCR carried out to investigate changes in expression of a number of genes regulating endochondral ossification. Results: Chondrocytes from fetal foals, grown as pellets, underwent hypertrophy and died by a process morphologically similar to that seen in vivo. Chondrocytes from horses age >5 months did not undergo hypertrophy in pellet culture. They formed intramembranous inclusion bodies and the cultures included cells of osteoblastic appearance. Pellets from neonatal foals cultured in FCS resembled pellets from older horses, however pellets grown in HS underwent hypertrophy but contained inclusion bodies. Chondrocytes from fetal foals formed a typical cartilage-like tissue grossly and histologically, and expressed the cartilage markers collagen type II and aggrecan mRNA. Expression of Sox9, collagen type II, Runx2, matrix metalloproteinase-13 and connective tissue growth factor mRNA increased at different times in culture. Expression of fibroblast growth factor receptor-3 and vascular endothelial growth factor mRNA decreased with time in culture. Conclusions: Freshly isolated cells from fetal growth cartilage cultured as pellets provide optimal conditions for studying hypertrophy and death of equine chondrocytes. Potential relevance: This culture system should greatly assist laboratory studies aimed at elucidating the pathogenesis of osteochondrosis. [source] Calcineurin Inhibition Ameliorates Structural, Contractile, and Electrophysiologic Consequences of Postinfarction RemodelingJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 9 2001LILI DENG M.S. Calcineurin Inhibition and Postinfarction Remodeling.Introduction: After myocardial infarction (MI), the heart undergoes an adaptive remodeling process characterized by hypertrophy of the noninfarcted myocardium. Calcineurin, a Ca2+, calmodulin-regulated phosphatase, has been shown to participate in hypertrophic signal transduction. Methods and Results: We investigated the effects of calcineurin inhibition by cyclosporin A on key structural, contractile, and electrophysiologic alterations of post-MI remodeling. Male Sprague-Dawley rats were divided into four groups: (1) sham-operated; (2) sham + cyclosporin A; (3) post-MI (left anterior descending coronary artery ligation); and (4) MI + cyclosporin A. Cyclosporin A (25 mg/kg/day) was initiated 2 days before surgery and continued for 30 days. Hypertrophy was evaluated by echocardiography and by changes in membrane capacitance of isolated myocytes from noninfarcted left ventricle (LV). The effects of cyclosporin A on hemodynamics and cardiac dimensions were investigated, and changes in diastolic function were correlated with changes in protein phosphatase 1 activity and the basal level of phosphorylated phospholamban. The effects of cyclosporin A on Kv4.2/Kv4.3 genes expression and transient outward K + current (Ito) density also were evaluated. One of 12 rats in the post-MI group and 2 of 12 rats in the post-MI + cyclosporin A group died within 48 hours after MI. There were no late deaths in either MI group. There was no evidence of heart failure (lung congestion and/or pleural effusion) in the two groups 4 weeks post-MI. Calcineurin phosphatase activity increased 1.9-fold in post-MI remodeled LV myocardium, and cyclosporin A administration resulted in an 86% decrease in activity. There were statistically significant decreases of LV end-diastolic pressure, LV end-diastolic diameter, and LV relative wall thickness in the post-MI + cyclosporin A group compared with the post-MI group. On the other hand, there was no significant difference in LV end-systolic diameter or peak rate of LV pressure increase between the two post-MI groups. Protein phosphatase 1 activity was elevated by 36% in the post-MI group compared with sham, and this correlated with a 79% decrease in basal level of p16, phospholamban. In the post-MI + cyclosporin A group, the increase in protein phosphatase 1 activity was much less (18% vs 36%; P < 0.05), and the decrease in basal level of p16-phospholamban was markedly ameliorated (20% vs 79%; P < 0.01). The decreases in mRNA levels of Kv4.2 and Kv4.3 and Ito density in the LV of the post-MI + cyclosporin A group were significantly less compared with the post-MI group. Conclusion: Our results show that calcineurin inhibition by cyclosporin A partially ameliorated post-MI remodeled hypertrophy, diastolic dysfunction, decrease in basal level of phosphorylated phospholamban, down-regulation of key K + genes expression, and decrease of K + current, with no adverse effects on systolic function or mortality in the first 4 weeks after MI. [source] Impulse conduction and gap junctional remodelling by endothelin-1 in cultured neonatal rat ventricular myocytesJOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2009Y. Reisner Abstract Endothelin-1 (ET-1) is an important contributor to ventricular hypertrophy and failure, which are associated with arrhythmogenesis and sudden death. To elucidate the mechanism(s) underlying the arrhythmogenic effects of ET-1 we tested the hypothesis that long-term (24 hrs) exposure to ET-1 impairs impulse conduction in cultures of neonatal rat ventricular myocytes (NRVM). NRVM were seeded on micro-electrode-arrays (MEAs, Multi Channel Systems, Reutlingen, Germany) and exposed to 50 nM ET-1 for 24 hrs. Hypertrophy was assessed by morphological and molecular methods. Consecutive recordings of paced activation times from the same cultures were conducted at baseline and after 3, 6 and 24 hrs, and activation maps for each time period constructed. Gap junctional Cx43 expression was assessed using Western blot and confocal microscopy of immunofluorescence staining using anti-Cx43 antibodies. ET-1 caused hypertrophy as indicated by a 70% increase in mRNA for atrial natriuretic peptide (P < 0.05), and increased cell areas (P < 0.05) compared to control. ET-1 also caused a time-dependent decrease in conduction velocity that was evident after 3 hrs of exposure to ET-1, and was augmented at 24 hrs, compared to controls (P < 0.01). ET-1 increased total Cx43 protein by ,40% (P < 0.05) without affecting non- phosphorylated Cx43 (NP-Cx43) protein expression. Quantitative confocal microscopy showed a ,30% decrease in the Cx43 immunofluorescence per field in the ET-1 group (P < 0.05) and a reduced field stain intensity (P < 0.05), compared to controls. ET-1-induced hypertrophy was accompanied by reduction in conduction velocity and gap junctional remodelling. The reduction in conduction velocity may play a role in ET-1 induced susceptibility to arrhythmogenesis. [source] What Is Left Ventricular Hypertrophy and Is There a Reason to Regress Left Ventricular Hypertrophy?JOURNAL OF CLINICAL HYPERTENSION, Issue 8 2009Matthew R. Weir MD First page of article [source] Hypertrophied hearts: what of sevoflurane cardioprotection?ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 4 2009J. R. LARSEN Background: Recent studies have demonstrated that inhalation anaesthetics, like sevoflurane, confer cardioprotection both experimentally and clinically. However, coexisting cardiac disease might diminish anaesthetic cardioprotection and could partly explain why the clinical results of cardioprotection with anaesthetics remain controversial , in contrast to solid experimental evidence. Concomitant left ventricular hypertrophy is found in some cardiac surgery patients and could change cardioprotection efficacy. Hypertrophy could potentially render the heart less susceptible to sevoflurane cardioprotection and more susceptible to ischaemic injury. We investigated whether hypertrophy blocks sevoflurane cardioprotection, and whether tolerance to ischaemia is altered by left ventricular hypertrophy, in an established experimental animal model of ischaemia,reperfusion. Methods: Anaesthetized juvenile pigs (n=7,12/group) were subjected to 45 min distal coronary artery balloon occlusion, followed by 120 min of reperfusion. Controls were given pentobarbital, while sevoflurane cardioprotection was achieved by 3.2% inhalation throughout the experiment. Chronic banding of the ascending aorta resulted in left ventricular hypertrophy development in two further groups and these animals underwent identical ischaemia,reperfusion protocols, with or without sevoflurane cardioprotection. Myocardial infarct sizes were compared post-mortem. Results: The mean myocardial infarct size (% of area-at-risk) was reduced from mean 55.0 (13.6%) (±SD) in controls to 17.5 (13.2%) by sevoflurane (P=0.001). Sevoflurane reduced the infarct size in hypertrophied hearts to 14.6 (10.4%) (P=0.001); however, in hypertrophic controls, infarcts were reduced to 34.2 (10.2%) (P=0.001). Conclusion: Sevoflurane abrogated ischaemic injury to similar levels in both normal and left ventricular hypertrophied hearts. [source] Sonographic evaluation of the sciatic nerve in patients with lower-limb amputationsMUSCLE AND NERVE, Issue 6 2010A. Salim Göktepe MD Abstract Hypertrophy of the sciatic nerve after lower-limb amputation in patients with sarcomas has been previously reported by magnetic resonance imaging; however, sonographic evaluation of the sciatic nerve after lower-limb amputation due to nonmalignant causes has not been done before. Therefore, the aim of this study was to perform imaging of the sciatic nerve in lower-limb amputees and to find out whether sonographic findings were related to clinical characteristics. Twenty-three males with lower-limb amputations due to traumatic injuries were enrolled. Sonographic evaluations were performed using a linear array probe (Aloka UST-5524-7.5 MHZ). Sciatic nerve diameters were measured bilaterally at the same level, and the values of the normal limbs were taken as controls. Sciatic nerve width and thickness values were found to be greater on the amputated sides than the normal sides (P = 0.001). The thickness values were greater in above-knee amputees than below-knee amputees (P = 0.05). Subjects with a neuroma also had thicker sciatic nerves (P = 0.04). The diameters were found not to change between subjects with different liners (P > 0.05), but they were correlated with time after amputation (r = 0.6, P = 0.006; r = 0.4, P = 0.05, respectively). Our results clearly show that the sciatic nerves were wider and thicker on the amputated sides. Amputation level, duration, and the presence of a neuroma seem to affect the eventual diameters of the nerves. Muscle Nerve, 2010 [source] Lipid signaling changes in smooth muscle remodeling associated with partial urinary bladder outlet obstructionNEUROUROLOGY AND URODYNAMICS, Issue 2 2006Edward LaBelle Abstract Aims Hypertrophy of the urinary bladder smooth muscle (detrusor) is associated with partial bladder outlet obstruction (PBOO). Hypertrophied detrusor smooth muscle (DSM) reveals altered contractile characteristics. In this study, we analyzed the lipid-dependent signaling system that includes phospholipase A2 in PBOO-induced DSM remodeling and hypertrophy to determine whether the release of arachidonic acid (AA) from phospholipid is altered in the detrusor. Methods Partial bladder outlet obstruction (PBOO) was produced by partial ligation of the urethra in New Zealand white rabbits. Two weeks after the surgery, the bladder function was studied by keeping the rabbits in metabolic cages for 24 hr. Bladders were removed from rabbits that had bladder dysfunction (increased urinary frequency and decreased void volume) and the DSM separated from mucosa and serosa. The isolated smooth muscle was incubated with [3H] AA to equilibrate the cytoplasmic AA. The level of AA release was compared with the level obtained with 2-week sham-operated rabbits. Results The rate of AA release was high in DSM from bladders with PBOO-induced hypertrophy. Carbachol stimulated AA release in control DSM but DSM from obstructed rabbits revealed no further increase from the elevated basal AA release. The half-maximal concentration of carbachol that was required to stimulate AA release from control samples of detrusor was 35 µM. Conclusions The increased levels of AA release that are observed in this tissue after PBOO indicate the activation of phospholipase A2. The finding that carbachol could induce contraction, but not an increase in AA, indicates that the carbachol-induced contraction in the obstructed bladders is independent of lipid signaling pathways that involve AA. It is possible that the increased rate of arachidonic acid release from obstructed bladders correlates with the enhanced rates of prostaglandin production reported by other investigators from the same tissue. Neurourol. Urodynam. © 2006 Wiley-Liss, Inc. [source] Miliary Neonatal Hemangiomatosis with Fulminant Heart Failure and Cardiac Septal Hypertrophy in Two InfantsPEDIATRIC DERMATOLOGY, Issue 4 2004A. H. O'Hagan M.B., M.R.C.P. We report two infants with this condition who had fulminant cardiac failure and cardiac septal hypertrophy. The first was a 5-day-old boy who presented with increasing numbers of cutaneous hemangiomata associated with worsening cardiac failure. Magnetic resonance imaging (MRI) showed extensive hepatic hemangioma. Despite treatment with systemic corticosteroids and subcutaneous interferon alfa-2b his disease progressed. Hepatic artery embolization was unsuccessful. The infant died of congestive cardiac failure at 6 weeks of age. Postmortem examination showed a massively enlarged cardiac interventricular septum and biventricular hypertrophy. The second patient was a 1-week-old girl who also had cutaneous hemangioma and cardiac decompensation. MRI showed extensive intrahepatic involvement. She was treated early with corticosteroids and interferon ,, which resulted in involution of the cutaneous and hepatic lesions. Cardiac septal hypertrophy did not persist at late follow-up, and the association of miliary neonatal hemangiomatosis and cardiac septal hypertrophy has not yet been established. [source] Congenital Hypertrophy of the Lateral Nail Folds of the Hallux: Clinical Features and Follow-Up of Seven CasesPEDIATRIC DERMATOLOGY, Issue 5 2000Bianca Maria Piraccini M.D. We describe the clinical picture and follow-up of seven patients with this abnormality. In three patients the affected toe showed an asymptomatic, dome-shaped, hypertrophic lip that partially covered the nail plate. Four patients had acute inflammatory changes due to toenail ingrowth, with considerable swelling and reddening of the hypertrophic lip that was painful on pressure. Topical treatment with steroids was useful to reduce inflammation and produced persistent remission in two patients. Follow-up showed a spontaneous disappearance of the hypertrophic nail fold in one of the seven patients. In two patients the hypertrophic lip partially regressed, but remained clearly visible, while in two patients it remained unchanged. In two patients surgical correction of the soft tissue abnormality was necessary due to painful nail ingrowth unresponsive to topical treatment. [source] Neural specialization for hovering in hummingbirds: Hypertrophy of the pretectal nucleus lentiformis mesencephaliTHE JOURNAL OF COMPARATIVE NEUROLOGY, Issue 2 2007Andrew N. Iwaniuk Abstract Hummingbirds possess an array of morphological and physiological specializations that allow them hover such that they maintain a stable position in space for extended periods. Among birds, this sustained hovering is unique to hummingbirds, but possible neural specializations underlying this behavior have not been investigated. The optokinetic response (OKR) is one of several behaviors that facilitates stabilization. In birds, the OKR is generated by the nucleus of the basal optic root (nBOR) and pretectal nucleus lentiformis mesencephali (LM). Because stabilization during hovering is dependent on the OKR, we predicted that nBOR and LM would be significantly enlarged in hummingbirds. We examined the relative size of nBOR, LM, and other visual nuclei of 37 species of birds from 13 orders, including nine hummingbird species. Also included were three species that hover for short periods of time (transient hoverers; a kingfisher, a kestrel, and a nectarivorous songbird). Our results demonstrate that, relative to brain volume, LM is significantly hypertrophied in hummingbirds compared with other birds. In the transient hoverers, there is a moderate enlargement of the LM, but not to the extent found in the hummingbirds. The same degree of hypertrophy is not, however, present in nBOR or the other visual nuclei measured: nucleus geniculatus lateralis, pars ventralis, and optic tectum. This selective hypertrophy of LM and not other visual nuclei suggests that the direction-selective optokinetic neurons in LM are critical for sustained hovering flight because of their prominent role in the OKR and gaze stabilization. J. Comp. Neurol. 500:211,221, 2007. © 2006 Wiley-Liss, Inc. [source] Bacteriologic Comparison of Tonsil Core in Recurrent Tonsillitis and Tonsillar Hypertrophy,THE LARYNGOSCOPE, Issue 12 2007Jin Hyeok Jeong MD Abstract Objectives: Although many bacteriology studies on tonsillar diseases have been completed, all have been confined to children and were characterized by a paucity of cases. The purpose of this study was to analyze the underlying bacterial pathogens in tonsillar disease. Methods: A retrospective study was performed on 824 patients who underwent elective tonsillectomy with or without adenoidectomy. We analyzed the differences between the bacterial pathogens in recurrent tonsillitis and tonsillar hypertrophy with regard to age, season, and antibiotic sensitivity. Results: Among 824 cases, 966 bacterial strains from the tonsil core were isolated. In recurrent tonsillitis, Staphylococcus aureus was the most common pathogen (30.3%), followed by Haemophilus influenzae (15.5%) and group A ,-hemolytic Streptococcus (Streptococcus pyogenes, 14.4%). In patients over 14 years of age, quite differently from other age groups, Klebsiella pneumoniae was isolated at a significantly higher percentage. In tonsillar hypertrophy, H. influenzae was isolated most commonly (31.4%) regardless of age, followed by S. pyogenes (24.2%), S. aureus (22.9%), and Streptococcus pneumoniae (12.6%). Furthermore, mixed infection was common because of its high resistance to penicillin. In both groups, S. pneumoniae was more common in younger patients, whereas K. pneumoniae was relatively common in adults. We found no differences in the detection rate by season; however, H. influenzae was frequently isolated in the tonsillar hypertrophy group regardless of seasonal variations. We also found no difference in the antibiotic sensitivity between the two groups; however, strains resistant to penicillin were relatively prevalent and showed a high sensitivity to third-generation cephalosporin. Conclusions: We observed some differences in the types of bacteria in the tonsillar core between the recurrent tonsillitis and tonsillar hypertrophy groups. Our study indicates that essential bacteria have been changing and, thus, we need to change our choice of antibiotics. [source] Bipolar Radiofrequency-Induced Thermotherapy of Turbinate Hypertrophy: Pilot Study and 20 Months' Follow-upTHE LARYNGOSCOPE, Issue 1 2003Jan Seeger MD Abstract Objectives/Hypothesis The present report is a pilot clinical study about a new bipolar ablation technique for the treatment of turbinate hypertrophy, which offers an alternative to conventional methods. Study Design Prospective, clinical. Methods From August 1999 to March 2000, a new bipolar radiofrequency system with acoustic feedback control was submucosally applied for the treatment of 38 patients with nasal airway obstruction of vasomotor (n = 31) or allergic (n = 7) genesis. The therapy was made ambulatory with surface anesthesia. Data were collected by questionnaire and rhinomanometry preoperatively and 2 and 20 months postoperatively. Results Nearly all patients reported an improvement of their nasal breathing, with 68% of them reporting a full and 29% a partial recovery. No significant differences were reported with regard to the response of the allergic versus the vasomotor rhinitis. On average, a definite benefit was observed after 2 weeks. Side effects, such as bleeding, synechia, or atrophic changes of the mucosa, which would have to be treated, were not observed. Conclusion The new bipolar radiofrequency thermotherapy presents an efficient option for the treatment of turbinate hypertrophy, which meets the requirements for an outpatient treatment. [source] Adenotonsillar Hypertrophy and Epstein-Barr Virus in Pediatric Organ Transplant Recipients,THE LARYNGOSCOPE, Issue 6 2001Nina L. Shapiro MD Abstract Objectives/Hypothesis Epstein-Barr virus,related (EBV-related) lymphoid hyperplasia of the tonsils and adenoids is a precursor to post-transplantation lymphoproliferative disorder (PTLD). The incidence of post-transplantation adenotonsillar hypertrophy, a potential early sign of PTLD or EBV-related lymphoid hyperplasia, is not known. We sought to identify potential risk factors for adenotonsillar hypertrophy manifested as EBV-related hyperplasia and early PTLD in the pediatric solid organ transplant population. Study Design Cross-sectional analysis. Methods We developed a 65-point questionnaire concerning obstructive sleep disorder and upper respiratory tract infections and an 8-point focused physical examination, to identify prevalence of and risk factors for adenotonsillar hypertrophy in the pediatric transplant population. We evaluated 120 pediatric solid organ transplant recipients by parental questionnaire and focused adenotonsillar physical examination. Results Of the 120 patients, 62 had undergone liver transplantation and 58 had undergone kidney transplantation. Overall, the mean questionnaire score was 8.36 (range, 0,40) and the mean physical examination score was 3.86 (range, 1,8). Patients whose EBV serological test result was negative at the time of transplant had higher scores for both the questionnaire (mean score, 10.24) and the physical examination (mean score, 4.56) than those whose EBV serological test result was positive at the time of transplantation (scores of 7.38 and 3.30 for questionnaire and physical examination, respectively). The difference in examination scores was statistically significant (P <.003). Conclusions Epstein-Barr virus seronegativity at the time of organ transplantation is a known risk factor for PTLD, with associated risk of developing EBV-related lymphoid hyperplasia. Our results indicate a higher incidence of symptoms and signs consistent with adenotonsillar hypertrophy in the EBV seronegative population. Adenotonsillar hypertrophy may be a precursor to EBV-related lymphoid hyperplasia and PTLD and must be identified in this patient population. [source] Critical Role for IL-6 in Hypertrophy and Fibrosis in Chronic Cardiac Allograft RejectionAMERICAN JOURNAL OF TRANSPLANTATION, Issue 8 2009J. A. Diaz Chronic cardiac allograft rejection is the major barrier to long term graft survival. There is currently no effective treatment for chronic rejection except re-transplantation. Though neointimal development, fibrosis, and progressive deterioration of graft function are hallmarks of chronic rejection, the immunologic mechanisms driving this process are poorly understood. These experiments tested a functional role for IL-6 in chronic rejection by utilizing serial echocardiography to assess the progression of chronic rejection in vascularized mouse cardiac allografts. Cardiac allografts in mice transiently depleted of CD4+ cells that develop chronic rejection were compared with those receiving anti-CD40L therapy that do not develop chronic rejection. Echocardiography revealed the development of hypertrophy in grafts undergoing chronic rejection. Histologic analysis confirmed hypertrophy that coincided with graft fibrosis and elevated intragraft expression of IL-6. To elucidate the role of IL-6 in chronic rejection, cardiac allograft recipients depleted of CD4+ cells were treated with neutralizing anti-IL-6 mAb. IL-6 neutralization ameliorated cardiomyocyte hypertrophy, graft fibrosis, and prevented deterioration of graft contractility associated with chronic rejection. These observations reveal a new paradigm in which IL-6 drives development of pathologic hypertrophy and fibrosis in chronic cardiac allograft rejection and suggest that IL-6 could be a therapeutic target to prevent this disease. [source] Cardiac Allograft Hypertrophy: A New Target for Therapy, a Surrogate Marker for Survival?AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009G. Torre-Amione Long-term heart transplant survival may not simply be limited by allograft vasculopathy, but also by diffuse myocardial injury in form of left ventricular hypertrophy. See also article by Raichlin et al in this issue on page 132. [source] Electrocardiographic Indices of Left Ventricular Hypertrophy and Repolarization Phase Share the Same Genetic Influences: A Twin StudyANNALS OF NONINVASIVE ELECTROCARDIOLOGY, Issue 4 2009Sara Mutikainen M.Sc. Background: Both left ventricular hypertrophy (LVH) and repolarization phase (RP) are known to be attributable to genetic influences, but less is known whether they share same genetic influences. The aim of this study was to investigate to what extent individual differences in electrocardiographic (ECG) LVH and RP are explained by genetic and environmental influences and whether these influences are shared between these two traits. Methods: Resting ECG recordings were obtained from 186 monozygotic and 203 dizygotic female twin individuals, aged 63 to 76 years. Latent factors, called LVH and RP, were formed to condense the information obtained from LVH indices (Cornell voltage and Cornell product) and T-wave amplitudes (leads V5 and II), respectively. Multivariate quantitative genetic modeling was used both to decompose the phenotypic variances into additive genetic, common environmental, and unique environmental influences, and for the calculation of genetic and environmental correlations between LVH and RP. Results: Additive genetic influences explained 16% of individual differences in LVH and 74% in RP. The remaining individual differences were explained by both common and unique environmental influences. The genetic correlation and unique environmental correlation between LVH and RP were ,0.93 and ,0.05, respectively. Conclusions: In older women without overt cardiac diseases, RP is under stronger genetic control than LVH. The majority of genetic influences are shared between LVH and RP whereas environmental influences are mainly specific to each. [source] | |||||||||||||||||||||||||||||||||||||||||||