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Heart Function (heart + function)

Distribution by Scientific Domains

Medical Sciences	72%
Life Sciences	24%

Distribution within Medical Sciences

Pharmacology & Pharmaceutical Medicine	37%
Cardiovascular Disease	11%
Anesthesia & Pain Management	6%

Selected Abstracts

Right Heart Function and Scleroderma: Insights from Tricuspid Annular Plane Systolic Excursion

ECHOCARDIOGRAPHY, Issue 2 2007
Chiu-Yen Lee M.D.
Objective: The purpose of this study was to evaluate the use of echocardiographic parameters as predictors of rehospitalization in scleroderma patients. Methods: Echocardiographic studies were conducted in 38 patients with systolic scleroderma (SSc) to assess cardiopulmonary function. Forty-five age-matched volunteers without any sign of heart failure served as the control group. Transmitral flow pattern, tricuspid annular plane systolic excursion (TAPSE), left ventricular ejection fraction (LVEF), and right ventricular ejection fraction (RVEF) were evaluated. All patients were subsequently followed for one year. Results: Peak transmitral early-diastolic velocity (mitral E) and TAPSE measurements were significantly different between SSc and control patients (mitral E: 74.1 ± 16.3 vs. 83.5 ± 17.0 cm/s with P = 0.012; TAPSE: 2.4 ± 0.43 vs. 1.9 ± 0.39 cm with P < 0.0001). LVEF was similar, but RVEF was lower in the SSc group (LVEF: 61.7 ± 9.7 vs. 61.7 ± 5.8% with P = 0.962; RVEF: 49.6 ± 6.8 vs. 39.2 ± 6.7% with P < 0.0001). A strong correlation was found between TAPSE and RVEF. A TAPSE less than 1.96 cm indicted a RVEF less than 40% with a sensitivity of 81% and specificity of 78%. Contrary to expectation, pulmonary artery systolic pressure (PASP) did not correlate well with RV function (r = 0.261, r2= 0.068, P = 0.016). Finally, the frequency of rehospitalization was inversely correlated with RVEF and TAPSE in SSc patients. Conclusions: We can predict the rehospitalization rate of SSc patients by TAPSE and RVEF, suggesting the involvement of heart, skin, lung, and other organs in scleroderma patients. [source]

Impaired Heart Function And Noradrenaline Release After Ischaemia In Stroke-Prone Spontaneously Hypertensive Rats

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 9 2000
Hong Chen
SUMMARY 1. Stroke-prone spontaneously hypertensive rats (SHRSP) are a strain of rat that exhibit severely high blood pressure and stroke attacks at an early age, but their heart function in vitro has seldom been studied in detail. Although the activity of the sympathetic nervous system is known to increase after myocardial ischaemia, there is little information about the cardiac release of noradrenaline (NA) associated with heart function after ischaemia in SHRSP. The aim of the present study was to examine heart function and cardiac NA release after ischaemia in SHRSP. 2. Isolated hearts of 4- and 8-month-old SHRSP and age-matched Wistar-Kyoto (WKY) rats were perfused in a working heart preparation and were subjected to 30 min ischaemia followed by 30 min reperfusion. Heart function and coronary flow were monitored throughout the experiment. Coronary effluent was collected for determination of NA using high- performance liquid chromatography coupled with electrochemical detection. 3. Under baseline conditions, cardiac output of 4-month-old SHRSP was slightly but significantly decreased compared with that of WKY rats (P < 0.05), although coronary flow was maintained normally at this age. Eight-month-old SHRSP showed a further impairment of systolic heart function, with lower coronary flow and higher coronary vascular resistance under baseline conditions. Elevated left ventricular end-diastolic pressure was evident in SHRSP at both ages before ischaemia. Heart function was severely damaged after 30 min global ischaemia in SHRSP from both age groups. Stroke-prone spontaneously hypertensive rats also showed lower coronary flow and higher coronary vascular resistance during reperfusion. 4. Coronary NA was not detectable in WKY rats or SHRSP at 4 months of age under baseline conditions. In 8-month-old SHRSP, pre-ischaemic NA release was significantly higher than that in age-matched WKY rat controls. The concentration of NA in the coronary effluent of SHRSP during reperfusion was also significantly higher than that of WKY rats at both ages. 5. These data demonstrate that SHRSP have early impairment of both systolic and diastolic heart function compared with WKY rats. Severe damage of heart function and coronary flow after ischaemia in SHRSP was accompanied with an increased release of NA, which may play a harmful role in heart function impairment in SHRSP after ischaemia. [source]

Molecular Adsorbents Recirculating System Dialysis for Liver Insufficiency and Sepsis Following Right Ventricular Assist Device after Cardiac Surgery

ARTIFICIAL ORGANS, Issue 8 2004
Otrud Vargas Hein
Abstract:, We report a case of right heart failure (RHF) and sepsis with liver insufficiency in a 70-year-old patient after coronary artery bypass graft surgery. Three hours after surgery the patient suddenly developed therapy refractory cardiac arrest caused by RHF. He had to have emergency surgery, under which the graft to the right coronary artery was revised and a right ventricular assist device was implanted. Heart function recovered and the assist device was explanted on day 1 after surgery. Thoracic closure was performed on day 5 after surgery. The patient went into septic shock on day 11. Liver dysfunction developed postoperatively and worsened the course of sepsis. Therefore, MARS (molecular adsorbents recirculating system) dialysis was performed once on day 20 after surgery. Liver function improved after MARS therapy and the patient recovered from sepsis. On day 46 the patient was transferred from the ICU of another hospital to one of the peripheral wards, to be finally discharged on day 67. [source]

Impaired Heart Function And Noradrenaline Release After Ischaemia In Stroke-Prone Spontaneously Hypertensive Rats

Mechanics and function in heart morphogenesis

DEVELOPMENTAL DYNAMICS, Issue 2 2005
Thomas Bartman
Abstract For years, biomechanical engineers have studied the physical forces involved in morphogenesis of the heart. In a parallel stream of research, molecular and developmental biologists have sought to identify the molecular pathways responsible for embryonic heart development. Recently, several studies have shown that these two avenues of research should be integrated to explain how genes expressed in the heart regulate early heart function and affect physical morphogenetic steps, as well as to conversely show how early heart function affects the expression of genes required for morphogenesis. This review combines the perspectives of biomechanical engineering and developmental biology to lay out an integrated view of the role of mechanical forces in heart development. Developmental Dynamics 233:373,381, 2005. © 2005 Wiley-Liss, Inc. [source]

Chronic effects of type 2 diabetes mellitus on cardiac muscle contraction in the Goto-Kakizaki rat

EXPERIMENTAL PHYSIOLOGY, Issue 6 2007
F. C. Howarth
Type 2 diabetes mellitus accounts for more than 90% of all cases of diabetes mellitus, and cardiovascular complications are the major cause of mortality and death in diabetic patients. The chronic effects of type 2 diabetes mellitus on heart function have been investigated in the Goto-Kakizaki (GK) rat. Experiments were performed in GK rats and age-matched Wistar control rats at 18 months of age. The progressive effects of diabetes on glucose metabolism were monitored periodically by application of the glucose tolerance test. Ventricular action potentials were measured in isolated, perfused heart. Shortening and intracellular Ca2+ were measured in electrically stimulated ventricular myocytes. The GK rats displayed mild fasting hyperglycaemia and progressively worsening glucose tolerance. At 18 months of age and 180 min after intraperitoneal injection of glucose (2 g (kg body weight),1), blood glucose was 436 ± 47 mg dl,1 in GK rats compared with 153 ± 18 mg dl,1 in control animals. Heart weight to body weight ratio was significantly increased in GK rats (4.10 ± 0.09 mg g,1, n= 5) compared with control animals (3.36 ± 0.22 mg g,1, n= 4). Spontaneous heart rate was slightly reduced in GK rats compared with control rats. Although the amplitude of shortening was not altered, the amplitude of the Ca2+ transient was significantly increased in myocytes from GK rats (0.78 ± 0.11 ratio units) compared with control rats (0.50 ± 0.06 ratio units). Despite progressively worsening glucose metabolism, at 18 months of age the contractile function of the heart appears to be well preserved. [source]

Correlation of ,-skeletal actin expression, ventricular fibrosis and heart function with the degree of pressure overload cardiac hypertrophy in rats

EXPERIMENTAL PHYSIOLOGY, Issue 3 2006
Donatella Stilli
We have analysed alterations of ,-skeletal actin expression and volume fraction of fibrosis in the ventricular myocardium and their functional counterpart in terms of arrhythmogenesis and haemodynamic variables, in rats with different degrees of compensated cardiac hypertrophy induced by infra-renal abdominal aortic coarctation. The following coarctation calibres were used: 1.3 (AC1.3 group), 0.7 (AC0.7) and 0.4 mm (AC0.4); age-matched rats were used as controls (C group). One month after surgery, spontaneous and sympathetic-induced ventricular arrhythmias were telemetrically recorded from conscious freely moving animals, and invasive haemodynamic measurements were performed in anaesthetized animals. After killing, subgroups of AC and C rats were used to evaluate in the left ventricle the expression and spatial distribution of ,-skeletal actin and the amount of perivascular and interstitial fibrosis. As compared with C, all AC groups exhibited higher values of systolic pressure, ventricular weight and ventricular wall thickness. AC0.7 and AC0.4 rats also showed a larger amount of fibrosis and upregulation of ,-skeletal actin expression associated with a higher vulnerability to ventricular arrhythmias (AC0.7 and AC0.4) and enhanced myocardial contractility (AC0.4). Our results illustrate the progressive changes in the extracellular matrix features accompanying early ventricular remodelling in response to different degrees of pressure overload that may be involved in the development of cardiac electrical instability. We also demonstrate for the first time a linear correlation between an increase in ,-skeletal actin expression and the degree of compensated cardiac hypertrophy, possibly acting as an early compensatory mechanism to maintain normal mechanical performance. [source]

Attenuation of changes in Gi -proteins and adenylyl cyclase in heart failure by an ACE inhibitor, imidapril

JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 3 2003
R. Sethi
Abstract Cardiac dysfunction in animals with congestive heart failure due to myocardial infarction (MI) is known to be associated with a wide variety of defects in receptor and post-receptor mechanisms. Since the heart function have been shown to be improved by treatment with different angiotensin converting enzyme (ACE) inhibitors, we examined the effects of imidapril, an ACE inhibitor, on changes in post-receptor mechanisms involving adenylyl cyclase (AC) and G proteins in the failing heart. Heart failure in rats was induced by occluding the coronary artery and 3 weeks later the animals were treated daily with 1 mg/kg (orally) imidapril for 5 weeks. The animals were assessed for their left ventricular function and crude membranes were isolated from the viable left ventricle and examined for AC activities as well as G-protein activities and expression. Animals with heart failure exhibited depressions in ventricular function and AC activities in the absence or presence of forskolin, NaF and Gpp(NH)p. The AC activity in the presence of pertussis toxin was increased whereas that in the presence of cholera toxin was decreased in the failing heart. Protein contents and mRNA levels for Gi -proteins were increased whereas those for Gs -proteins were unaltered in the infarcted heart. All these changes due to MI were prevented by imidapril treatment. The results indicate that the depressed cardiac function in the failing heart may partly be due to the direct effects of changes in AC and Gi proteins. [source]

Effects of myostatin deletion in aging mice

AGING CELL, Issue 5 2009
Michael R. Morissette
Summary Inhibitors of myostatin, a negative regulator of skeletal muscle mass, are being developed to mitigate aging-related muscle loss. Knock-out (KO) mouse studies suggest myostatin also affects adiposity, glucose handling and cardiac growth. However, the cardiac consequences of inhibiting myostatin remain unclear. Myostatin inhibition can potentiate cardiac growth in specific settings (Morissette et al., 2006), a concern because of cardiac hypertrophy is associated with adverse clinical outcomes. Therefore, we examined the systemic and cardiac effects of myostatin deletion in aged mice (27,30 months old). Heart mass increased comparably in both wild-type (WT) and KO mice. Aged KO mice maintained twice as much quadriceps mass as aged WT; however, both groups lost the same percentage (36%) of adult muscle mass. Dual-energy X-ray absorptiometry revealed increased bone density, mineral content, and area in aged KO vs. aged WT mice. Serum insulin and glucose levels were lower in KO mice. Echocardiography showed preserved cardiac function with better fractional shortening (58.1% vs. 49.4%, P = 0.002) and smaller left ventricular diastolic diameters (3.41 vs. 2.71, P = 0.012) in KO vs. WT mice. Phospholamban phosphorylation was increased 3.3-fold in KO hearts (P < 0.05), without changes in total phospholamban, sarco(endo)plasmic reticulum calcium ATPase 2a or calsequestrin. Aged KO hearts showed less fibrosis by Masson's Trichrome staining. Thus, myostatin deletion does not affect aging-related increases in cardiac mass and appears beneficial for bone density, insulin sensitivity and heart function in senescent mice. These results suggest that clinical interventions designed to inhibit skeletal muscle mass loss with aging could have beneficial effects on other organ systems as well. [source]

Aging in inbred strains of mice: study design and interim report on median lifespans and circulating IGF1 levels

AGING CELL, Issue 3 2009
Rong Yuan
Summary To better characterize aging in mice, the Jackson Aging Center carried out a lifespan study of 31 genetically-diverse inbred mouse strains housed in a specific pathogen-free facility. Clinical assessments were carried out every 6 months, measuring multiple age-related phenotypes including neuromuscular, kidney and heart function, body composition, bone density, hematology, hormonal levels, and immune system parameters. In a concurrent cross-sectional study of the same 31 strains at 6, 12, and 20 months, more invasive measurements were carried out followed by necropsy to assess apoptosis, DNA repair, chromosome fragility, and histopathology. In this report, which is the initial paper of a series, the study design, median lifespans, and circulating insulin-like growth factor 1 (IGF1) levels at 6, 12, and 18 months are described for the first cohort of 32 females and 32 males of each strain. Survival curves varied dramatically among strains with the median lifespans ranging from 251 to 964 days. Plasma IGF1 levels, which also varied considerably at each time point, showed an inverse correlation with a median lifespan at 6 months (R = ,0.33, P = 0.01). This correlation became stronger if the short-lived strains with a median lifespan < 600 days were removed from the analysis (R = ,0.53, P < 0.01). These results support the hypothesis that the IGF1 pathway plays a key role in regulating longevity in mice and indicates that common genetic mechanisms may exist for regulating IGF1 levels and lifespan. [source]

Salutary effects of Corydalis yanhusuo extract on cardiac hypertrophy due to pressure overload in rats

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 8 2007
Chengping Wen
We have evaluated the effects of an alcohol extract from the rhizome of Corydalis yanhusuo W.T. (CY), a well-known traditional Chinese medicinal herb, on pressure-overloaded cardiac hypertrophy induced by transverse abdominal aorta constriction (TAAC) in rats. Rats were given vehicle or CY extract (200 or 50 mg kg,1 per day) from the second week after induction of pressure overload, for a period of 7 weeks. Haemodynamic parameters, relative heart weight and myocyte cross-sectional area were measured in each group. We also estimated left ventricular (LV) collagen volume fraction (CVF) using Masson trichrome staining, and type I collagen expression by Western blot assay. Chronic TAAC caused notable cardiac hypertrophy and heart dysfunction. Significant collagen deposition and greater type I collagen expression were found in model control rats. These changes were not significantly reversed after treatment with 50 mgkg,1 CY, whereas 200 mgkg,1 significantly improved heart function and prevented cardiac hypertrophy, with parallel reductions in myocardial fibrosis, as evidenced by reduced LV CVF and reduced levels of type I collagen. In conclusion, chronic treatment of rats with CY extract attenuated development of cardiac hypertrophy. [source]

Iso-S -petasin, a hypotensive sesquiterpene from Petasites formosanus, depresses cardiac contraction and intracellular Ca2+ transients in adult rat ventricular myocytes

JOURNAL OF PHARMACY AND PHARMACOLOGY: AN INTERNATI ONAL JOURNAL OF PHARMACEUTICAL SCIENCE, Issue 1 2003
Lucy B. Esberg
ABSTRACT Petasites formosanus is an indigenous species of the medicinal plant Petasites which has been used to treat hypertension. Both S -petasin and its isoform iso-S -petasin have been shown to be the effective ingredients in P. formosanus. However, their effect on heart function has not been revealed. This study was to examine the effect of iso-S -petasin on cardiac contractile function at the myocyte level. Ventricular myocytes were isolated from adult rat hearts and were stimulated to contract at 0.5 Hz under 1.0 mm extracellular Ca2+. Contractile properties were evaluated using an lonOptix MyoCam system including peak shortening (PS), time to PS (TPS), time to 90% re-lengthening (TR90) and maximal velocity of shortening/re-lengthening (±dL/dt). Intracellular Ca2+ properties were assessed by fura-2 and presented as Ca2+ -induced Ca2+ release (CICR) and intracellular Ca2+ decay. Acute application of iso-S -petasin (10,7 to 10,4 M) elicited a concentration-dependent inhibition in PS and CICR, with maximal inhibitions of 51.0% and 31.0%, respectively. iso-S -petasin also induced a concentration-dependent inhibition of ± dL/dt without affecting TPS, TR90, baseline intracellular Ca2+ level or intracellular Ca2+ decay. Elevation of extracellular Ca2+ from 1.0 mm to 2.7 mm significantly antagonized the iso-S -petasin-induced depression in PS and CICR. These results demonstrated a direct depressant action of iso-S -petasin on ventricular contraction, which may work in concert with its antihypertensive action to reduce the cardiac load. The iso-S -petasin-induced decrease in CICR may play a role in its cardiac depressant effect. [source]

Effects of Alcohol Withdrawal on 24 Hour Ambulatory Blood Pressure Among Alcohol-Dependent Patients

ALCOHOLISM, Issue 12 2003
Ramón Estruch
Background: Although epidemiologic studies have reported an association between alcohol intake and high blood pressure (BP), the results of intervention studies have shown inconsistent results. We embarked on a study to determine whether different subgroups of alcohol-dependent patients may be identified in relation to the effect of alcohol on BP. Methods: Fifty alcohol-dependent men (mean age, 41.4 years) received 0.4 g of ethanol per kilogram of body weight every 4 hr in 200 ml of orange juice during 24 hr and the same amount of orange juice without ethanol during another 24 hr. Twenty-four hour ambulatory BP monitoring was performed during ethanol and orange juice intakes, as was hormonal and biochemical analysis. Results: Thirty-five (75%) alcohol-dependent men were normotensive and 15 (30%) hypertensive. Eighteen (51%) normotensive and 12 (80%) hypertensive subjects showed a significant decrease in 24 hr mean BP after ethanol withdrawal (mean decrease of 8.4 mm Hg [95% confidence interval, ,11.2 to ,5.7] and 12.5 mm Hg [confidence interval, ,16.2 to ,8.8], respectively) and were considered as sensitive to alcohol. The remaining alcohol-dependent subjects were considered as resistant to alcohol. Normotensive subjects sensitive to ethanol showed a significantly greater left ventricular mass and a significantly lower ejection fraction than those normotensive patients whose BP did not change after ethanol withdrawal (both p < 0.01). Conclusions: More than three fourths of the hypertensive and more than half of the normotensive alcohol-dependent patients showed sensitivity to the pressor effects of ethanol. Impairment also was observed in heart function in normotensive patients sensitive to the pressor effects of ethanol. [source]

Joint generalized estimating equations for multivariate longitudinal binary outcomes with missing data: an application to acquired immune deficiency syndrome data

JOURNAL OF THE ROYAL STATISTICAL SOCIETY: SERIES A (STATISTICS IN SOCIETY), Issue 1 2009
Stuart R. Lipsitz
Summary., In a large, prospective longitudinal study designed to monitor cardiac abnormalities in children born to women who are infected with the human immunodeficiency virus, instead of a single outcome variable, there are multiple binary outcomes (e.g. abnormal heart rate, abnormal blood pressure and abnormal heart wall thickness) considered as joint measures of heart function over time. In the presence of missing responses at some time points, longitudinal marginal models for these multiple outcomes can be estimated by using generalized estimating equations (GEEs), and consistent estimates can be obtained under the assumption of a missingness completely at random mechanism. When the missing data mechanism is missingness at random, i.e. the probability of missing a particular outcome at a time point depends on observed values of that outcome and the remaining outcomes at other time points, we propose joint estimation of the marginal models by using a single modified GEE based on an EM-type algorithm. The method proposed is motivated by the longitudinal study of cardiac abnormalities in children who were born to women infected with the human immunodeficiency virus, and analyses of these data are presented to illustrate the application of the method. Further, in an asymptotic study of bias, we show that, under a missingness at random mechanism in which missingness depends on all observed outcome variables, our joint estimation via the modified GEE produces almost unbiased estimates, provided that the correlation model has been correctly specified, whereas estimates from standard GEEs can lead to substantial bias. [source]

B-type natriuretic peptide (BNP) and N-terminal-proBNP for heart failure diagnosis in shock or acute respiratory distress

ACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 3 2006
L. Bal
Background:, Plasma B-type natriuretic peptide (BNP) assay is recommended as a diagnostic tool in emergency-room patients with acute dyspnea. In the intensive care unit (ICU), the utility of this peptide remains a matter of debate. The objectives of this study were to determine whether cut-off values for BNP and N-terminal-proBNP (NT-proBNP) reliably diagnosed right and/or left ventricular failure in patients with shock or acute respiratory distress, and whether non-cardiac factors led to an increase in these markers. Methods:, Plasma BNP and NT-proBNP levels and echocardiographic parameters of cardiac dysfunction were determined in 41 patients within 24 h of the onset of shock or acute respiratory distress. Results:, BNP and NT-proBNP levels were higher in the 25 patients with heart failure than in the other 16 patients: 491.7 ± 418 pg/ml vs. 144.3 ± 128 pg/ml and 2874.4 ± 2929 pg/ml vs. 762.7 ± 1128 pg/ml, respectively (P < 0.05). In the diagnosis of cardiac dysfunction, BNP > 221 pg/ml and NT-proBNP > 443 pg/ml had 68% and 84% sensitivity, respectively, and 88% and 75% specificity, respectively, but there was a substantial overlap of BNP and NT-proBNP values between patients with and without heart failure. BNP and NT-proBNP were elevated, but not significantly, in patients with isolated right ventricular dysfunction. Patients with renal dysfunction and normal heart function had significantly higher levels of BNP (258.6 ± 144 pg/ml vs. 92.4 ± 84 pg/ml) and NT-proBNP (2049 ± 1320 pg/ml vs. 118 ± 104 pg/ml) than patients without renal dysfunction. Conclusion:, Both BNP and NT-proBNP can help in the diagnosis of cardiac dysfunction in ICU patients, but cannot replace echocardiography. An elevated BNP or NT-proBNP level merely indicates the presence of a ,cardiorenal distress' and should prompt further investigation. [source]

Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features

PACING AND CLINICAL ELECTROPHYSIOLOGY, Issue 9 2002
ANTONIO FRANCO FOLINO
FOLINO, A.F., et al.: Heart Rate Variability in Arrhythmogenic Right Ventricular Cardiomyopathy Correlation with Clinical and Prognostic Features. The identification of subjects with arrhythmogenic right ventricular cardiomyopathy (ARVC) at higher risk for sudden death is an unresolved issue. An influence of the autonomic activity on the genesis of ventricular arrhythmias was postulated. Heart rate variability (HRV) analysis provides a useful method to measure autonomic activity, and is a predictor of increased risk of death after myocardial infarction. For these reasons, the aim of the study was to evaluate HRV and its correlations with ventricular arrhythmias, heart function, and prognostic outcome in patients with ARVC. The study included 46 patients with ARVC who were not taking antiarrhythmic medications. The diagnosis was made by ECG, echocardiography, angiography, and endomyocardial biopsy. Exercise stress test and Holter monitoring were obtained in all patients. Time-domain analysis of HRV was expressed as the standard deviation of all normal to normal NN intervals (SDNN) detected during 24-hour Holter monitoring. Thirty healthy subjects represented a control group for HRV analysis. The mean follow-up was 10.8 ± 1.86 years. SDNN was reduced in patients with ARVC in comparison with the control group (151 ± 36 vs 176 ± 34, P = 0.00042). Moreover, there was a significant correlation of this index with the age of the patients (r =,0.59, P < 0.001), with the left (r = 0.44, P = 0.002) and right (r = 0.47, P = 0.001) ventricle ejection fraction, with the right ventricular end diastolic volume (r =,0.62, P < 0.001), and with the ventricular arrhythmias, detected during the same Holter record used for HRV analysis (patients with isolated ventricular ectopic beats < 1,000/24 hours, 184 ± 34; patients with isolated ventricular ectopic beats > 1,000/24 hours and/or couplets, 156 ± 25; patients with repetitive ventricular ectopic beats (,3) and/or ventricular tachycardia, 129 ± 25; P < 0.001). During follow-up two patients showed a transient but significant reduction of SDNN and a concomitant increase of the arrhythmic events. In eight patients an episode of sustained ventricular tachycardia occurred, but the mean SDNN of this subgroup did not differ from the mean value of the remaining patients (152 ± 15 vs 150 ± 39; P = NS). Only one subject died after heart transplantation during follow-up (case censored). Time-domain analysis of HRV seems to be a useful method to assess the autonomic influences in ARVC. A reduction of vagal influences correlates with the extent of the disease. The significant correlation between SDNN and ventricular arrhythmias confirmed the influences of autonomic activity in the modulation of the electrical instability in ARVC patients. However, SDNN was not predictive of spontaneous episodes of sustained ventricular tachycardia. [source]

Protective effect of Lycium barbarum on doxorubicin-induced cardiotoxicity

PHYTOTHERAPY RESEARCH, Issue 11 2007
Yan-Fei Xin
Abstract The objective of this work was to explore the hypothesis that Lycium barbarum (LB) may be protective against doxorubicin (DOX)-induced cardiotoxicity through antioxidant-mediated mechanisms. Male SD rats were treated with distilled water or a water extract of LB (25 mg/kg, p.o.) daily and saline or DOX (5 mg/kg, i.v.) weekly for 3 weeks. Mortality, general condition and body weight were observed during the experiment. DOX-induced cardiotoxicity was assessed by electrocardiograph, heart antioxidant activity, serum levels of creatine kinase (CK) and aspartate aminotransferase (AST) and histopathological change. The DOX group showed higher mortality (38%) and worse physical characterization. Moreover, DOX caused myocardial injury manifested by arrhythmias and conduction abnormalities in ECG (increased QT and ST intervals and ST elevation), a decrease of heart antioxidant activity, an increase of serum CK and AST, as well as myocardial lesions. Pretreatment with LB significantly prevented the loss of myofibrils and improved the heart function of the DOX-treated rats as evidenced from lower mortality (13%), normalization of antioxidative activity and serum AST and CK, as well as improving arrhythmias and conduction abnormalities. These results suggested that LB elicited a typical cardioprotective effect on DOX-related oxidative stress. Furthermore, in vitro cytotoxic study showed the antitumor activity of DOX was not compromised by LB. It is possible that LB could be used as a useful adjunct in combination with DOX chemotherapy. Copyright © 2007 John Wiley & Sons, Ltd. [source]

Fetal dilated cardiomyopathy: an unsuspected presentation of methylmalonic aciduria and hyperhomocystinuria, cblC type,

PRENATAL DIAGNOSIS, Issue 3 2009
Isabelle De Bie
Abstract Objective To report the prenatal presentation with dilated cardiomyopathy of methylmalonic aciduria and homocystinuria, cblC type [cobalamin C (cblC) deficiency] (MIM 277400). Method We describe a boy with cblC deficiency who presented prenatally with fetal ultrasound findings of dilated cardiomyopathy and growth restriction. Results Dilated cardiomyopathy and growth retardation were detected in the third trimester of an initially uncomplicated pregnancy. Investigations were negative for chromosomal and other known causes. Growth restriction persisted but fetal heart function improved. Postnatal biochemical evaluation revealed combined methylmalonic acidemia and homocystinemia. Molecular investigations confirmed cblC deficiency. Initiation of treatment was followed by rapid clinical improvement. Conclusion Prenatal dilated cardiomyopathy can be the presenting sign of cblC deficiency. Inborn errors of metabolism should be considered in the investigation of prenatally diagnosed dilated cardiomyopathy in view of the possible impact on treatment and future reproductive options, in some of these conditions. Copyright © 2009 John Wiley & Sons, Ltd. [source]

Successful Long-Term Outcome of the First Combined Heart and Kidney Transplant in a Patient with Systemic AL Amyloidosis

AMERICAN JOURNAL OF TRANSPLANTATION, Issue 1 2009
V. Audard
Simultaneous cardiac and renal involvement is associated with a particularly poor prognosis in patients with AL amyloidosis (AL-A). We report the first case of a successful long-term outcome of combined heart and kidney transplantation not followed by autologous stem cell transplantation in a patient with systemic AL-A. The recipient was a 46-year-old man with end-stage renal failure associated with serious cardiac involvement in the context of AL-A. Before transplantation, two courses of oral melphalan plus prednisone induced partial hematologic remission, as shown by the decrease in circulating free light chain with no improvement of renal or heart function. The patient underwent combined heart and kidney transplantation as a rescue treatment. During the follow-up period (36 months), plasma cell dyscrasia remains in complete remission, with normal free lambda light chain levels and no recurrence of amyloid deposition on heart and kidney grafts. This case report demonstrates that combined heart and kidney transplantation not systematically associated with stem cell transplantation may be considered an additional therapeutic option in AL-A patients with severe organ dysfunction and partial hematologic remission. [source]

Right heart function during one-lung ventilation , observations using transoesophageal echocardiography

ANAESTHESIA, Issue 12 2009
J. N. Wilkinson
No abstract is available for this article. [source]

Prediction of the External Work of the Native Heart From the Dynamic H-Q Curves of the Rotary Blood Pumps During Left Heart Bypass

ARTIFICIAL ORGANS, Issue 9 2010
Yoshimasa Yokoyama
Abstract The ventricular performance is dependent on the drainage effect of rotary blood pumps (RBPs) and the performance of RBPs is affected by the ventricular pulsation. In this study, the interaction between the ventricle and RBPs was examined using the pressure-volume (P-V) diagram of the ventricle and dynamic head pressure-bypass flow (H-Q) curves (H, head pressure: arterial pressure minus ventricular pressure vs. Q, bypass flow) of the RBPs. We first investigated the relationships in a mock loop with a passive fill ventricle, followed by validation in ex vivo animal experiments. An apical drainage cannula with a micro-pressure sensor was especially fabricated to obtain ventricular pressure, while three pairs of ultrasonic crystals placed on the heart wall were used to derive ventricular volume. The mock loop-configured ventricular apical,descending aorta bypass revealed that the external work of the ventricle expressed by the area inside the P-V diagrams (EWHeart) correlated strongly with the area inside dynamic H-Q curves (EWVAD), with the coefficients of correlation being R2 = 0.869 , 0.961. The results in the mock loop were verified in the ex vivo studies using three Shiba goats (10,25 kg in body weight), showing the correlation coefficients of R2 = 0.802 , 0.817. The linear regression analysis indicated that the increase in the bypass flow reduced pulsatility in the ventricle expressed in EWHeart as well as in EWVAD. Experimental results, both mock loop and animal studies, showed that the interaction between cardiac external work and H-Q performance of RBPs can be expressed by the relationships "EWHeart versus EWVAD." The pulsatile nature of the native heart can be expressed in the area underneath the H-Q curves of RBPs EWVAD during left heart bypass indicating the status of the level of assistance by RBPs and the native heart function. [source]

Long-Term Evaluation of Myoblast Seeded Patches Implanted on Infarcted Rat Hearts

ARTIFICIAL ORGANS, Issue 6 2010
Marie-Noëlle Giraud
Abstract Cell transplantation presents great potential for treatment of patients with severe heart failure. However, its clinical application was revealed to be more challenging than initially expected in experimental studies. Further investigations need to be undertaken to define the optimal treatment conditions. We previously reported on the epicardial implantation of a bio-engineered construct of skeletal myoblast-seeded polyurethane and its preventive effect on progression toward heart failure. In the present study, we present a long-term evaluation of this functional outcome. Left anterior descending coronary ligation was performed in female Lewis rats. Two weeks later, animals were treated with either epicardial implantation of biograft, acellular scaffold, sham operation, or direct intramyocardial skeletal myoblast injection. Functional assessments were performed with serial echocardiographies every 3 months and end point left ventricle pressure was assessed. Hearts were then harvested for histological examinations. Myocardial infarction induced a slow and progressive reduction in fractional shortening after 3 months. Progression toward heart failure was significantly prevented for up to 6 months after injection of myoblasts and for up to 9 months following biograft implantation. Nevertheless, this effect vanished after 12 months, with immunohistological examinations revealing an absence of the transplanted myoblasts within the scaffold. We demonstrated that tissue therapy is superior to cell therapy for stabilization of heart function. However, beneficial effects are transient. [source]

Ductular Cholestasis, an Unusual Form of Intrahepatic Cholestasis, Associated With Cardiogenic Shock and Ventricular Assist Device

ARTIFICIAL ORGANS, Issue 2 2010
Alberto Mohedano-Gómez
Abstract Ventricular assist devices have been shown to be effective in advanced heart failure selected patients. They often have borderline end-organ function, what facilitates organ dysfunction. Liver failure is difficult to manage and leads to increased morbidity and mortality. We report a case of ductular cholestasis, an unusual cholestatic hepatic failure with untractable coagulopathy, developed during the use of a magnetic levitation centrifugal pump, implanted as a bridge to heart transplantation, in a patient with cardiogenic shock (as an end-stage disease of idiopathic dilated cardiomyopathy). We discussed the pathophysiology of this entity and the possible related factors, including the assist device. Preemptive interventions have been advocated as the primary way of treatment. Preoperative optimization of heart function and avoidance of visceral hypoperfusion and sepsis may play a major role. [source]

Effect of lifestyle factors and hormone therapy on heart function by serial echocardiography in postmenopausal women

AUSTRALIAN AND NEW ZEALAND JOURNAL OF OBSTETRICS AND GYNAECOLOGY, Issue 1 2010
Soo-Keat KHOO
Background:, There is conflicting information on the effects of oestrogen on the heart in women, especially those using postmenopausal hormone therapy. Whilst some studies reported a beneficial effect, others showed adverse outcomes. The interplay of lifestyle factors and type/timing of therapy remains to be clarified. Aim:, The aim of this study was to determine the effects of lifestyle and hormone therapy on heart function and structure in postmenopausal women. Method:, As part of a large longitudinal study of women randomly recruited from an urban population, the study assessed 410 suitable women by echocardiography in Year 1 and Year 5 of the study by two independent cardiologists. Results:, In lifestyle characteristics, the difference in age and body mass (as markers of cardiovascular risk) was in favour of never-users versus hormone therapy-users. Using an arbitrary cut-off ,15% change for an effect, we found lifestyle factors had minimal effect on the two measured parameters , ejection fraction, left ventricular mass. Effects of hormone therapy were variable and mixed; greatest effect was found for an ,early start' of hormone therapy with oestrogen-only preparation , the risk of reduced ejection fraction was decreased [hazard ratio (HR) 0.42, confidence interval = 0.17,1.03, P = 0.06] and risk of increased left ventricular mass was increased (HR 2.21, 1.09,4.49, P = 0.03). Conclusion:, Our findings add to the evidence that oestrogen given to postmenopausal women has a mixed effect on the heart, with effect best shown when started early. [source]

Procyanidins Produce Significant Attenuation of Doxorubicin-Induced Cardiotoxicity via Suppression of Oxidative Stress

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 3 2009
Wei Li
The major side effect of doxorubicin is oxidative injury-related cardiotoxicity, which has dramatically hindered its usage. Procyanidins from grape seeds are potent free radical scavengers that have been shown to protect against anthracycline-induced cardiotoxicity. In the present study, we tested whether procyanidins would prevent the doxorubicin-induced cardiotoxicity in rats. Rats were intraperitoneally treated with doxorubicin at a cumulative dose of 15 mg/kg with and without pre-administration of procyanidins. Our data showed that doxorubicin led to cardiac function deterioration, myocardial injury and increased oxidative stress in cardiac tissues. The cardiac function deterioration by doxorubicin included increased QT-interval and ST-interval in electrocardiograph (ECG) and decreased left ventricular developed pressure. Doxorubicin-induced myocardial injury was shown by the increased creatine kinase, alanine aminotransferase and aspartate aminotransferase in serum as well as in myocardial lesions. Pretreatment with procyanidin (150 mg/kg daily) effectively hindered the adverse effects of doxorubicin, such as myocardial injury and impaired heart function. Procyanidin pretreatment attenuated cytoplasmic vacuolization, increased left ventricular developed pressure and improved the ECG. The cardioprotective effect of procyanidin corresponded to the decrease of lipid peroxidation and the increase of cardiac antioxidant potency in doxorubicin-treated rats that were also given procyanidin. An in vitro cytotoxic study showed that procyanidins did not attenuate the antineoplastic activity of doxorubicin to A549 adenocarcinoma cells. All the above lines of evidence suggest that procyanidins protect cardiomyocytes from doxorubicin-induced cardiotoxicity via suppression of oxidative stress. [source]

The Role of Myocardial KATP -Channel Blockade in the Protective Effects of Glibenclamide against Ischaemia in the Rat Heart

BASIC AND CLINICAL PHARMACOLOGY & TOXICOLOGY, Issue 2 2002
Roger J. Legtenberg
This study addresses the possible involvement of KATP channels in this beneficial action of glibenclamide. We hypothesized that if glibenclamide improved postischaemic cardiac function by blocking of KATP channels, opening of these KATP channels should result in the opposite, namely detrimental effects on postischaemic heart function. Postischaemic functional loss and coronary blood flow were recorded during treatment with glibenclamide (4 ,mol.l,1; n=5), the KATP channel openers pinacidil (1 ,mol.l,1; n=5) and diazoxide (30 ,mol.l,1; n=5), the combination of glibenclamide with pinacidil (n=5) and glibenclamide with diazoxide (n=5), and vehicle (n=8). Both pinacidil and diazoxide significantly increased coronary blood flow 2,3 times, which was abolished by glibenclamide pre- and postischaemically. This confirms that under both flow conditions glibenclamide significantly blocks KATP channels in the coronary vasculature. The 12 min. global ischaemic incident resulted in a cardiac functional loss of 22.2±2.9% during vehicle. Glibenclamide reduced the cardiac functional loss to 4.3±1.2% (P<0.01). Interestingly, both pinacidil and diazoxide reduced the cardiac functional loss to 4.0±1.5% (P<0.01) and 2.9±1.4% (P<0.001), respectively. The combination pinacidil+glibenclamide resulted in additional protection compared with the individual components (0.6±0.1 versus 4.0±1.5%, P<0.05). Thus, in contrast to its effect on coronary vascular tone, the glibenclamide-induced improvement of postischaemic cardiac function may not be mediated through blockade of the KATP channel. Alternative mechanisms may be operative, such as uncoupling of the mitochondrial respiratory chain, thereby preconditioning the hearts against stunning. [source]

Treatment of statin adverse effects with supplemental Coenzyme Q10 and statin drug discontinuation

BIOFACTORS, Issue 1-4 2005
Peter H. Langsjoen
Abstract Fifty consecutive new cardiology clinic patients who were on statin drug therapy (for an average of 28 months) on their initial visit were evaluated for possible adverse statin effects (myalgia, fatigue, dyspnea, memory loss, and peripheral neuropathy). All patients discontinued statin therapy due to side effects and began supplemental CoQ10 at an average of 240 mg/day upon initial visit. Patients have been followed for an average of 22 months with 84% of the patients followed now for more than 12 months. The prevalence of patient symptoms on initial visit and on most recent follow-up demonstrated a decrease in fatigue from 84% to 16%, myalgia from 64% to 6%, dyspnea from 58% to 12%, memory loss from 8% to 4% and peripheral neuropathy from 10% to 2%. There were two deaths from lung cancer and one death from aortic stenosis with no strokes or myocardial infarctions. Measurements of heart function either improved or remained stable in the majority of patients. We conclude that statin-related side effects, including statin cardiomyopathy, are far more common than previously published and are reversible with the combination of statin discontinuation and supplemental CoQ10. We saw no adverse consequences from statin discontinuation. [source]

,-Adrenoceptor stimulation potentiates insulin-stimulated PKB phosphorylation in rat cardiomyocytes via cAMP and PKA

BRITISH JOURNAL OF PHARMACOLOGY, Issue 1 2010
Jorid T Stuenæs
Background and purpose:, Genetic approaches have documented protein kinase B (PKB) as a pivotal regulator of heart function. Insulin strongly activates PKB, whereas adrenaline is not considered a major physiological regulator of PKB in heart. In skeletal muscles, however, adrenaline potentiates insulin-stimulated PKB activation without having effect in the absence of insulin. The purpose of the present study was to investigate the interaction between insulin and ,-adrenergic stimulation in regulation of PKB phosphorylation. Experimental approach:, Cardiomyocytes were isolated from adult rats by collagenase, and incubated with insulin, isoprenaline, and other compounds. Protein phosphorylation was evaluated by Western blot and phospho-specific antibodies. Key results:, Isoprenaline increased insulin-stimulated PKB Ser473 and Thr308 phosphorylation more than threefold in cardiomyocytes. Isoprenaline alone did not increase PKB phosphorylation. Isoprenaline also increased insulin-stimulated GSK-3, Ser9 phosphorylation approximately twofold, supporting that PKB phosphorylation increased kinase activity. Dobutamine (,1 -agonist) increased insulin-stimulated PKB phosphorylation as effectively as isoprenaline (more than threefold), whereas salbutamol (,2 -agonist) only potentiated insulin-stimulated PKB phosphorylation by approximately 80%. Dobutamine, but not salbutamol, increased phospholamban Ser16 phosphorylation and glycogen phosphorylase activation (PKA-mediated effects). Furthermore, the cAMP analogue that activates PKA (dibutyryl-cAMP and N6 -benzoyl-cAMP) increased insulin-stimulated PKB phosphorylation by more than threefold without effect alone. The Epac-specific activator 8-(4-chlorophenylthio)-2,-O-methyl-cAMP (007) increased insulin-stimulated PKB phosphorylation by approximately 50%. Db-cAMP and N6 -benzoyl-cAMP, but not 007, increased phospholamban Ser16 phosphorylation. Conclusions and implications:, ,-adrenoceptors are strong regulators of PKB phosphorylation via cAMP and PKA when insulin is present. We hypothesize that PKB mediates important signalling in the heart during ,-adrenergic receptors stimulation. [source]

EFFECT OF BENAZEPRIL ON HEART RATE TURBULENCE IN PATIENTS WITH DILATED CARDIOMYOPATHY

CLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 7 2007
Jiang-Hua Zhong
SUMMARY 1Heart rate (HR) turbulence describes short-term sinus rhythmic fluctuation after a single premature ventricular beat. Turbulence onset (TO) and turbulence slope (TS) are two essential parameters in HR turbulence. Turbulence onset and TS have been used to evaluate cardiac autonomic nerve function. 2In the present study, we measured the HR turbulence in dilated cardiomyopathy (DCM) and determined the possible role of benazepril, an angiotensin-converting enzyme inhibitor (ACEI), on these parameters. There were three groups: control, DCM and DCM treated with benazepril. The control group consisted of normal subjects with PVB, but no structural heart disease. Ambulatory electrocardiogram, blood pressure and echocardiography were analysed. 3There was an increase in TO and a decrease in TS in DCM patients. Benazepril treatment (10 mg/day, p.o.) reduced those changes. There were no significant differences in blood pressure and left ventricular ejection fraction (LVEF) between DCM patients and DCM patients treated with benazepril. 4Linear regression analysis showed that TO was negatively correlated with LVEF, whereas TS was positively correlated with LVEF, in the DCM group. After benazepril treatment, the correlations between TO and TS and LVEF disappeared. 5It is concluded that the TO and TS of HR turbulence are altered in patients with DCM. These alterations indicate a dysfunction of the autonomic control of cardiac electrophysiology in DCM patients. Although TO and TS are correlated with LVEF in DCM patients, the effect of benazepril in improving HR turbulence parameters is not a result of its action on heart function, which suggests a new beneficial effect of ACEI in the treatment of DCM patients. [source]