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Ventricular Contractility (ventricular + contractility)
Kinds of Ventricular Contractility Selected AbstractsLeft Ventricular Function in Male Patients with Secondary HypogonadismECHOCARDIOGRAPHY, Issue 3 2007Oben Baysan M.D. Background: In addition to the effects on ventricular repolarization, testosterone could also affect left ventricular performance. The enhancement of left ventricular contractility in testosterone-deficient rats following testosterone replacement implies to the possible testosterone effect. Objectives: The aim of the current study is to reveal the alterations of left ventricular functions, if any, in secondary hypogonadal male patients. Methods: Thirty-four males with secondary hypogonadism comprised the study group. The control group consisted of 30 healthy subjects. Echocardiographic measurements including left ventricular dimensions, ejection fraction, mitral inflow, and left ventricular outflow parameters were obtained from all subjects. Tissue Doppler parameters were also measured from left ventricular lateral wall and interventricular septum. Results: Left ventricular diameters, wall thicknesses, and performance parameters were similar in both groups. Mitral inflow parameters showed a statistically insignificant difference. Pulse-wave tissue Doppler interpretation of hypogonadal and healthy subjects were similar in terms of lateral and septal basal segment Sm, Em, and Am wave velocities. Conclusions: Regarding the findings of previous studies that showed impaired myocardial contractility and lusitropy in testosterone deficient rats and our study results, further studies are needed for better understanding of testosterone's effects on human myocardium. [source] An abnormal gene expression of the ,-adrenergic system contributes to the pathogenesis of cardiomyopathy in cirrhotic rats,HEPATOLOGY, Issue 6 2008Giulio Ceolotto Decreased cardiac contractility and ,-adrenergic responsiveness have been observed in cirrhotic cardiomyopathy, but their molecular mechanisms remain unclear. To study ,-adrenergic,stimulated contractility and ,-adrenergic gene expression patterns, 20 Wistar Kyoto rats were treated with carbon tetrachloride to induce cirrhosis and 20 rats were used as controls. Left ventricular contractility was recorded in electrically driven isolated hearts perfused at constant flow with isoproterenol (10,10 to 10,6 M). A cardiac gene expression profile was obtained using a microarray for the myocyte adrenergic pathway. The cardiac contractility maximal response to isoproterenol was significantly reduced in cirrhotic rats in comparison to control rats, whereas the half-maximal effective concentration was not different. In cirrhotic rats, cardiac gene expression analysis showed a significant overexpression of G protein alpha,inhibiting subunit 2 (G,i2), cyclic nucleotide phosphodiesterase (PDE2a), regulator of G-protein signaling 2 (RGS2), and down-expression of adenylate cyclase (Adcy3). These results indicate that overexpression of G,i2, PDE2a, and RGS2 down-regulates the ,-adrenergic signaling pathway, thus contributing to the pathogenesis of cirrhotic cardiomyopathy. (HEPATOLOGY 2008;48:1913-1923.) [source] Differential effects of sevoflurane and propofol anesthesia on left ventricular,arterial coupling in dogsACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 8 2010Y. L. J. M. DERYCK Background: General anesthetics interfere with arterial and ventricular mechanical properties, often altering left ventricular,arterial (LVA) coupling. We hypothesized that sevoflurane and propofol alter LVA coupling by different effects on arterial and ventricular properties. Methods: Experiments were conducted in six anesthetized open-chest dogs for the measurement of left ventricular pressure and aortic pressure and flow. Measurements were performed during anesthesia with 0.5, 1.0 and 1.5 minimum alveolar concentration sevoflurane and 12, 24 and 36 mg/kg/h propofol. LVA coupling was assessed as the ratio of ventricular end-systolic elastance (Ees, measuring ventricular contractility) to effective arterial elastance (Ea, measuring ventricular afterload). The steady component of afterload, arterial tone, was assessed by systemic vascular resistance and arterial pressure,flow curves. The pulsatile component of afterload was assessed by aortic impedance and compliance. Results: Sevoflurane decreased aortic pressure and cardiac output more than propofol. Sevoflurane reduced arterial tone, increased arterial stiffness and did not affect wave reflections. It increased Ea, decreased Ees and reduced LVA coupling. Propofol reduced arterial tone, did not affect arterial stiffness and decreased wave reflections. It did not affect Ea, Ees or LVA coupling. Conclusions: Sevoflurane increased ventricular afterload and decreased ventricular performance, thereby altering LVA coupling. Propofol did not affect ventricular afterload or ventricular performance, thereby preserving LVA coupling. Thus, propofol preserves LVA coupling in dogs better, and might be a better choice for patients with compromised left ventricular function. [source] Surgical Repair of a Congenital Left Ventricular AneurysmJOURNAL OF CARDIAC SURGERY, Issue 1 2007Mustafa Cikirikcioglu M.D., Ph.D. A 9-year-old boy with complaints of dyspnea and palpitation was diagnosed with a left ventricular aneurysm originating from the left ventricle free wall. Aneurysm resection and endoventricular patch repair was performed. Postoperative follow-up was uncomplicated and follow-up echocardiographs showed normal left ventricular contractility. [source] Validation of a New Noninvasive Device for the Monitoring of Peak Endocardial Acceleration in Pigs: Implications for Optimization of Pacing Site and ConfigurationJOURNAL OF CARDIOVASCULAR ELECTROPHYSIOLOGY, Issue 7 2008PIERRE BORDACHAR M.D. Introduction: The peak of endocardial acceleration (PEA) is an index of myocardial contractility. We aimed to (1) demonstrate that the PEA measured by the noninvasive cutaneous precordial application of an accelerometer sensor is related to left ventricular (LV) dP/dt max and (2) assess the usefulness of PEA monitoring during graded ischemia and during different configurations of sequential biventricular pacing. Methods and Results: Measurements of invasive LV dP/dt max were compared with measurements of transcutaneous PEA in seven pigs at baseline and during acute drug infusions; increased heart rate; right, left, biventricular and sequential biventricular pacing before and after graded ischemia induced by the constriction of the left anterior descending coronary artery. A consistent PEA signal was obtained in all animals. PEA changes were highly related to LV dP/dt max changes (r= 0.93; P < 0.001). The changes of LV contractility induced by the different pacing configurations were detected by PEA analysis in the absence of ischemia (r= 0.94; P < 0.001) and in the presence of ischemic LV dysfunction (r= 0.91; P < 0.001). Conclusion: Noninvasive PEA measurement allows monitoring of left ventricular contractility and may be a useful tool to detect global effect of ventricular ischemia and to optimize the choice of both pacing site and pacing configuration. [source] Short-Term Acetaldehyde Exposure Depresses Ventricular Myocyte Contraction: Role of Cytochrome P450 Oxidase, Xanthine Oxidase, and Lipid PeroxidationALCOHOLISM, Issue 4 2003Nicholas S. Aberle II Background: Chronic alcoholism leads to the development of alcoholic cardiomyopathy, manifested as ventricular dilation and impaired ventricular contractility. However, the specific toxic mechanism responsible for alcoholic cardiomyopathy remains unclear. One major candidate toxin is the first metabolic product of ethanol, acetaldehyde (ACA). This study was designed to examine the role of cytochrome P450 oxidase 2E1 (CYP 2E1), xanthine oxidase, and lipid peroxidation in the short-term ACA exposure-induced mechanical defects in adult rat ventricular myocytes. Methods: Mechanical and intracellular Ca2+ properties were evaluated by an IonOptix SoftEdge® system. Lipid peroxidation was assessed with malondialdehyde levels by using high-performance liquid chromatography. Results: Short-term (4- to 6-hr) culture of myocytes with ACA (1,100 ,M) in sealed containers with silicone septum depressed cell-shortening amplitude, maximal velocity of shortening/relengthening, and prolonged duration of relengthening, as well as intracellular Ca2+ clearing without any effect on the duration of shortening and electrically stimulated an intracellular Ca2+ increase. It is interesting to note that the ACA-induced effects on myocyte mechanical properties were abolished with co-treatment of the lipid peroxidation inhibitor butylated hydroxytoluene (20 ,M), the CYP 2E1 inhibitor diallyl sulfide (100 ,M), and the xanthine oxidase inhibitor allopurinol (100 ,M). Short-term incubation of ACA with the myocytes also produced a significant increase of the lipid peroxidation end product malondialdehyde, which may be prevented by butylated hydroxytoluene. Conclusions: Collectively, these data provided evidence that ACA depressed cardiomyocyte mechanical function at micromolar levels, possibly through mechanisms related to CYP oxidase, xanthine oxidase, and lipid peroxidation. [source] Echocardiographic changes and risk factors for left ventricular hypertrophy in children and adolescents after renal transplantationPEDIATRIC TRANSPLANTATION, Issue 3 2004Amr A. El-Husseini Abstract:, Long-term consequences of cardiac alteration in children with chronic renal failure and after renal transplantation are largely unknown. In chronic uremia, cardiomyopathy manifests itself as systolic dysfunction, concentric left ventricular hypertrophy (LVH) or left ventricular dilatation. The correction of uremic state by renal transplantation leads to normalization of left ventricular contractility, regression of LVH and improvement of cavity volume and so dialysis patients with uremic cardiomyopathy would benefit from renal transplantation. We studied 73 patients, aged 17 yr or less, who underwent renal transplantation in our center. This cross-sectional study was performed 4.6 yr (median) after transplantation. Of the total, 48 were males and 25 were females. Transthoracic echocardiographic examination was performed for all cases. The effects of clinical, demographic, biochemical and therapeutic data on echocardiographic parameters were assessed. Multivariate analysis was used to assess the relation between the risk factors and the left ventricular muscle mass index. The most common echocardiographic abnormalities were the LVH (47.9%), left atrial enlargement (31.5%) and left ventricular dilatation and systolic dysfunction (13.7% for each). The pretransplant dialysis, arteriovenous fistula, acute rejection, cumulative steroid dose per square meter surface area, post-transplant hypertension, anemia and graft dysfunction were significant risk factors for LVH by univariate analysis. The significant factors by multivariate analysis were pretransplant dialysis, post-transplant hypertension and anemia. From this study we may conclude that LVH is a common problem among renal transplant children and adolescents. Early transplantation, control of hypertension and correction of anemia may be beneficial regarding left ventricular function and structure. [source] Vasopressin in the treatment of vasodilatory shock in childrenPEDIATRICS INTERNATIONAL, Issue 2 2005Satoshi Masutani Abstract,Background:,Many recent studies suggest that vasopressin deficiency is an important cause of catecholamine-resistant hypotension with vasodilation in adults, but little is known about vasopressin deficiency in children. Methods:,To clarify the usefulness of vasopressin administration in pediatric cathecolamine-resistant hypotension with preserved ventricular contractility, urinary output and blood pressure response to vasopressin were retrospectively analyzed in 12 consecutive patients (15 instances) who were treated with vasopressin. The causes of vasodilation were central nervous system disturbance (n = 5), side-effect of drug (n = 5), and infection (n = 5). Plasma vasopressin concentration was measured six times before vasopressin administration and five times during vasopressin administration. Results:,Patients were divided into four groups according to their response to vasopressin administration. In group 1 (n = 5), urinary output increased to > 3 mL/kg per h within 3 h after vasopressin administration. In group 2 (n = 4), urinary output increased to > 3 mL/kg per h from 3 to 5 h after vasopressin administration. In group 3 (n = 4), urinary output did not increase to > 3 mL/kg per min within 5 h after vasopressin administration, but systolic blood pressure increased to > 120% of the level at the time of vasopressin administration. All remaining patients were classified into group 4 (n = 3). Plasma vasopressin concentration were low considering the markedly hypotensive state in all six instances. Plasma vasopressin concentration during vasopressin administration were significantly increased compared with before administration (P < 0.05). No apparent side-effects were observed in this series. Conclusion:,Vasopressin deficiency may occur in catecholamine-resistant hypotension of pediatric patients due to various causes including central nervous system disturbance, drug induced hypotension and sepsis. Small doses of vasopressin administration seems to be very effective in such conditions by increasing blood pressure and urinary output. [source] Longitudinal estimation of signal-averaged electrocardiograms in patients with Kawasaki diseasePEDIATRICS INTERNATIONAL, Issue 1 2002Yukio Kuramochi Abstract Background:,Myocarditis associated with Kawasaki (KD) disease is prominent, but rarely detected by conventional methods. The hypothesis of this study is to see if signal-averaged electrocardiogram can detect myocarditis with KD. Methods:,We obtained signal-averaged electrocardiograms from 71 patients with KD (mean age 2.8 ± 2.9 years) in the acute (1st,4th week), subacute (5,7th week), and chronic (8th week or later) phases (mean study period 3.5 ± 1.7 years). Sixteen patients who had pericardial effusion, bundle branch block or myocardial ischemia were excluded from this study. The results were compared with those of Holter and 12-lead electrocardiograms, echocardiography and serum myocardial enzymes. They were also contrasted with the course of each patient. Results:,The incidence of abnormal findings on signal-averaged electrocardiogram was 18.2% in the acute phase versus 10.9% in the subacute and chronic phases. It differed significantly higher than the other conventional tests (P < 0.05). Four patients had abnormalities of signal-averaged electrocardiograms through all three phases. Among these four, two had reduced left ventricular contractility. However, these changes were transient and resolved in the subacute phase. All patients had good courses and no residue. Conclusion:,This study shows the possibility that signal-averaged electrocardiogram is more useful to detect myocarditis associated with KD than the other conventional tests. However, we could not define the prognostic value of abnormal signal-averaged electrocardiograms during this study period. [source] Methods for prenatal assessment of fetal cardiac functionPRENATAL DIAGNOSIS, Issue 13 2009Tim Van Mieghem Abstract Fetal cardiac function is increasingly recognized as a marker of disease severity and prognosis in selected fetal conditions. Magnetic resonance imaging (MRI) has been used in experimental (animal) fetal cardiology but the lack of a noninvasive fetal electrocardiogram (ECG) to trigger image acquisition remains a major limiting factor precluding its application in humans. Fetal medicine specialists are therefore limited to ultrasound to evaluate human fetal cardiac function. In this review, we aim to provide a complete overview of the different ultrasound techniques that can be used for fetal cardiac function assessment and we discuss their (theoretical) strengths and shortcomings. Conventional methods include M-mode assessment of ventricular contractility and Doppler assessment of the precordial veins and cardiac output (CO). More recent techniques such as the measurement of the myocardial performance index (MPI), myocardial motion analysis with tissue Doppler, speckle tracking and three-dimensional (3D) ultrasound techniques are also discussed. Copyright © 2009 John Wiley & Sons, Ltd. [source] Fully Autonomous Preload-Sensitive Control of Implantable Rotary Blood PumpsARTIFICIAL ORGANS, Issue 9 2010Andreas Arndt Abstract A pulsatility-based control algorithm with a self-adapting pulsatility reference value is proposed for an implantable rotary blood pump and is to be tested in computer simulations. The only input signal is the pressure difference across the pump, which is deduced from measurements of the pump's magnetic bearing. A pulsatility index (PI) is calculated as the mean absolute deviation from the mean pressure difference. As a second characteristic, the gradient of the PI with respect to the pump speed is derived. This pulsatility gradient (GPI) is used as the controlled variable to adjust the operating point of the pump when physiological variables such as the systemic arterial pressure, left ventricular contractility, or heart rate change. Depending on the selected mode of operation, the controller is either a linear controller or an extremum-seeking controller. A supervisory mechanism monitors the state of the system and projects the system into the region of convergence when necessary. The controller of the GPI continuously adjusts the reference value for PI. An underlying robust linear controller regulates the PI to the reference value in order to take into account changes in pulmonary venous return. As a means of reacting to sudden changes in the venous return, a suction detection mechanism was included. The control system is robustly stable within a wide range of physiological variables. All the clinician needs to do is to select between the two operating modes. No other adjustments are required. The algorithm showed promising results which encourage further testing in vitro and in vivo. [source] Physiological Control of a Rotary Blood Pump With Selectable Therapeutic Options: Control of Pulsatility GradientARTIFICIAL ORGANS, Issue 10 2008Andreas Arndt Abstract A control strategy for rotary blood pumps meeting different user-selectable control objectives is proposed: maximum support with the highest feasible flow rate versus medium support with maximum ventricular washout and controlled opening of the aortic valve (AoV). A pulsatility index (PI) is calculated from the pressure difference, which is deduced from the axial thrust measured by the magnetic bearing of the pump. The gradient of PI with respect to pump speed (GPI) is estimated via online system identification. The outer loop of a cascaded controller regulates GPI to a reference value satisfying the selected control objective. The inner loop controls the PI to a reference value set by the outer loop. Adverse pumping states such as suction and regurgitation can be detected on the basis of the GPI estimates and corrected by the controller. A lumped-parameter computer model of the assisted circulation was used to simulate variations of ventricular contractility, pulmonary venous pressure, and aortic pressure. The performance of the outer control loop was demonstrated by transitions between the two control modes. Fast reaction of the inner loop was tested by stepwise reduction of venous return. For maximum support, a low PI was maintained without inducing ventricular collapse. For maximum washout, the pump worked at a high PI in the transition region between the opening and the permanently closed AoV. The cascaded control of GPI and PI is able to meet different control objectives and is worth testing in vitro and in vivo. [source] Cardioprotection from ischemia-reperfusion injury due to Ras-GTPase inhibition is attenuated by glibenclamide in the globally ischemic heartCELL BIOCHEMISTRY AND FUNCTION, Issue 4 2007Ibrahim Al-Rashdan Abstract The present study was designed to see if acute local inhibition of Ras-GTPase before or after ischemia (during perfusion) would produce protection against ischemia and reperfusion (I/R)-induced cardiac dysfunction. The effect of glibenclamide, an inhibitor of cardiac mitochondrial ATP-sensitive potassium (mitoKATP) channels, on Ras-GTPase-mediated cardioprotection was also studied. A 40,min episode of global ischemia followed by a 30,min reperfusion in perfused rat hearts produced significantly impaired cardiac function, measured as left ventricular developed pressure (Pmax) and left ventricular end-diastolic pressure (LVEDP). Perfusion with Ras-GTPase inhibitor FPT III before I/R [FPT(pre)], significantly enhanced cardiac recovery in terms of left ventricular contractility. Pmax was significantly higher at the end of 30,min reperfusion in FPT(pre)-treated hearts compared to pre-conditioned hearts. However, the degree of improvement in left ventricular contractility was significantly less when FPT III was given only after ischemia during reperfusion [FPT(post)]. Combination treatment with FPT III and glibenclamide before I/R resulted in significant reduction of FPT III-mediated cardioprotection. These data suggest that activation of Ras-GTPase signaling pathways during ischemia are critical in the development of left ventricular dysfunction and that opening of mitoKATP channels, at least in part, contributes to cardioprotection produced by Ras-GTPase inhibition. Copyright © 2006 John Wiley & Sons, Ltd. [source] | |||||||||||||