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Left Ventricular Contractility (leave + 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] 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] 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] 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] | ||||||||||