Home About us Contact
|
Home About us Contact | ||
|
|
||
Contractile Reserve (contractile + reserve)
Selected AbstractsContractile Reserve Assessed Using Dobutamine Echocardiography Predicts Left Ventricular Reverse Remodeling after Cardiac Resynchronization Therapy: Prospective Validation in Patients with Left Ventricular DyssynchronyECHOCARDIOGRAPHY, Issue 6 2010F.R.C.P.C., Mario Sénéchal M.D. Background: The presence of viable myocardium may predict response to cardiac resynchronization therapy (CRT). The aim of this study is to evaluate in patients with left ventricular (LV) dyssynchrony whether response to CRT is related to myocardial viability in the region of the pacing lead. Methods: Forty-nine consecutive patients with advanced heart failure, LV ejection fraction < 35%, QRS duration > 120 ms and intraventricular asynchronism , 50 ms were included. Dobutamine stress echocardiography was performed within the week before CRT implantation. Resting echocardiography was performed 6 months after CRT implantation. Viability in the region of LV pacing lead was defined as the presence of viability in two contiguous segments. Response to CRT was defined by evidence of reverse LV remodeling (,15% reduction in LV end-systolic volume). Results: Thirty-one patients (63%) were identified as responders at follow-up. The average of viable segments was 5.9 ± 2 in responders and 3.2 ± 3 in nonresponders (P = 0.0003). Viability in the region of the pacing lead had a sensitivity of 94%, a specificity of 67%, a positive predictive value of 83%, and a negative predictive value of 86% for the prediction of response to CRT. Conclusions: In patients with LV dyssynchrony, reverse remodeling after CRT requires viability in the region of the pacing lead. This simple method using echocardiography dobutamine for the evaluation of local viability (i.e., viability in two contiguous segments) may be useful to the clinician in choosing the best LV lead positioning. (Echocardiography 2010;27:668-676) [source] Usefulness and Limitation of Dobutamine Stress Echocardiography to Predict Acute Response to Cardiac Resynchronization TherapyECHOCARDIOGRAPHY, Issue 1 2010F.R.C.P.C., Mario Sénéchal M.D. Background: It has been hypothesized that a long-term response to cardiac resynchronization therapy (CRT) could correlate with myocardial viability in patients with left ventricular (LV) dysfunction. Contractile reserve and viability in the region of the pacing lead have not been investigated in regard to acute response after CRT. Methods: Fifty-one consecutive patients with advanced heart failure, LV ejection fraction , 35%, QRS duration > 120 ms, and intraventricular asynchronism , 50 ms were prospectively included. The week before CRT implantation, the presence of viability was evaluated using dobutamine stress echocardiography. Acute responders were defined as a ,15% increase in LV stroke volume. Results: The average of viable segments was 5.8 ± 1.9 in responders and 3.9 ± 3 in nonresponders (P = 0.03). Viability in the region of the pacing lead had an excellent sensitivity (96%), but a low specificity (56%) to predict acute response to CRT. Mitral regurgitation (MR) was reduced in 21 patients (84%) with acute response. The presence of MR was a poor predictor of response (sensibility 93% and specificity 17%). However, combining the presence of MR and viability in the region of the pacing lead yields a sensibility (89%) and a specificity (70%) to predict acute response to CRT. Conclusion: Myocardial viability is an important factor influencing acute hemodynamic response to CRT. In acute responders, significant MR reduction is frequent. The combined presence of MR and viability in the region of the pacing lead predicts acute response to CRT with the best accuracy. (Echocardiography 2010;27:50-57) [source] Global and right ventricular end-diastolic volumes correlate better with preload after correction for ejection fractionACTA ANAESTHESIOLOGICA SCANDINAVICA, Issue 5 2010M. L. N. G. MALBRAIN Background: Volumetric monitoring with right ventricular end-diastolic volume indexed (RVEDVi) and global end-diastolic volume indexed (GEDVi) is increasingly being suggested as a superior preload indicator compared with the filling pressures central venous pressure (CVP) or the pulmonary capillary wedge pressure (PCWP). However, static monitoring of these volumetric parameters has not consistently been shown to be able to predict changes in cardiac index (CI). The aim of this study was to evaluate whether a correction of RVEDVi and GEDVi with a measure of the individual contractile reserve, assessed by right ventricular ejection fraction (RVEF) and global ejection fraction, improves the ability of RVEDVi and GEDVi to monitor changes in preload over time in critically ill patients. Methods: Hemodynamic measurements, both by pulmonary artery and by transcardiopulmonary thermodilution, were performed in 11 mechanically ventilated medical ICU patients. Correction of volumes was achieved by normalization to EF deviation from normal EF values in an exponential fashion. Data before and after fluid administration were obtained in eight patients, while data before and after diuretics were obtained in seven patients. Results: No correlation was found between the change in cardiac filling pressures (,CVP, ,PCWP) and ,CI (R2 0.01 and 0.00, respectively). Further, no correlation was found between ,RVEDVi or ,GEDVi and ,CI (R2 0.10 and 0.13, respectively). In contrast, a significant correlation was found between ,RVEDVi corrected to RVEF (,cRVEDVi) and ,CI (R2 0.64), as well as between ,cGEDVi and ,CI (R2 0.59). An increase in the net fluid balance with +844 ± 495 ml/m2 resulted in a significant increase in CI of 0.5 ± 0.3 l/min/m2; however, only ,cRVEDVi (R2 0.58) and ,cGEDVi (R2 0.36) correlated significantly with ,CI. Administration of diuretics resulting in a net fluid balance of ,942 ± 658 ml/m2 caused a significant decrease in CI with 0.7 ± 0.5 l/min/m2; however, only ,cRVEDVi (R2 0.80) and ,cGEDVi (R2 0.61) correlated significantly with ,CI. Conclusion: Correction of volumetric preload parameters by measures of ejection fraction improved the ability of these parameters to assess changes in preload over time in this heterogeneous group of critically ill patients. [source] Sildenafil-mediated neovascularization and protection against myocardial ischaemia reperfusion injury in rats: role of VEGF/angiopoietin-1JOURNAL OF CELLULAR AND MOLECULAR MEDICINE, Issue 6b 2008Srikanth Koneru Abstract Sildenafil citrate (SC), a drug for erectile dysfunction, is now emerging as a cardiopulmonary drug. Our study aimed to determine a novel role of sildenafil on cardioprotection through stimulating angiogenesis during ischaemia (I) reperfusion (R) at both capillary and arteriolar levels and to examine the role of vascular endothelial growth factor (VEGF) and angiopoietin-1 (Ang-1) in this mechanistic effect. Rats were divided into: control sham (CS), sildenafil sham (SS), control + IR (CIR) and sildenafil + IR (SIR). Rats were given 0.7 mg/kg, (i.v) of SC or saline 30 min. before occlusion of left anterior descending artery followed by reperfusion (R). Sildenafil treatment increased capillary and arteriolar density followed by increased blood flow (2-fold) compared to control. Treatment with sildenafil demonstrated increased VEGF and Ang-1 mRNA after early reperfusion. PCR data were validated by Western blot analysis. Significant reduction in infarct size, cardiomyocyte and endothelial apoptosis were observed in SC-treated rats. Increased phosphorylation of Akt, eNOS and expression of anti-apoptotic protein Bcl-2, and thioredoxin, hemeoxygenase-1 were observed in SC-treated rats. Echocardiography demonstrated increased fractional shortening and ejection fraction following 45 days of reperfusion in the treatment group. Stress testing with dobutamine infusion and echocardiogram revealed increased contractile reserve in the treatment group. Our study demonstrated for the first time a strong additional therapeutic potential of sildenafil by up-regulating VEGF and Ang-1 system, probably by stimulating a cascade of events leading to neovascularization and conferring myocardial protection in in vivo I/R rat model. [source] Cardiac evaluation of haemodialysis-related hypotension using dobutamine stress echocardiographyNEPHROLOGY, Issue 3 2001Don Poldermans SUMMARY: Haemodialysis-related hypotension occurs in approximately 30% of patients. Myocardial ischaemia and/or insufficient contractile reserve in response to sympathetic stress may be involved in the pathogenesis of hypotension during dialysis. Using dobutamine stress echocardiography, left ventricular function at rest, myocardial contractile reserve and the presence and extent of ischaemia can be assessed in a non-invasive way. This short review will focus on the potential value of dobutamine stress echocardiography for the evaluation of hypotension-prone haemodialysis patients. [source] CREATINE KINASE INHIBITOR IODOACETAMIDE ANTAGONIZES CALCIUM-STIMULATED INOTROPY IN CARDIOMYOCYTESCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 2 2009Jun Ren SUMMARY 1Inhibition of creatine kinase is known to suppress cardiac contractile reserve in intact hearts, although the underlying mechanism has not been elucidated. 2The present study was designed to examine whether cardiac depression induced by creatine kinase inhibition was due to action at the level of the essential contractile element, namely cardiomyocytes. Adult rat cardiomyocytes were perfused with the creatine kinase inhibitor iodoacetamide (90 µmol/L) for 90 min. Mechanical and intracellular Ca2+ properties were evaluated using edge-detection and fluorescence microscopy, respectively. Myocytes were superfused with normal (1.3 mmol/L) or high (3.3 mmol/L) extracellular Ca2+ contractile buffer. Mechanical function was examined, including peak shortening (PS), maximal velocity of shortening/relengthening (±dL/dt), time to 90% PS (TPS90), time to 90% relengthening (TR90) and integration of shortening/relengthening (normalized to PS). Intracellular Ca2+ transients were evaluated using the following indices: resting and rise of fura-2 fluorescence intensity (,FFI) and intracellular Ca2+ decay time constant. 3The results indicate that elevated extracellular Ca2+ stimulated cardiomyocyte positive inotrope, manifested as increased PS, ±dL/dt, area of shortening, resting FFI and ,FFI associated with a shortened TR90 and intracellular Ca2+ decay time constant. High extracellular Ca2+ did not affect TPS90 and area of relengthening. Iodoacetamide ablated high Ca2+ -induced increases in PS, ±dL/dt, area of shortening, resting FFI, ,FFI and shortened TR90 and intracellular Ca2+ decay time constant. Iodoacetamide itself significantly enhanced the area of relengthening and TR90 without affecting other indices. 4Collectively, these data demonstrate that inhibition of creatine kinase blunts high extracellular Ca2+ -induced increases in cardiomyocyte contractile response (i.e. cardiac contractile reserve). [source] | ||||||||||