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LV End-diastolic Pressure (lv + end-diastolic_pressure)
Selected AbstractsCardiac function during mild hypothermia in pigs: increased inotropy at the expense of diastolic dysfunctionACTA PHYSIOLOGICA, Issue 1 2010H. Post Abstract Aim:, The induction of mild hypothermia (MH; 33 °C) has become the guideline therapy to attenuate hypoxic brain injury after out-of-hospital cardiopulmonary resuscitation. While MH exerts a positive inotropic effect in vitro, MH reduces cardiac output in vivo and is thus discussed critically when severe cardiac dysfunction is present in patients. We thus assessed the effect of MH on the function of the normal heart in an in vivo model closely mimicking the clinical setting. Methods:, Ten anaesthetized, female human-sized pigs were acutely catheterized for measurement of pressure,volume loops (conductance catheter), cardiac output (Swan-Ganz catheter) and for vena cava inferior occlusion. Controlled MH (from 37 to 33 °C) was induced by a vena cava inferior cooling catheter. Results:, With MH, heart rate (HR) and whole body oxygen consumption decreased, while lactate levels remained normal. Cardiac output, left ventricular (LV) volumes, peak systolic and end-diastolic pressure and dP/dtmax did not change significantly. Changes in dP/dtmin and the time constant of isovolumetric relaxation demonstrated impaired active relaxation. In addition, MH prolonged the systolic and shortened the diastolic time interval. Pressure,volume analysis revealed increased end-systolic and end-diastolic stiffness, indicating positive inotropy and reduced end-diastolic distensibility. Positive inotropy was preserved during pacing, while LV end-diastolic pressure increased and diastolic filling was substantially impaired due to delayed LV relaxation. Conclusion:, MH negatively affects diastolic function, which, however, is compensated for by decreased spontaneous HR. Positive inotropy and a decrease in whole body oxygen consumption warrant further studies addressing the potential benefit of MH on the acutely failing heart. [source] Analysis of Left Atrial Volume Change Rate for Evaluation of Left Ventricular Diastolic FunctionECHOCARDIOGRAPHY, Issue 7 2004F.E.S.C., Ming-Jui Hung M.D. An excellent correlation exists between the change in the left atrial (LA) angiographic area and posterior aortic wall motion. The aim of the study was to define the role of posterior aortic wall motion, indicating LA volume change, during the left ventricular (LV) phase for the assessment of LV diastolic function. A total of 155 patients underwent echocardiography after cardiac catheterization. Study patients were classified into four groups according to the ratio of early-to-late transmitral flow velocity (E/A ratio) and/or LV end-diastolic pressure (EDP): 42 patients with LVEDP < 15 mmHg and E/A ratio >1 (normal filling); 46 patients with E/A < 1 (impaired relaxation); 46 patients with LVEDP , 15 mmHg and E/A > 1 and <2 (pseudonormal filling); 21 patients with E/A > 2, E , 70 cm/s, and E-wave deceleration time ,160 ms (restrictive filling). The slopes of early and late (slopes E and A) diastolic motion of LA wall were derived from M-mode analysis, together with the LV isovolumic time constant Tau from cardiac catheterization. Values of slope E/A decreased in restrictive filling, pseudonormal filling, and impaired relaxation as compared with normal filling (0.41 ± 0.14, 0.69 ± 0.15, and 0.56 ± 0.23 vs 1.25 ± 0.26, P < 0.001, respectively) and correlated inversely with the isovolumic time constant Tau (r = 0.79, P < 0.001). In cases for which a value of slope E/A < 1 was obtained, indicating a relaxation abnormality, the M-mode derived pattern of LA wall motion identified the underlying abnormal LV diastolic function with a sensitivity of 98.3%, a specificity of 100%, a positive predictive value of 100%, and a negative predictive value of 95.2%. Analysis of the slope of LA wall motion, indicating LA volume change rate, during LV diastolic phase is useful in evaluating LV diastolic function. It provides a new noninvasive index that correlates well with invasive index of LV relaxation. [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] Estimation of Left Ventricular Filling Pressure by Doppler Echocardiography in Dogs with Pacing-Induced Heart FailureJOURNAL OF VETERINARY INTERNAL MEDICINE, Issue 3 2008K.E. Schober Background: Congestive heart failure (CHF) is a common clinical syndrome characterized by elevated filling pressure. Hypothesis: Doppler echocardiographic (DE) variables of left ventricular (LV) filling can predict a decline of LV end-diastolic pressure (LVEDP) induced by acute preload reduction in dogs with compensated CHF. Animals: Five male hound dogs. Methods: Dogs previously instrumented with a transvenous cardiac pacemaker and a LV pressure gauge were paced at 160,180 bpm to induce mild CHF characterized by LVEDP > 20 mmHg. LVEDP and 9 DE variables of LV filling derived from diastolic time intervals, transmitral and pulmonary venous flow, and tissue Doppler imaging were measured simultaneously at baseline and 30, 60, 120, and 240 minutes after furosemide (4 mg/kg, IV) or placebo (0.9% saline, IV). Repeated measures analysis of variance and correlation analysis were used to determine the association between the decline of LVEDP after furosemide and DE measures of LV filling pressure (LVFP). Results: Furosemide but not placebo decreased LVEDP (P < .001). The ratio of early transmitral flow velocity to LV isovolumic relaxation time (E : IVRT) predicted LVEDP best (R2= .50; P < .001). Correlations were also found between LVEDP and IVRT, E, ratio between E and late diastolic transmitral flow velocity (E : A), and early diastolic velocity of the mitral annulus (Ea). The ratio of E to Ea (E : Ea) was not useful in the prediction of LVEDP in this model. Conclusion and Clinical Importance: E : IVRT can be used to predict LVFP in dogs with mild left-sided CHF induced by rapid pacing. [source] Downregulation of survival signalling pathways and increased apoptosis in the transition of pressure overload-induced cardiac hypertrophy to heart failureCLINICAL AND EXPERIMENTAL PHARMACOLOGY AND PHYSIOLOGY, Issue 11 2009Xiao-Mei Li Summary 1.,Transition from compensated left ventricular (LV) hypertrophy to decompensated heart failure was characterized using a pressure-overload induced model to elucidate the temporal relationship between cardiomyocyte apoptosis and survival signalling in this transition. 2.,Mice were subjected to transverse aortic constriction (TAC) or sham operation for 1,16 weeks and were studied by echocardiography, catheterization and histology. Relevant gene expression and phosphorylation of extracellular signal-regulated kinase (ERK) 1/2, Akt and glycogen synthase kinase (GSK)-3, were determined. 3.,Transverse aortic constriction resulted in myocyte hypertrophy and fibrosis from Week 4 and a progressive increase in left ventricular (LV) dimensions and wall thicknesses with maintained contractile function by Week 12. However, a sharp decline in contractile function and elevated LV end-diastolic pressure from 12 to 16 weeks were observed after TAC, indicating functional decompensation. 4.,Following TAC, mRNA levels of atrial natriuretic peptide, B-type natriuretic peptide, ,-myosin heavy chain (MHC) and transforming growth factor-,1 were increased time dependently, whereas mRNA expression of ,-MHC, sarcoplasmic/endoplasmic reticulum calcium ATPase 2a and Bcl-2 were decreased. The ratio of Bcl-2/Bax was decreased and this was consistent with progressively increased myocyte apoptosis demonstrated by terminal deoxyribonucleotidyl transferase-mediated dUTP,digoxigenin nick end-labelling staining. Phosphorylation of ERK1/2 was increased by Week 4, but decreased thereafter. Levels of phosphorylated Akt declined from Week 8, whereas GSK3, phosphorylation increased from 1 to 8 weeks, then decreased from Week 12 after TAC. 5.,In conclusion, TAC resulted in early concentric and late eccentric hypertrophy with eventual development of LV dysfunction. This transition was temporally associated with a progressive increase in cell size, fibrosis and myocyte apoptosis. Downregulation of ERK1/2, Akt and GSK3, and enhanced cardiomyocyte apoptosis are implicated as important mechanisms in the transition from compensated hypertrophy to heart failure. [source] | ||||||||||