| BackgroundAcute decompensated heart failure is the rapid onset or deterioration of symptoms and signs in patients with previous diagnosis of heart failure, which may be caused by a trigger such as an arrhythmia or respiratory infections. With complicated conditions, ADHF has a high re-hospitalization rate and mortality. The cardiac structure and functions are severely impaired. Additionally, the intracavitary flow field changes, with less beneficialvortex and stored energy. The energy loss further impairs systolic and diastolic functions.Inotropes are important parts for improving symptoms and stabilize hemodynamics in the ADHF treatment. Levosimendan is a novel inotrope as type II Ca2+sensitizer, which increase affinity of troponin C (TnC) for Ca2+to performe positive inotropic effect. Additionally, levosimendan has been found to have vasodilation and anti-inflammation effect.The evaluation of treatment in ADHF includesmany aspects. Besides symptoms and signs, the cardiac structure, dysfunction and intracavitary flow field also play important parts. Echocardiography is the most common used tool for evaluating cardiac function, including systolic and diastolic function. Except the assessment of global and regional function based on wall motion, the newly developed vector flow mapping (VFM) is also able to evaluate the flow field and hemodynamics in the ventricles. At present, the effect of levosimendan on the change of intracavitary flow field is not clear.The study aim to appraise the effect of levosimendan treatment on the alterations of cardiac structures, functions and flow field in ADHF patients to illustrate the short-term effect comprehensively.Objective1. To evaluate the clinical effect of Levosimendan on the changes of cardiac structures and functions of the patients in the treatment of acute decompensated heart failure.2. To evaluate the clinical effect of Levosimendan on the changes ofintracavitary flow field of the patients in the treatment of acute decompensated heart failure.Method1. PatientsA total of 29 ADHF patients admitted to hospital (NYHA class III-IV), containing 24 males and 5 females with an average age 62 years old, were divided into levosimendan group (n=15) and conventional therapy group (n=14) randomly. All the patients were given conventional oxygen, diuretics, vasodilators, lanatoside C etc. to improve symptoms. Besides, levosimendan treatment was started with a loading dose given as an venous infusion of 12 μg/kg over 10 min, followed by a continuous infusion of 0. lug/(kg*min) for 24 hours with electrocardiogram monitoring.After stabilization, all patients went on medications like ACEI or ARB, beta-blockers and mineralocorticoid receptor antagonist.15 healthy volunteers matching in terms of age and gender were enrolled meanwhile. All of them received clinical assessment, blood examinations and echocardiography to exclude heart diseases.2. Clinical dataAll the ADHF patients’medical history, symptoms and signs, ECG, blood pressure, heart rate were recorded. Serological examinations are taken to measure NT-pro BNP, cTn I, liver function, renal function, serum lipid, uric acid, complete blood count etc.Assess NYHA class before and 7 days after levosimendan treatment respectively to judge the clinical improvement.3. EchocardiographyEchocardiography examinations for all the patients were taken before and 7 days after levosimendantreatment respectively (ALOKA F75 with UST-52105 probe). 2-DE was performed to acquire PL AX, AP4, AP3, AP2 dynamic images and measure LVEDD, LVESD, LVPWd, IVSd, LaD, SaD, LVEDV, LVESV, LVEF (by bi-plane Simpson method), CO, LAV. Calculate sphericity index (SI), LVEDVi, LVESVi, LAVi and CI.PW Doppler was performed to measure peak E and A of mitral inflow velocities. TDI was used to assess mitral annular velocities s, e, and a. PW-PW mode was used to acquire mitral and aortic inflow velocities simultaneously to measure IVRT, FVCT, ET, and calculate Tei index.Three cycles of dynamic Color-Doppler flow images of AP4, AP3 and AP2 were stored digitally in VFM mode and exported to DAS-RSI workshop for further analysis. The average energy loss in the whole left ventricle chamber of 7 phases, including isovolumetric contraction phase (PI), rapid ejection phase (P2), slow ejection phase (P3), isovolumetric diastole phase (P4), rapid filling phase (P5), slow filling phase (P6) and atrial systole phase (P7), were recorded.4. StatisticsSPSS 20.0 software (SPSS Inc., Chicago, USA) was used for statistic analysis. After normality and homogeneity of variances test, all the normal distributions were described as mean±standard deviation and non-normal distributions as M (Q1, Q3). Count data were expressed as frequency or rate (%). For two samples’comparison, Student’s t-test was used for normal distributions, whereas Mann-Whitney U test. A P<0.05 was considered statistically significant.Results1. Baseline clinical dataNo statistically significant differences exist between levosimendan group and conventional therapy group in terms of sex, age, BSA, HR, BP, NYHA class and primary heart diseases (P>0.05). Serum K+of levosimendan is higher (P<0.05), but K+of both groups are normal.2. Left ventricular structureBefore treatment, no statistically significant differences exist between two groups in terms of LVPWd, LVIDd, LVIDs, IVSd, LaD, SaD, SI (P>0.05). After conventional treatment, SaD decreased with statistical significance (P<0.05). LVPWd, LVIDd, LVIDs, IVSd, SI and LaD didn’t change significantly (P>0.05). After levosimendan treatment, all the indexes didn’t change significantly (P>0.05). There were no significant differences between two groups after treatment (P>0.05).3. Systolic functionBefore treatment, no statistically significant differences exist between two groups in terms of LVEDVi, LVESVi, LVEF, SV, CO, CI, s, Tei (P>0.05). After conventional treatment, LVESVi decreased and LVEF increased with statistical significance (P<0.05). After levosimendan treatment, LVEF, SV increased and LVEDVi, LVESVi decreased (P<0.05), other indexes didn’t change significantly (P>0.05). There were no significant differences between two groups after treatment (P>0.05).4. Diastolic functionBefore treatment, no statistically significant differences exist between group A and group B in terms of DT, E, A, E/A, e(1), e(s), E/e, IVRT, LAVi (P>0.05). After conventional treatment, A increased with statistical significance (P<0.05). Other indexes didn’t change significantly (P>0.05). After levosimendan treatment, all the indexes didn’t change significantly (P>0.05). There were no significant differences between two groups after treatment (P>0.05).5. Energy loss of HF group and normal control groupThere are 7 phases including isovolumetric contraction phase (P1), rapid ejection phase (P2), slow ejection phase (P3), isovolumetric diastole phase (P4), rapid filling phase (P5), slow filling phase (P6), atrial systole phase (P7). Compared with normal control group, the lower EL in heart failure groups of P1, P2, P3 in A2C, lower EL of PI, P3 in A3C and lower EL of P3 in A4C had statistical significance (P<0.05). Other indexes didn’t change significantly (P>0.05).6. Energy loss of HF treatmentBefore treatment, no statistically significant differences exist between two groups in terms of EL of P1-P7 in all 3 chambers (P>0.05). After conventional treatment, EL of all phases in A2C didn’t change significantly (P>0.05). EL of P4 in A3C and P7 in A4C decreased (P>0.05). After levosimendan treatment, EL of all phases in 3 chambers didn’t change significantly (P>0.05). There were no significant differences between two groups in terms of EL of P1-P7 in A2C and A4C (P>0.05). In A3C, EL of P1, P3 and P4 is higher after levosimendan treatment (P<0.05).Conclusion1. The energy loss in systolic phases decreases in patients of ADHF.2. Levosimendan and conventional treatment can decrease LVEDV, LVESV and increase LVEF, thus can improve LV systolic function in patients of ADHF.3. Levosimendan treatment can increase energy loss in systolic phase and improveintracavitary flow field. |
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