Abstract
Aims
Despite new therapeutic options, patients with heart failure (HF) still progress to advanced stage. Among new therapeutic options, Levosimendan was recently approved in order to treat patients hospitalized for acute decompensated heart failure (ADHF) with severe systolic dysfunction. The pharmacological effects of Levosimendan consist of inotropy, vasodilatation, and cardioprotection through the increase of calcium sensitivity. These effects should be monitored with echocardiography and in particular with speckle tracking and tri-dimensional echocardiography which appear to be useful in LV systolic function detection and monitoring. In this study we aim to evaluate the effect of slow infusion of Levosimendan on the non-invasive measurement of cardiac output, the speckle tracking parameters and the tri-dimensional echocardiography measurements in advanced ADHF patients.
Methods and results
This is a prospective observational study evaluating Levosimendan efficacy through advanced echocardiography. We enrolled 11 patients with diagnosis of ADHF who respect the recent ESC criteria of ‘advanced heart failure’. Patients underwent to blood sample examination to measure electrolytes, creatinine, and NTproBNP. Patients underwent to advanced echocardiography examination (performed for each patient pre- and post-Levosimendan infusion) with tri-dimensional echocardiography and global longitudinal strain assessment. Furthermore patients underwent to non-invasive cardiac output and cardiac index collection through impedance cardiography pre- and post-Levosimendan infusion. All patients were followed for 30 days after discharge for all cause of mortality and HF re-hospitalization. A total of 11 patients affected by advanced ADHF were included in this study. Mean age was 73.8 ± 4.7 years. 72.7% (n 8) patients were men. 81.9% (n 9) of patients recognize ischaemic heart disease as HF etiology. At admission mean systolic arterial pressure was 100 ± 17 mmHg, mean NTproBNP was 24 445 ± 12 194 pg/ml and mean serum creatinine was 1.55 ± 0.84 mg/dl. At tri-dimensional echocardiography mean LV ejection fraction (LVEF) was 19.7 ± 5.7% and at bi-dimensional echocardiography mean tricuspid anular plane systolic excursion (TAPSE) and pulmonary arterial systolic pressure (PASP) were, respectively, 12.5 ± 2.7 mm and 48 ± 16 mmHg. Mean LV global longitudinal strain (GLS) was −3.0 ± 1.8. Mean furosemide in-hospital infusion was 306 ± 102 mg/die and mean urine output 1436 ± 496 ml. None developed significant ventricular or supraventricular arrhythmias. All patients were treated with betablockers during infusion. At 30 days of follow-up two patients died and 1 patient was re-hospitalized. Evaluating the differences among our variables pre- and post-Levosimendan infusion, we found that NTproBNP was significantly reduced post-Levosimendan infusion (P = 0.01). Among ICG non-invasive measurement, we found significant differences in stroke volume (SV) and cardiac output (CO) in terms of significant improvement (P = 0.001 for both). Analysing tri-dimensional echocardiography variables, we observed a significant improvement of LVEF (P = 0.003), SV (P = 0.03) and 3-D LV GLS (P = 0.002). Furthermore, we observed a significant reduction in end-systolic volume (ESV) post-Levosimendan infusion (P = 0.02). Among bi-dimensional echocardiography measurements, there was a significant reduction in end-diastolic diameter of right ventricle (EDDRV) and in B-lines count (respectively, P = 0.02 and P = 0.002). Moreover, we observed a significant improvement in TAPSE (P = 0.003) and in LV GLS (P = 0.004).
Conclusions
Our study showed that slow Levosimendan infusion (12.5 mg at velocity of 0.05–1 mcg/kg/min) without bolus could be considered in advanced ADHF patients to improve cardiac performance without severe adverse events. ICG and echocardiography in-hospital evaluation seemed to be necessary to understand treatment success and patients status improvement as well as cardiac function benefit.
Relation of primary and secondary cardiac arrests or sustained ventricular tachycardia to sudden death risk in advanced heart failure
