Methods and results: Non-invasive hemodynamic parameter (stroke volume, SV, cardiac output, CO, Systemic Vascular Resistance, SVI) were obtained by the Niccomo Device (Medis, Germany) through a bioimpedence technique. Measurements with this device have been shown to be accurate, highly reproducible and sensitivity to normal hemodynamic changes. In this ongoing study, the first 16 acute HF patients enrolled had the following clinical characteristics: mean age 69±16, 31% females, ischemic aetiology 31%, hypertensive 25%, idiopathic 44%, LVEF 39±20%, BNP 1348±1198 pg/mL. Despite clinical stabilization of the patient, after 48-72 hrs from admission, HR was persistently elevated (79,5± 8,5 bpm) and Ivabradine 5 mg bid was started on-top of standard care (beta blockers 62,5 %, diuretics 81,25%, ACE i 62,5%, ARB 12,5%, MRA 56,25%). Measurement were made at the baseline (48-72hrs from admission), after 24-48-72 hrs from starting Ivabradine and at the time of discharge. Treatment with ivabradine was well tolerated in all patients. HR was progressively reduced from 79,5 ± 8,4bpm to 64,2 ±10,1 bpm at hospital discharge, p<0.01. We observed a significant hemodynamic improvement by HR control with an increase of stroke volume (baseline 74,4±9,4 ml vs 85,49±16,4 ml at discharge, p 0,017), and only a minimal reduction of cardiac output (baseline 6,6 ±0,7 L/min vs 5,32 ±1 L/min at discharge, P=ns). All other measures of heart work were also significantly affected by reducing HR.
In conclusion: The strategy of the early administration of ivabradine, during a decompensated episode of HF to control HR on top of usual care including beta-blockers, is feasible and safe. The effect of lowering HR may save energy without affecting cardiac output as confirmed by the significant increase of stroke .