Ivabradine for hemodynamic optimization and catecholamine weaning in cardiogenic shock: a retrospective cohort study

Background Heart rate control may represent a key therapeutic target in cardiogenic shock (CS), particularly in patients who experience failure of catecholamine weaning. Ivabradine, a selective sinus node inhibitor, could improve ventriculo-arterial coupling and hemodynamic stability; however, clinical data in this setting remain scarce. Methods We conducted a retrospective cohort study in the Cardiology Department of our University Hospital, between July 2024 and May 2025. Thirty-nine critically ill patients with CS requiring continuous catecholamine infusion and unsuccessful initial weaning attempts received ivabradine at a dose of 5 mg twice daily. Hemodynamic, echocardiographic, and biological parameters were assessed at baseline and after 48 hours. Results The median dobutamine dose at the time of ivabradine introduction was 8 μg/kg/min. Norepinephrine was used in 64.1% of cases, with a median dose of 1 μg/min. After 48 hours, ivabradine significantly reduced heart rate (103 ± 25.5 to 84.9 ± 19.3 bpm; p < 0.001). This reduction was associated with improved stroke volume (21.98 [18.84–25.12] to 29.83 [25.12–31.40] mL; p < 0.001), increased cardiac power output (0.39 ± 0.16 to 0.46 ± 0.14 W; p = 0.001), and better ventriculo-arterial coupling (6.08 ± 3.20 to 4.5 ± 2.11; p < 0.001). Mean arterial pressure increased (+8.6 mmHg; p < 0.001), while lactate levels significantly decreased (3 [2.8–4] to 1.8 [1.5–3] mmol/L; p < 0.001). Successful catecholamine withdrawal was achieved in 77% of patients. Conclusions In this single-center retrospective study, ivabradine safely improved hemodynamic parameters and ventriculo-arterial coupling, facilitating catecholamine withdrawal in the majority of patients with cardiogenic shock and prior weaning failure. These findings support further prospective evaluation of ivabradine in this high-risk population