Ivabradine in cardiogenic shock with catecholamine weaning failure: focus on the atrial fibrillation subpopulation

Background

The management of cardiogenic shock (CS) and failure of catecholamine weaning is challenging, particularly in patients with concomitant atrial fibrillation (AF). Because ivabradine primarily acts on the sinus node, its role in patients with AF remains uncertain. We therefore specifically evaluated the hemodynamic effects of ivabradine in the atrial fibrillation subpopulation of patients with CS and unsuccessful catecholamine withdrawal.

Methods

This subgroup analysis included 12 patients with atrial fibrillation selected from a cohort of 39 individuals admitted to the Cardiology Department of our University Hospital, for cardiogenic shock with a failed catecholamine weaning study, between July 2024 and May 2025. All patients received ivabradine at a dose of 5 mg twice daily. Clinical, echocardiographic, and hemodynamic parameters were assessed at baseline and 48 hours after treatment initiation.

Results

In this atrial fibrillation subgroup, heart rate significantly decreased from 111.75 ± 31.06 bpm to 89.08 ± 20.09 bpm (p = 0.005). Importantly, this reduction was not associated with hemodynamic deterioration. Systolic arterial pressure increased from 101.75 ± 16.35 mmHg to 106.83 ± 10.63 mmHg, although not reaching statistical significance (p = 0.284). Mean arterial pressure rose modestly from 87.38 ± 12.66 mmHg to 92.69 ± 9.16 mmHg (p = 0.186), and diastolic pressure remained overall stable.

Echocardiographic assessment demonstrated significant improvements. Velocity time integral increased from 7 (6–8) cm to 9.5 (8–10) cm (p < 0.001), and stroke volume significantly improved from 21.98 (18.84–25.12) mL to 29.83 (25.12–31.4) mL (p < 0.001). Cardiac output showed a slight, non-significant increase (2.56 ± 0.87 to 2.69 ± 0.76 L/min; p = 0.540), and cardiac power output rose modestly without statistical significance (0.44 ± 0.18 to 0.49 ± 0.16 W; p = 0.146). Systemic vascular resistance remained stable (p = 0.740). Notably, ventriculo-arterial coupling significantly improved from 6.55 ± 2.77 to 4.78 ± 1.61 (p = 0.002), reflecting enhanced cardiovascular efficiency even in the context of atrial fibrillation.

Conclusions

Among patients with cardiogenic shock and prior catecholamine weaning failure, the atrial fibrillation subpopulation demonstrated significant heart rate reduction and improvement in stroke volume and ventriculo-arterial coupling after ivabradine initiation, without deterioration of arterial pressure or vascular resistance. These findings suggest that ivabradine may be hemodynamically safe and potentially beneficial even in selected CS patients with atrial fibrillation, warranting further prospective investigationEvolution of hemodynamic parameters