Successful withdrawal of catecholamine with ivabradine administration in catecholamine-dependent heart failure
Kohei Azuma1, Masanori Asakura1, Koichi Nishimura1
1Department of Cardiovascular and Renal Medicine, Hyogo College of Medicine, Nishinomiya, Japan.
Insights
Ivabradine successfully treated catecholamine-dependent heart failure in a patient intolerant to beta-blockers. This heart rate-lowering agent improved stroke volume and reduced afterload, allowing for catecholamine withdrawal.
Area of Science:
- Cardiology
- Pharmacology
Background:
- Catecholamine-dependent heart failure presents a significant therapeutic challenge, particularly when patients are intolerant to standard beta-blocker therapy.
- Acute decompensated heart failure (ADHF) refractory to conventional treatments requires novel therapeutic approaches.
Observation:
- A 39-year-old male patient with severe systolic cardiac failure presented with ADHF refractory to standard treatments.
- The patient could not tolerate beta-blockers or dobutamine tapering.
- Persistent high heart rate (HR) above 100 bpm was noted.
Findings:
- Ivabradine administration led to a significant increase in stroke volume (SV).
- The patient's HR was reduced, enabling successful tapering of dobutamine.
- Hemodynamic assessment indicated a reduction in afterload following ivabradine initiation.
Implications:
- Ivabradine offers a viable therapeutic option for catecholamine-dependent ADHF patients intolerant to beta-blockers.
- This case highlights ivabradine's potential to improve cardiac function and reduce afterload in complex heart failure scenarios.
- Further research into ivabradine's role in managing refractory heart failure is warranted.
Abstract:
Ivabradine is a heart rate (HR)-lowering agent that blocks hyperpolarization-activated cyclic nucleotide-gated channel in the sinus node without a negative inotropic effect on cardiac function. Here we report a case of catecholamine-dependent heart failure, who was intolerant to β blockers, and successfully withdrew catecholamine by administering ivabradine. A 39-year-old male acute decompensated heart failure (ADHF) patient with severe systolic cardiac failure, refractory to diuretic and dobutamine treatment was transferred to our hospital. In addition to titration of dobutamine support, intra-aortic balloon pump, mechanical ventilation, and continuous hemodiafiltration therapy were initiated. These mechanical supports could stabilize ADHF and were removed. Upon stabilization of ADHF, we attempted to initiate a low dose of bisoprolol and taper dobutamine, but the patient could not tolerate even a low dose of bisoprolol nor tapering of dobutamine. Since his HR was consistently above 100 beats per minute and ivabradine was reported to improve stroke volume (SV), we initiated ivabradine, and his SV remarkably increased after initiation. Consequently, the dose of dobutamine was successfully tapered. Also, additional clinical advantage of ivabradine, assessed through hemodynamic parameters, appeared to be a reduction in afterload. <Learning objective: Ivabradine is a heart rate (HR)-lowering agent that blocks the hyperpolarization-activated cyclic nucleotide-gated channel in the sinus node without a negative inotropic effect. In this present catecholamine-dependent advanced heart failure case, the patient could not tolerate even a low dose of bisoprolol nor tapering of dobutamine. Being intolerant to beta-blockers, we initiated the administration of ivabradine. And the initiation of ivabradine resulted in not only the reduction of HR, but also the improvement in stroke volume resulting in the reduction of afterload.>.
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