Slide 1: Med Update! A 45-year-old male with heart failure (EF 30%) is being discharged. This is his fourth hospitalization in the last year for CHF exacerbations. He has an AICD. His vital signs are BP 115/70, HR 76, RR 12, and SO2 99% on room air. An EKG shows the patient is in sinus rhythm. Current meds: sacubatril-valsartan 97-103mg bid, metoprolol succinate 200mg daily, spironolactone 50mg daily, furosemide 40mg bid. Which of the following medication changes should you consider? A) Add amlodipine. B) Add ivabradine. C) Increase dose of metoprolol. D) Add lisinopril.
Slide 2: B) Add ivabradine. Ivabradine was FDA approved in 2015 after it was shown to reduce the risk of hospitalization in patients with stable symptomatic heart failure with reduced EF (<35%) who are intolerant of beta blockers OR have not met their target heart rate (70 bpm) on maximum doses of beta blockade. (This is a class IIb recommendation from the AHA/ACC!)
Slide 3: How’s it work? Ivabradine works by directly inhibiting hyperpolarization-activated cyclic nucleotide-gated (HCN) channels in the sinoatrial node, which are responsible for the funny (If) current that results in automatic SA node depolarization. As such, it works downstream of the adrenergic receptors, providing an alternative method of negative chronotropy. Ivabradine has no effect on inotropy. [Diagram of SA node automaticity]
- Swedberg K, Komajda M, Böhm M, et al. Ivabradine and outcomes in chronic heart failure (SHIFT): a randomised placebo-controlled study. Lancet. 2010 Sep 11;376(9744):875-85. PMID 20801500
Tags: cardiology, chronotropy, electrophysiology, funny current, heart failure, ivabradine, SA node