ArticleJournal of cardiovascular pharmacology2025
Heart Rate Lowering With Ivabradine and Burden of Symptoms in Patients With Postural Orthostatic Tachycardia Syndrome.
Article in Journal of cardiovascular pharmacology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.
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Who cites it
3 citing papers in PubMed.
- A Randomized Crossover Trial of Ivabradine, Propranolol, and Placebo in Postural Orthostatic Tachycardia Syndrome: A Detailed Description.JACC. Advances · 2026Article
- Postural Orthostatic Tachycardia Syndrome and Orthostatic Hypotension Following Hematopoietic Stem Cell Transplantation.JACC. CardioOncology · 2025Article
- Determinants of Exercise Intolerance in Postural Orthostatic Tachycardia Syndrome: A Systematic Review.Exercise, sport & movement · 2025Article
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Authors and funding
8 authors.
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Abstract
abstractPostural orthostatic tachycardia syndrome (POTS) is a clinical syndrome of tachycardia on standing leading to palpitations, dizziness, chest pain, and/or fatigue. An exaggerated norepinephrine response with standing is often present in POTS, but it remains unclear whether the tachycardia is compensatory for a reduced stroke volume or whether the tachycardia is itself causing the symptoms of POTS. We herein report the effects of heart rate (HR) lowering with ivabradine, a selective I f channel blocker, on symptom burden in patients with POTS. After ivabradine treatment, there was a significant reduction in the change in HR with standing in all patients from 40 (30-70) to 15 (8-19) bpm ( P = 0.011), without significant changes in blood pressure. The Malmö score was significantly reduced in all patients from 86 (74-92) to 39 (32-66) ( P = 0.005). A correlation between change in HR with standing and the change in Malmö score (R = +0.828; R 2 quadratic = 0.635; P < 0.001) was present. The parallel improvement in HR response and symptoms with ivabradine suggests that the tachycardia response in POTS may not be considered compensatory but rather central to the pathophysiology of POTS symptoms.
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