ArticleBritish journal of pharmacology2015
Pleiotropic, heart rate-independent cardioprotection by ivabradine.
Article in British journal of pharmacology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
32 citing papers in PubMed, 70 citations in OpenAlex.
- Adaptation of Arterial Wall Viscosity to the Short-Term Reduction of Heart Rate: Impact of Aging.Journal of the American Heart Association · 2022Trial
- Efficacy of Ivabradine in Combination with Beta-Blockers Versus Uptitration of Beta-Blockers in Patients with Stable Angina (CONTROL-2 Study).Advances in therapy · 2018Trial
- β-Blockers and ivabradine differentially affect cardiopulmonary function and left ventricular filling index.Clinical research in cardiology : official journal of the German Cardiac Society · 2016Trial
- Ivabradine as a Cardio-Protective Agent Against Anthracycline-Induced Cardiotoxicity: A Narrative Review.Cardiovascular drugs and therapy · 2026Review
- Achieved targeted heart rate following ivabradine therapy correlates with left ventricular reverse remodeling in non-ischemic dilated cardiomyopathy.Scientific reports · 2025Article
- Chronic administration of ivabradine improves cardiac Ca handling and function in a rat model of Duchenne muscular dystrophy.Scientific reports · 2025Article
- Article
- Effects of ivabradine on myocardial autophagia and apoptosis in isoprenaline-induced heart failure in mice.Iranian journal of basic medical sciences · 2024Article
- Heart rate reduction after genetic ablation of L-type CaFrontiers in cardiovascular medicine · 2023Article
- Five-year results of heart rate control with ivabradine or metoprolol succinate in patients after heart transplantation.Clinical research in cardiology : official journal of the German Cardiac Society · 2022Article
- Alternative Targets for Modulators of Mitochondrial Potassium Channels.Molecules (Basel, Switzerland) · 2022Review
- The Bradycardic Agent Ivabradine Acts as an Atypical Inhibitor of Voltage-Gated Sodium Channels.Frontiers in pharmacology · 2022Article
- Topical Neck Cooling Without Systemic Hypothermia Attenuates Myocardial Ischemic Injury and Post-ischemic Reperfusion Injury.Frontiers in cardiovascular medicine · 2022Article
- Ivabradine increases the high frequency gain ratio in the vagal heart rate transfer function via an interaction with muscarinic potassium channels.Physiological reports · 2021Article
- Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro.Brain sciences · 2021Article
- New Cardiomyokine Reduces Myocardial Ischemia/Reperfusion Injury by PI3K-AKT Pathway Via a Putative KDEL-Receptor Binding.Journal of the American Heart Association · 2021Article
- Ivabradine Ameliorates Cardiac Diastolic Dysfunction in Diabetic Mice Independent of Heart Rate Reduction.Frontiers in pharmacology · 2021Article
- Ivabradine and Blood Pressure Reduction: Underlying Pleiotropic Mechanisms and Clinical Implications.Frontiers in cardiovascular medicine · 2021Article
- Targeting myocardial ischaemic injury in the absence of reperfusion.Basic research in cardiology · 2020Review
- The role of mitochondrial reactive oxygen species, NO and HJournal of cellular and molecular medicine · 2020Review
Corrections and comments
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Authors and funding
6 authors at 4 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
background and purposeIn pigs, ivabradine reduces infarct size even when given only at reperfusion and in the absence of heart rate reduction. The mechanism of this non-heart rate-related cardioprotection is unknown. Hence, in the present study we assessed the pleiotropic action of ivabradine in more detail. EXPERIMENTAL APPROACH: Anaesthetized mice were pretreated with ivabradine (1.7 mg · kg(-1) i.v.) or placebo (control) before a cycle of coronary occlusion/reperfusion (30/120 min ± left atrial pacing). Infarct size was determined. Isolated ventricular cardiomyocytes were exposed to simulated ischaemia/reperfusion (60/5 min) in the absence and presence of ivabradine, viability was then quantified and intra- and extracellular reactive oxygen species (ROS) formation was detected. Mitochondria were isolated from mouse hearts and exposed to simulated ischaemia/reperfusion (6/3 min) in glutamate/malate- and ADP-containing buffer in the absence and presence of ivabradine respectively. Mitochondrial respiration, extramitochondrial ROS, mitochondrial ATP production and calcium retention capacity (CRC) were assessed. KEY
resultsIvabradine decreased infarct size even with atrial pacing. Cardiomyocyte viability after simulated ischaemia/reperfusion was better preserved with ivabradine, the accumulation of intra- and extracellular ROS decreased in parallel. Mitochondrial complex I respiration was not different without/with ivabradine, but ivabradine significantly inhibited the accumulation of extramitochondrial ROS, increased mitochondrial ATP production and increased CRC. CONCLUSION AND IMPLICATIONS: Ivabradine reduces infarct size independently of a reduction in heart rate and improves ventricular cardiomyocyte viability, possibly by reducing mitochondrial ROS formation, increasing ATP production and CRC.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.