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      Ivabradine and AF: Coincidence, Correlation or a New Treatment?

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          Abstract

          Ivabradine is a heart rate-lowering agent that inhibits pacemaker funny current (I f). It has been approved by the European Medicines Agency and the US Food and Drug Administration for patients with stable angina and heart failure (HF). AF is a common issue especially in ischaemic heart disease and HF patients. In contrast to experimental findings and a limited number of clinical trials that demonstrate the emerging role of ivabradine for heart rate control in AF or maintenance of sinus rhythm, there is accumulating contradictory data indicating that there is, in fact, an increased incidence of new-onset AF among people who are taking ivabradine in clinical practice. This article reviews the most recent evidence highlighting the diversity of data in relation to the use of ivabradine and the onset of AF and whether it has a legitimate role in AF treatment and the maintenance of sinus rhythm.

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          Ivabradine for patients with stable coronary artery disease and left-ventricular systolic dysfunction (BEAUTIFUL): a randomised, double-blind, placebo-controlled trial.

          Kim Fox, Ian Ford, P Gabriel Steg … (2008)
          Ivabradine specifically inhibits the I(f) current in the sinoatrial node to lower heart rate, without affecting other aspects of cardiac function. We aimed to test whether lowering the heart rate with ivabradine reduces cardiovascular death and morbidity in patients with coronary artery disease and left-ventricular systolic dysfunction. Between December, 2004, and December, 2006, we screened 12 473 patients at 781 centres in 33 countries. We enrolled 10 917 eligible patients who had coronary artery disease and a left-ventricular ejection fraction of less than 40% in a randomised, double-blind, placebo-controlled, parallel-group trial. 5479 patients received 5 mg ivabradine, with the intention of increasing to the target dose of 7.5 mg twice a day, and 5438 received matched placebo in addition to appropriate cardiovascular medication. The primary endpoint was a composite of cardiovascular death, admission to hospital for acute myocardial infarction, and admission to hospital for new onset or worsening heart failure. We analysed patients by intention to treat. The study is registered with ClinicalTrials.gov, number NCT00143507. Mean heart rate at baseline was 71.6 (SD 9.9) beats per minute (bpm). Median follow-up was 19 months (IQR 16-24). Ivabradine reduced heart rate by 6 bpm (SE 0.2) at 12 months, corrected for placebo. Most (87%) patients were receiving beta blockers in addition to study drugs, and no safety concerns were identified. Ivabradine did not affect the primary composite endpoint (hazard ratio 1.00, 95% CI 0.91-1.1, p=0.94). 1233 (22.5%) patients in the ivabradine group had serious adverse events, compared with 1239 (22.8%) controls (p=0.70). In a prespecified subgroup of patients with heart rate of 70 bpm or greater, ivabradine treatment did not affect the primary composite outcome (hazard ratio 0.91, 95% CI 0.81-1.04, p=0.17), cardiovascular death, or admission to hospital for new-onset or worsening heart failure. However, it did reduce secondary endpoints: admission to hospital for fatal and non-fatal myocardial infarction (0.64, 95% CI 0.49-0.84, p=0.001) and coronary revascularisation (0.70, 95% CI 0.52-0.93, p=0.016). Reduction in heart rate with ivabradine does not improve cardiac outcomes in all patients with stable coronary artery disease and left-ventricular systolic dysfunction, but could be used to reduce the incidence of coronary artery disease outcomes in a subgroup of patients who have heart rates of 70 bpm or greater.
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            Ivabradine in stable coronary artery disease without clinical heart failure.

            Kim Fox, Ian Ford, Philippe Gabriel Steg … (2014)
            An elevated heart rate is an established marker of cardiovascular risk. Previous analyses have suggested that ivabradine, a heart-rate-reducing agent, may improve outcomes in patients with stable coronary artery disease, left ventricular dysfunction, and a heart rate of 70 beats per minute or more. We conducted a randomized, double-blind, placebo-controlled trial of ivabradine, added to standard background therapy, in 19,102 patients who had both stable coronary artery disease without clinical heart failure and a heart rate of 70 beats per minute or more (including 12,049 patients with activity-limiting angina [class ≥II on the Canadian Cardiovascular Society scale, which ranges from I to IV, with higher classes indicating greater limitations on physical activity owing to angina]). We randomly assigned patients to placebo or ivabradine, at a dose of up to 10 mg twice daily, with the dose adjusted to achieve a target heart rate of 55 to 60 beats per minute. The primary end point was a composite of death from cardiovascular causes or nonfatal myocardial infarction. At 3 months, the mean (±SD) heart rate of the patients was 60.7±9.0 beats per minute in the ivabradine group versus 70.6±10.1 beats per minute in the placebo group. After a median follow-up of 27.8 months, there was no significant difference between the ivabradine group and the placebo group in the incidence of the primary end point (6.8% and 6.4%, respectively; hazard ratio, 1.08; 95% confidence interval, 0.96 to 1.20; P=0.20), nor were there significant differences in the incidences of death from cardiovascular causes and nonfatal myocardial infarction. Ivabradine was associated with an increase in the incidence of the primary end point among patients with activity-limiting angina but not among those without activity-limiting angina (P=0.02 for interaction). The incidence of bradycardia was higher with ivabradine than with placebo (18.0% vs. 2.3%, P<0.001). Among patients who had stable coronary artery disease without clinical heart failure, the addition of ivabradine to standard background therapy to reduce the heart rate did not improve outcomes. (Funded by Servier; SIGNIFY Current Controlled Trials number, ISRCTN61576291.).
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              Efficacy of ivabradine, a new selective I(f) inhibitor, compared with atenolol in patients with chronic stable angina.

              Martial Bourassa, Kim Fox, Michal Tendera … (2005)
              Ivabradine, a new I(f) inhibitor which acts specifically on the pacemaker activity of the sinoatrial node, is a pure heart rate lowering agent. Ivabradine has shown anti-ischaemic and anti-anginal activity in a placebo-controlled trial. The objective of this study was to compare the anti-anginal and anti-ischaemic effects of ivabradine and the beta-blocker atenolol. In a double-blinded trial, 939 patients with stable angina were randomized to receive ivabradine 5 mg bid for 4 weeks and then either 7.5 or 10 mg bid for 12 weeks or atenolol 50 mg od for 4 weeks and then 100 mg od for 12 weeks. Patients underwent treadmill exercise tests at randomization (M(0)) and after 4 (M(1)) and 16 (M(4)) weeks of therapy. Increases in total exercise duration (TED) at trough at M(4) were 86.8+/-129.0 and 91.7+/-118.8 s with ivabradine 7.5 and 10 mg, respectively and 78.8+/-133.4 s with atenolol 100 mg. Mean differences (SE) when compared with atenolol 100 mg were 10.3 (9.4) and 15.7 (9.5) s in favour of ivabradine 7.5 and 10 mg (P<0.001 for non-inferiority). TED at M(1) improved by 64.2+/-104.0 s with ivabradine 5 mg and by 60.0+/-114.4 s with atenolol 50 mg (P<0.001 for non-inferiority). Non-inferiority of ivabradine was shown at all doses and for all criteria. The number of angina attacks was decreased by two-thirds with both ivabradine and atenolol. Ivabradine is as effective as atenolol in patients with stable angina.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arrhythm Electrophysiol Rev
                Journal ID (iso-abbrev): Arrhythm Electrophysiol Rev
                Journal ID (publisher-id): AER
                Title: Arrhythmia & Electrophysiology Review
                Publisher: Radcliffe Cardiology
                ISSN (Print): 2050-3369
                ISSN (Electronic): 2050-3377
                Publication date (Print): 12 February 2020
                Volume: 8
                Issue: 4
                Pages: 300-303
                Affiliations
                [1. ] Cardiology and Angiology Unit, Department of Clinical and Experimental Internal Medicine, Medical Research Institute, University of Alexandria, Egypt
                [2. ] Department of Cardiology, Faculty of Medicine, University of Alexandria, Egypt
                [3. ] Michigan State University, East Lansing, MI, US
                [4. ] Department of Cardiology, Faculty of Medicine, Ain Shams University, Cairo, Egypt
                Author notes

                Disclosure: The authors have no conflicts of interest to declare.

                Correspondence: Mahmoud Hassan Abdelnabi, Cardiology and Angiology Unit, Department of Clinical and Experimental Internal Medicine, Medical Research Institute, University of Alexandria, Egypt. E: Mahmoud.hassan.abdelnabi@ 123456outlook.com
                Article
                DOI: 10.15420/aer.2019.30.2
                PMC ID: 7358942
                SO-VID: 3bc1e947-e92c-498c-8202-466e10b8ee5d
                Copyright © Copyright © 2019, Radcliffe Cardiology
                License:

                This work is open access under the CC-BY-NC 4.0 License which allows users to copy, redistribute and make derivative works for non-commercial purposes, provided the original work is cited correctly.

                History
                Date received : 09 March 2019
                Date accepted : 08 January 2019
                Page count
                Pages: 3
                Categories
                Subject: Electrophysiology and Ablation

                Keywords: ivabradine,heart rate,angina,if current,if channels,heart failure,acute coronary syndromes,af
                Data availability:
                Keywords: ivabradine, heart rate, angina, if current, if channels, heart failure, acute coronary syndromes, af

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