Ivabradine 5mg tablets

IntroductionIn patients with acute illness, compensatory tachycardia initially serves to maintain adequate cardiac output, oxygen delivery and tissue oxygenation but may persist despite appropriate fluid and vasopressor resuscitation or may be secondary to inotropic therapy. Sustained tachycardia is a predictor of adverse outcomes in critical illness. Ivabradine, a highly selective inhibitor of the sinoatrial node's pacemaker current (If or "funny" current), mitigates tachycardia by modulating diastolic depolarization slope without affecting contractility.AimTo report the existing evidence on the use of ivabradine in critically ill patients and assess its effect on rate control.MethodsA systematic literature search was performed up to May 2024 in the MEDLINE/PubMed®, Cochrane Controlled Clinical Trial register, EMBASE® and Scopus® databases. The search included: P- only original studies conducted in humans admitted to the Intensive Care Unit (ICU); I - when ivabradine administration was tested; C - in presence or absence of a control group; O - for any outcome; S - including case reports, randomized and observational trials, published in English in peer-reviewed journals.ResultsAfter the first screening, 39 studies were assessed for eligibility on a total of 682 records identified. Among those, 29 were excluded; 10 studies (4 randomized controlled trial, 5 case report/series, 1 prospective observational), including a total of 243 patients, were included in the qualitative analysis, 6 studies were included in the quantitative analysis. The use of ivabradine resulted in a pooled mean heart rate reduction of 18.70 [12.70-24.80] bpm (p ConclusionsIvabradine may be a useful alternative to beta-blocker in the management of inappropriate sinus tachycardia. Yet, evidence is limited and inconsistent. Larger randomized trials are needed to investigate the potential benefits or hazards of ivabradine use on hemodynamics and long-term outcomes.

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Postural orthostatic tachycardia syndrome (POTS) is a condition defined by symptoms of orthostatic intolerance and a sustained heart rate (HR) increment of ≥ 30 beats per minute (bpm) upon postural change to the upright position in the absence of orthostatic hypotension, defined as a sustained decrease in systolic blood pressure (SBP) of ≥ 20 mmHg or a decrease in diastolic blood pressure (DBP) of ≥ 10 mmHg within 3 min of standing. In children, a sustained HR increment of at least 40 bpm is required for diagnosis of POTS. POTS is a common condition in adults and children suffering from myalgic encephalomyelitis/chronic fatigue syndrome (ME/CFS). In daily clinical practice, therapeutic recommendations are rare and evidence is missing. The objective of this review is to present the current knowledge on non-pharmacological and pharmacological approaches in POTS with a special focus on POTS therapy in children and people with ME/CFS. Of 3853 studies, 45 studies were included in the systematic review. Evidence on therapy in POTS is rare and large randomized controlled trials (RCT) on single interventions are needed. Non-pharmacological approaches such as the use of compression garments, physical training, salt supplementation and transdermal vagal nerve stimulation could be possible treatment options in POTS because they are easy to implement as first-line therapeutic measures in clinical practice. For pharmaceuticals, several studies showed significant effects following therapy with ivabradine and β-adrenergic blocking agents. There are single studies which imply that midodrine (hydrochloride) and pyridostigmine seem to have a beneficial effect on hemodynamics in POTS.

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BackgroundCongenital junctional ectopic tachycardia (CJET) is a rare but life-threatening arrhythmia in neonates and infants, often refractory to conventional antiarrhythmic therapy. Ivabradine, a selective inhibitor of hyperpolarization-activated cyclic nucleotide-gated channels, has emerged as a promising drug for CJET management.AimTo evaluate the efficacy and safety of ivabradine in the management of CJET. Specifically, this study aims to analyze the dosing strategies, treatment outcomes, and the role of ivabradine as monotherapy or adjunct therapy in patients who have previously received other antiarrhythmic medications. Additionally, this review seeks to assess the impact of ivabradine on heart rate (HR) control, rhythm conversion, and its overall safety profile to provide evidence-based insights into its clinical use for CJET management.MethodsThis systematic review aims to evaluate the outcomes of ivabradine, either as monotherapy or as an adjunctive therapy, in the treatment of CJET. A comprehensive literature search was conducted across multiple electronic databases to identify relevant studies investigating the use of ivabradine in CJET. Stringent inclusion and exclusion criteria were applied to ensure the inclusion of high-quality, peer-reviewed studies. Data extraction and quality assessment were performed independently by two reviewers.ResultsTen studies, comprising 6 case reports, 3 case series, and 1 cohort study, met the inclusion criteria. Ivabradine doses ranged from 0.025 to 0.28 mg/kg/dose, administered either as monotherapy or in combination with various antiarrhythmic medications. Overall, ivabradine demonstrated promising results in achieving HR control, conversion to sinus rhythm, or stabilization of junctional rhythm. No significant adverse effects related to ivabradine were reported.ConclusionThe available evidence suggests that ivabradine may be an effective adjunctive therapy or, in some cases, a potential monotherapy for the management of CJET, particularly in cases refractory to traditional antiarrhythmic medications. However, the current evidence is limited by the small sample sizes and retrospective nature of the included studies. Well-designed prospective studies with larger cohorts and longer follow-up periods are warranted to further elucidate the role of ivabradine in CJET management.

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BackgroundIvabradine was initially introduced for heart failure and coronary artery disease patients, with its interesting feature of heart rate reduction without reducing heart contractility or blood pressure. In recent years, however, the use of ivabradine evolved for arrhythmia, including for focal atrial tachycardia (FAT). This systematic review aims to evaluate all the existing evidence on ivabradine for focal atrial tachycardia and synthesize information on its use, including efficacy and safety.MethodsA comprehensive literature search was conducted in three large databases: PubMed, ScienceDirect, and Scopus, following the PRISMA guidelines, using the search terms of: (ivabradine) AND (atrial tachycardia). Studies were included if they reported the use of Ivabradine for FAT in humans. Studies on atrial tachycardia outside of focal mechanisms or any other arrhythmias were excluded.ResultsThe search strategy resulted in 375 articles: 63 from PubMed, 262 from ScienceDirect, and 50 from Scopus, which subsequently resulted in 19 articles included for final review after a meticulous filtering process. The included studies were 11 case reports, 4 case series, and 4 observational studies discussing the outcome of ivabradine for focal atrial tachycardia.ConclusionEvidence from small cohorts and case reports suggests promising outcomes and a good safety profile of ivabradine for FAT, but larger, well-designed and more robust studies are needed. Recognizing an automaticity-driven FAT is key to considering ivabradine, especially when FAT persists despite cardioversion or standard therapy.

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