Ivabradine 7.5mg tablets

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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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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PurposeAnthracyclines are widely used anticancer agents but are limited by dose-dependent cardiotoxicity. Ivabradine selectively reduces heart rate without negative inotropy and may offer cardio protection in cancer patients, though its efficacy in anthracycline-induced cardiotoxicity (AIC) remains unclear.MethodsWe conducted a systematic review and meta-analysis of randomized controlled trials (RCTs) comparing ivabradine versus placebo in adult patients receiving anthracycline therapy. PubMed, Cochrane Central, Embase, Web of Science, Google Scholar, Scopus and ClinicalTrials.gov, and reference lists were searched through August 2025. Outcomes included left ventricular ejection fraction (LVEF), heart rate, blood pressure, NT-proBNP, and strain-based parameters. Risk of bias was assessed with the Cochrane RoB 2 tool.ResultsThree RCTs (n = 210) met inclusion criteria. Ivabradine showed no significant effect on LVEF (MD 0.32%, 95% CI - 0.90 to 1.54; p = 0.61) or NT-proBNP. Heart rate reduction was directionally favorable but not statistically significant (MD - 4.11 bpm, 95% CI - 8.69 to 0.46; p = 0.08). Systolic and diastolic blood pressure were unchanged. Strain-based outcomes were inconsistently reported, precluding pooled analysis.ConclusionsGiven the limited sample size, heterogeneity, and variability in endpoint definitions, current evidence is insufficient to establish a definitive cardioprotective role for ivabradine in AIC. Larger, rigorously designed trials with standardized imaging and biomarker endpoints are needed to determine its role.

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BACKGROUND: Postoperative junctional ectopic tachycardia (JET) is a frequent, hemodynamically consequential arrhythmia after congenital heart surgery. Ivabradine is increasingly used off-label, but its effectiveness and safety in pediatric postoperative JET remain uncertain. METHODS: We conducted a systematic review and single‑arm meta‑analysis of studies enrolling children (< 18 years) with postoperative JET treated with oral or nasogastric ivabradine. Outcomes included conversion to sinus rhythm, time to conversion, recurrence, use of concomitant antiarrhythmic drugs (AADs), adverse events (AEs) (bradycardia, hypotension, QT prolongation, atrioventricular block), and all‑cause mortality. Study‑level event rates were pooled as proportions using random‑effects models. RESULTS: Five studies (1 randomized trial arm, 3 cohorts, 1 case series; N = 87) met the inclusion criteria. Ivabradine dosing ranged from 0.05 to 0.1 mg/kg every 12 h. Across ivabradine‑based regimens, the pooled conversion proportion was 98.8% (95% CI 93.8–100), with reported mean times to stable sinus rhythm between 7.1 and 55.5 h. The pooled JET recurrence proportion was 3% (95% CI 0–12.1). Concomitant intravenous or oral AADs were used in 48.3% of patients (95% CI 10.4–87.2). No ivabradine-attributed bradycardia, hypotension, QT-interval prolongation, or new/worsening atrioventricular block was reported; all‑cause mortality was 2.1% (95% CI 0–10.1), attributed in the primary reports to postoperative complications rather than directly to ivabradine. In a sensitivity analysis restricted to two studies with ≤ 25% concomitant antiarrhythmic drug use, the conversion proportion remained high (98%), but confidence intervals for recurrence and mortality were wide. CONCLUSIONS: In the small, predominantly observational studies available, ivabradine-based regimens were associated with high conversion to sinus rhythm and low short-term recurrence of postoperative JET, with no hemodynamic or conduction AEs reported among 87 patients. Interpretation is limited by nonrandomized designs, frequent cotreatment with other AADs, short follow‑up, and regional concentration of data; the pooled proportions should be viewed as exploratory summaries rather than estimates of ivabradine’s independent effect. Multicentre randomized trials are needed to define causal efficacy, optimal dosing, and longer‑term safety. TRIAL REGISTRATION: This systematic review and single-arm meta-analysis was prospectively registered with PROSPERO (CRD420251080412).

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BackgroundPersistent sinus tachycardia affects up to 40% of patients after heart transplantation and is linked with graft dysfunction, impaired diastolic filling, and increased morbidity. Conventional rate-limiting therapies such as beta-blockers and calcium channel blockers are quite often contraindicated due to risks of bradyarrhythmia or hypotension. Ivabradine, a selective I(f) channel inhibitor, reduces heart rate (HR) without negative inotropic or hypotensive effects.AimTo evaluate the efficacy and safety of ivabradine in heart transplant recipients.MethodsA comprehensive search of PubMed, EMBASE, Scopus, Cochrane Library, and Google Scholar was conducted from inception to April 15, 2025. Eligible studies evaluated ivabradine in heart transplant recipient vs placebo or metoprolol, reporting HR, mortality, left ventricular mass (LVM), or safety. Data were independently extracted by two reviewers, and quality was assessed. Review Manager 5.4 performed pooled analyses using random-effects models. Mean differences (MD) or standardized MD (SMD) were calculated for continuous outcomes, and risk ratios for dichotomous outcomes.ResultsOf 415 records identified, four studies comprising 264 patients (126 ivabradine, 138 control) met the inclusion criteria. Ivabradine significantly reduced resting HR compared with controls (MD = -11.06 beats per minute; 95%CI: -19.50 to -2.62; P I 2 = 93%). Sensitivity analysis demonstrated consistent findings (SMD = -6.74; 95%CI: -9.23 to -4.24; I 2 = 0%). No significant difference in all-cause mortality was observed (MD = 0.52; 95%CI: 0.17-1.64; P = 0.27; I 2 = 85%). Pooled analysis of LVM revealed no significant effect of ivabradine (MD = -3.57 g; 95%CI: -29.21 to 22.08; P = 0.79; I 2 = 73%), with sensitivity analysis confirming neutrality. Adverse events were rare and mostly comparable between groups.ConclusionIvabradine reduces HR effectively in heart transplant recipients without added adverse outcomes, supporting its use as safe and well-tolerated alternative when conventional agents are unsuitable. Despite potential clinical benefit, small sample size and heterogeneity the need for larger randomized trials to confirm long-term outcomes and establish ivabradine's role in post-transplant care.

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