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Background: Beta blockers, mainly propranalol, are usually administered to control heart rate in patients with thyrotoxicosis, especially when congestive heart failure presents. However, when thyrotoxicosis is not controlled, heart rate may be difficult to control even with maximal doses of propranolol. This presentation alerts physicians to the possibility of using ivabradine, a selective inhibitor of the sinoatrial pacemaker, for the control of heart rate. Case presentation: We present a 37-year-old woman with thyrotoxicosis and congestive heart failure whose heart rate was not controlled with a maximal dose of beta blockers during a thyroid storm. The addition of ivabradine, a selective inhibitor of the sinoatrial pacemaker, controlled her heart rate within 48 hours. Conclusion: Ivabradine should be considered in patients with thyrotoxicosis, including those with heart failure, in whom beta blockers are insufficient to control heart rate

Ivabradine increases stroke volume, but does not have a negative impact on blood pressure (BP). Thus, a patient with low BP can benefit from treatment with ivabradine. A 72-year-old Japanese woman with asthma and chronic bronchitis presented with dyspnea. Her heart rate (HR) was 126 beats per minute and an electrocardiogram showed sinus tachycardia. The chest X-ray showed cardiomegaly and pulmonary congestion. A transthoracic echocardiogram (TTE) showed reduced left ventricular ejection function (LVEF) and severe functional mitral regurgitation (MR). We diagnosed her with inappropriate sinus tachycardia (IST) and heart failure (HF) due to tachycardia-induced cardiomyopathy. After resolving the pulmonary congestion with diuretics, we administered a minimum dose of bisoprolol, which resulted in re-exacerbation of the HF. Because IST was persistent, we initiated treatment with ivabradine. As soon as ivabradine was started, the HR decreased, the BP gradually increased, and HF compensation was achieved. Bisoprolol was continued and losartan was started. In summary, we used ivabradine for a patient with tachycardia, low BP, a low LVEF, and severe MR. By optimizing the medical therapy, exercise tolerance improved and she was discharged. The serum brain natriuretic peptide was significantly reduced and TTE showed an improved LVEF and reduced MR.

Objective Heart rate modulation therapy using ivabradine reduces both morbidity and mortality in patients with systolic heart failure. However, the target heart rate for this patient population remains to be elucidated. Methods In this prospective observational study, we included patients with heart failure and a reduced ejection fraction who received 5.0 mg/day of ivabradine for three days. At baseline and three days later, the overlap length between E-wave and A-wave using trans-mitral Doppler echocardiography, as well as the cardiac output using AESCLONE mini, were simultaneously measured. The associations between Δ overlap length and Δ cardiac output were then investigated. Results Eight patients [77 (53, 87) years old, 2 men] were included. The heart rate decreased from 81 (69, 104) bpm down to 64 (57, 79) bpm (p=0.012). The overlap length increased in four patients and decreased in the other four patients. During the time period of ivabradine therapy, patients who had a greater decrease in overlap length had a greater increase in cardiac output (r=0.84, p=0.009). Conclusion Decreases in the overlap length between E-wave and A-wave by Doppler echocardiography were associated with an increase in the cardiac output while on ivabradine therapy. The implications of Doppler echocardiography-guided heart rate modulation therapy targeting a minimal overlap length therefore require further evaluation in larger, prospective studies.

Angina is a significant contributor to disability and impairment in quality of life in patients with chronic coronary syndromes (CCS). An elevated heart rate (HR) may trigger myocardial ischemia by increasing oxygen consumption and decreasing the diastolic time, compromising the coronary flow. HR-lowering strategies offer symptom control and prevent cardiovascular events in subgroups of patients with CCS. However, the best therapeutic approach to achieve the desired HR in patients with CCS can be challenging based on efficacy and tolerability. Guidelines usually propose β-blockers and/or non-dihydropyridine calcium channel blockers (CCB) for angina patients with elevated HR. Nonetheless, there is no clear evidence of greater antianginal efficacy of this strategy versus an alternative HR-lowering agent. Ivabradine reduces the HR by blocking the If current in the sinoatrial node without affecting myocardial contractility or vascular tone. The magnitude of the HR reduction by ivabradine is proportional to the initial HR, which decreases the risk of significant bradycardia. Ivabradine increases the diastolic time and the coronary flow reserve to a greater extent than β-blockers and favors collateralization, improving the regional blood flow. We present two clinical cases of patients with symptomatic CCS in whom HR control with ivabradine was fundamental for symptom control and improvement in left ventricular (LV) function. An earlier combination of ivabradine plus β-blockers would have provided more rapid symptom control and improved LV function in the first case. In the second case, the primary mechanism responsible for angina was most likely a coronary vasomotor abnormality, in which the use of β-blockers aggravated the discomfort. The combination of a dihydropyridine CCB plus ivabradine was highly influential in symptom control. Due to its effects beyond HR reduction and good tolerability, ivabradine should be considered an essential ally in managing patients with angina and high HR with or without LV dysfunction.

Aims Heart failure (HF) causes significant morbidity and mortality, but the rates and characteristics of people with HF in Australia are not well studied. SHAPE set out to describe the characteristics of HF patients seen in the real‐world setting. Methods We analysed anonymized patient data extracted from the clinical software of 43 participating GP clinics for the 5 year period from 1 July 2013 to 30 June 2018. Patients were stratified into ‘definite’ and ‘probable’ HF based on a hierarchy of selection criteria and analysed for their clinical characteristics. Symptoms and signs of HF and ejection fraction data were searched for within the free text of the medical notes. Results Of the 1.12 million adults seen regularly, 20 219 were classified as having definite or probable HF. The mean age of the population was 69.8 years, 50.6% were female, and mean body mass index was 31.2 kg/m2. Fewer than 1 in 6 had the HF diagnosis optimally recorded. Only 3.2% (650 patients) had their left ventricular ejection fraction (EF) quantified: 40.9% had an EF ≥50% and 59.1% had an EF

Introduction and objectives Ivabradine reduces heart rate by blocking the I(f) current and preserves blood pressure and stroke volume through unknown mechanisms. Caveolin-3 protects the heart by forming protein complexes with several proteins, including extracellular matrix (ECM)-metalloproteinase-inducer (EMMPRIN) and hyperpolarization-activated cyclic nucleotide-gated channel 4 (HN4), a target of ivabradine. We hypothesized that ivabradine might also exert cardioprotective effects through inhibition of ECM degradation. Methods In a porcine model of cardiogenic shock , we studied the effects of ivabradine on heart integrity, the levels of MMP-9 and EMMPRIN , and the stability of caveolin-3/HCN4 protein complexes with EMMPRIN. Results Administration of 0.3 mg/kg ivabradine significantly reduced cardiogenic shock-induced ventricular necrosis and expression of MMP-9 without affecting EMMPRIN mRNA , protein, or protein glycosylation (required for MMP activation). However, ivabradine increased the levels of the caveolin-3/LG-EMMPRIN (low-glycosylated EMMPRIN) and caveolin-3/HCN4 protein complexes and decreased that of a new complex between HCN4 and high-glycosylated EMMPRIN formed in response to cardiogenic shock. We next tested whether caveolin-3 can bind to HCN4 and EMMPRIN and found that the HCN4/EMMPRIN complex was preserved when we silenced caveolin-3 expression, indicating a direct interaction between these 2 proteins. Similarly, EMMPRIN-silenced cells showed a significant reduction in the binding of caveolin-3/HCN4, which regulates the I(f) current, suggesting that, rather than a direct interaction, both proteins bind to EMMPRIN. Conclusions In addition to inhibition of the I(f) current, ivabradine may induce cardiac protection by inhibiting ECM degradation through preservation of the caveolin-3/LG-EMMPRIN complex and control heart rate by stabilizing the caveolin-3/HCN4 complex.

Ivabradine, which reduces heart rate (HR) without affecting sympathetic nerve activity, improves mortality and morbidity in patients with systolic dysfunction. However, its impact on up-titrating a concomitant beta-blocker dose in such a cohort, via increasing cardiac output and blood pressure and improving tolerability to beta-blockers, remains unknown. In this single-center, prospective, randomized control trial, patients with systolic dysfunction, defined as left ventricular ejection fraction50%, sinus rhythm, heart rate75 bpm, systolic blood pressure between 90 and 110 mmHg, and New York Heart Association functional class III or IV, who are refractory to up-titration of a beta-blocker due to symptomatic hypotension, dizziness, or worsening heart failure, were assigned to the 20 ivabradine arm or the 20 conventional therapy arm and followed-up for 6 months. The primary outcome is the daily dose of beta-blocker at 6-months follow-up. The secondary outcomes are echocardiographic parameters including overlap between E-wave and A-wave in transmitral diastolic filling flow, plasma B-type natriuretic peptide level, 6-minute walk distance, and heart failure readmission rate. By conducting this study, we hope to demonstrate the clinical benefit of ivabradine therapy in up-titrating beta-blockers and improving clinical outcomes in patients with systolic dysfunction.

Congenital junctional ectopic tachycardia (CJET) is a rare tachyarrhythmia that remains difficult to manage, with suboptimal control in most cases. Here, we report literature research on the use of ivabradine in the treatment of pediatric junctional ectopic tachycardia (JET), both congenital and postoperative, and describe the successful use of ivabradine–flecainide association for CJET therapy resistant to other antiarrhythmic agents. This new drug combination was effective in completely suppressing JET. Ivabradine–flecainide combination may be considered a new therapeutic strategy of CJET with a satisfactory efficacy/tolerability ratio in patients resistant to conventional drug combinations.

We present the case of a 64-year-old man who presented to our outpatient clinic with intermittent palpitations and presyncopal events. In 2009, he underwent dual chamber pacemaker implantation in another institution for 2nd degree heart block. Pharmacological treatment attempts with β‑blocker, calcium channel antagonists and ivabradine remained clinically unsuccessful. Up to this point in time, no documentation of clinical tachycardia, which was reported to result in a heart rate of around 160 beats/minute, was obtained. The patient presented to our clinic for further electrophysiological evaluation.

Objectives This study sought to compare the efficacy of ivabradine and amiodarone in the management of postoperative junctional ectopic tachycardia (JET) after cardiac surgery in children. Background JET is a serious arrhythmia occurring in children after cardiac surgery and requires aggressive management. Amiodarone has been conventionally used in its treatment. Recent studies have reported the utility of ivabradine in this regard. Methods In this open-label randomized controlled trial, 94 children (age ≤18 years) who developed postoperative JET were allocated to receive either amiodarone or ivabradine. The primary endpoint was restoration of normal sinus rhythm. Results Sinus rhythm was achieved in 43 out of the 46 patients (93.5%) in the amiodarone group and 46 out of the 48 patients (95.8%) in the ivabradine group (mean difference of treatment effect: 2.3%; 95% confidence interval: −6.7% to 11.5%). The median (interquartile range) time taken to achieve sinus rhythm conversion was similar in both the groups: 21.5 (17–30.2) hours versus 22 (13.4–38.5) hours (p = 0.36)]. The time taken to rate control of JET was significantly less in the amiodarone group: median 7.0 (5.5–9.5) hours versus 8.0 (5.8–10.8) hours (p = 0.02)]. No drug-related adverse events were observed in the ivabradine group. Conclusions Oral ivabradine is not inferior to intravenous amiodarone in converting postoperative JET to sinus rhythm. There was no difference in time taken to sinus rhythm conversion between the groups, although the rate control was earlier in patients who received amiodarone. Monotherapy with ivabradine may be considered as an alternative to amiodarone in the management of postoperative JET. (Comparison of Two Drugs, Ivabradine and Amiodarone, in the Management of Junctional Ectopic Tachycardia, an Abnormality in Cardiac Rhythm in Patients Under 18 years Who Undergo Cardiac Surgery: CTRI/2018/08/015182 )

This report describes two cases of tachycardia-induced cardiomyopathy secondary to incessant ectopic atrial tachycardia (EAT) in an infant presenting with severe left ventricular dysfunction and hemodynamic instability. The two cases were managed differently. The first required mechanical ventilation and was resistant to conventional antiarrhythmic drugs. After the initiation of enteral ivabradine (0.15mg/kg) the heart rate slowed with significant improvement in hemodynamics, peripheral perfusion and sinus rhythm was restored after 12 hours. Ivabradine was continued and the patient was discharged home after 10 days of hospitalization. The second case was managed by early initiation of ivabradine and resulted in restoration of sinus rhythm within 4 hours, thus avoiding trials of conventional anti-arrhythmic drugs with unstable hemodynamic profile. The infant was discharged after 5 days of hospitalization on ivabradine..

Heart rate modulation therapy using ivabradine improves mortality and morbidity in patients with systolic dysfunction. However, a target heart rate remains uncertain. Echocardiography-guided ivabradine therapy, in which we attempt to approach zero overlap between two diastolic filling inflow waves, has recently been proposed to maximize cardiac output, facilitate reverse remodeling, and reduce mortality and morbidity, instead of using an absolute value for the target heart rate. Prospective studies are needed to validate the clinical implication of these therapeutic strategies. Also, this concept should be expanded to other clinical scenarios.

Aims Ivabradine has been used in patients who have chronic heart failure (HF) with reduced ejection fraction (HFrEF) and concomitant sinus heart rate ≥70 bpm. This administration for acute HFrEF remains a concern. This study used a real‐world multicentre database to investigate the effects of ivabradine among patients with acute decompensated HFrEF before discharge. Methods and results This study retrospectively identified patients with acute decompensated HFrEF who were administered ivabradine at discharge from two multicentre HF databases. Propensity score matching was performed to adjust for confounders. Cardiovascular mortality, all‐cause mortality, and recurrent HF rehospitalization risks were then compared between those with and without ivabradine treatment. After 1:2 propensity score matching, 876 patients (age, 60.7 ± 14.6 years; female, 23.2%; left ventricular ejection fraction, 28.2% ± 7.8%; and heart rate at discharge, 84.3 ± 13.8 bpm) were included in the final analysis, including 292 and 584 patients with and without ivabradine treatment at discharge, respectively. No significant differences were observed in baseline characteristics between the two groups. At 1 year follow‐up, patients in the ivabradine group had significantly lower heart rates (77.6 ± 14.7 vs. 81.1 ± 16.3 bpm; P = 0.005) and lower HF severity symptoms (New York Heart Association Functional class, 2.1 ± 0.7 vs. 2.3 ± 0.9; P

Background: Chronic heart failure (CHF) is a clinical status and a progressive health disorder extremely related to increased morbidity and mortality worldwide. Accordingly, this study aimed to assess systematic review of literature on cost-effectiveness done in patients with heart failure receiving Ivabradine plus standard treatment compared with standard treatment alone. Areas covered: This study is a systematic review in which all published articles related to the study topic were assessed in time range of 2014�2020. In order to find articles, internet search in foreign databases of PubMed, Embase, ISI/Web of Science (WoS), SCOPUS, Global Health databases, through keywords related to the objective was performed. Six articles out of 1524 article related to final topic were assessed. In addition, quality of studies was evaluated using CHEERS checklist. In six countries investigated (Iran, Thailand, Australia, United States of America, United Kingdom, and Greece), willingness-to-pay (WTP) thresholds higher cost per QALY, and highest ICER for Ivabradine was in USA (55,600 /QALY) and the lowest was in Thailand (10,616/QALY). Most items of CHEERS were estimated in the studies and studies had good quality. Expert opinion: Regarding our investigation, ivabradine combined with standard care was more cost-effective than standard care alone in most of the evaluated studies, although the cost of this intervention was higher than its effectiveness. However, the threshold chosen by each country can have a significant impact on these results. And to have a more accurate result, it is required to pay more attention to the income level in different countries. © 2021 Informa UK Limited, trading as Taylor & Francis Group.

Since 1953, sinus tachycardia has been defined as a heart rate (HR) in sinus rhythm of >100 beats per minute (bpm). However, this number has never been formally evaluated, and no established threshold values for special groups, such as those with heart failure (HF) accompanied by a reduced ejection fraction (HFrEF). Herein, we provided evidence that lowering the HR of patients with HFrEF to

Background Acute kidney injury (AKI) with sepsis increases mortality significantly. The pathophysiology of AKI during sepsis is complex and multifactorial. Lower heart rate is associated with better survival in patients with multiple organ dysfunction syndrome (MODS), a disease mostly caused by sepsis. In our study, we hypnotized that use of ivardrabine as heart rate reducing agent in septic patient with renal impairment may improve renal function. Results Fifty patients with sepsis with early renal impairment were divided in 1: 1 ratio to receive Ivabradine (group I) or not (group C). The average age of the included patients was almost 45 years, chest disorders were the main cause of sepsis in both groups. There were statistically significant differences between both groups in terms of reduction of heart rate group (I) (68.13 ± 3.34) versus (group C) (87.04 ± 3.23) and (P < 0.001) also, improvement in eGFR by Cystatin c in group (I) (103.32 ± 6.96) versus (group C) (96.25 ± 6.36) and (P < 0.001) also vasopressor dosage consumption (P < 0.001). As regards secondary outcomes, there were no statistically significant differences between study’s groups in terms of length of hospital stay (P = 0.390), need for hemodialysis (P = 0.384), and mortality (P = 1.000). Conclusions We concluded that Ivabradine as an adjuvant therapy in septic patients with renal impairment is promising agent to reduce such impairment. Trial registration Pan African Clinical Trial Registry: Identification number for the registry is PACTR201911806644230.

Ischaemic Heart Disease (IHD) and Chronic Obstructive Pulmonary Disease (COPD) are common diseases that rank highest in the Global Burden of Disease Study (2019). IHD and COPD are often combined, making diagnosis and treatment of patients difficult in actual clinical practice. The aim of the study was to identify problems in the diagnosis and treatment of patients with a combination of chronic IHD and COPD, based on a retrospective analysis of medical records. Patient’s adherence to treatment was also assessed with the Morisky Scale (MMAS-8). The analysis of 108 inpatient charts with a combination of chronic IHD and COPD was carried out. The quality of diagnosis and treatment of IHD was evaluated in accordance with the order of the Ministry of Health of Ukraine N152 dated March 02 2016, considering the recommendations of the European Society of Cardiology (2019). It was found that smoking history was in 23.1% of patients, a body mass index (BMI) was calculated in 51,9%, and a carotid ultrasound examination was carried out in 7.4% of cases. The total cholesterol level was determined in 59.2% of patients, while the level of low-density lipoprotein cholesterol (LDL-C) was determined in only 43.5%. Transthoracic echocardiography (TTE) was performed in 62.9 % of patients, but stress-echocardiography and exercise ECG were not performed. Daily ECG monitoring was performed in 60.2% of cases. The levels of brain natriuretic peptide (BNP) or N-terminal proBNP (NT-proBNP) were not detrmined to precise etiology of dyspnea. It was also found that beta-blockers (29.6% of patients), ivabradine (11.1% of patients) and statins (65.7% of patients) are seldom administered to patients with IHD and COPD. The targeted doses of these drugs are not reached. Fixed combinations of long-term bronchodilalarors were insufficiently used in therapy of COPD. However, patients' adherence to basic IHD and COPD therapy is weak. 45.4 % of patients were non-adherent to treatment, 43.5% were medium-adherent, and only 11.1% of patients were adherent to treatment.

Background: Septic shock is associated with excessive sympathetic outflow, high plasma catecholamine levels, myocardial depression, vascular hypo-reactivity, and autonomic dysfunction. Typically, patients have a low resistance, high cardiac output circulation with tachycardia and arterial hypotension that may be poorly or even nonresponsive to exogenous catecholamine vasopressors. The aim of the present study was to compare the effect of ivabradine vs bisoprolol for heart rate control on the hemodynamics and clinical outcomes in patients with septic shock. Methods: The study was carried out on 90 patients, aging from 18 to 60 years of both sex presented with septic shock in ICU. Patients were randomly classified into 3 equal groups each of 30 patients. Group I (Control group) received conventional therapy. Group II (Bisoprolol group) received conventional therapy plus bisoprolol 5 mg once daily & one placebo pill on 12 hrs interval via nasogastric tube for 7 days. Group III (Ivabradine group) received conventional therapy plus ivabradine 5 mg twice daily on 12 hrs interval via nasogastric tube for 7 days. Results: Both bisoprolol and ivabradine effectively lowered heart rate in septic shock patients but ivabradine was more effective than bisoprolol. Both bisoprolol and ivabradine did not affect mean blood pressure, with ivabradine being more effective in maintaining blood pressure than bisoprolol. Noradrenaline dose was lower in ivabradine group in comparison with the other two groups. As regard to stroke volume & cardiac output, there was improvement in ivabradine group in comparison with bisoprolol and control groups. As regard to serum lactate level, there was improvement in ivabradine group in comparison with the other two groups. Both bisoprolol & ivabradine resulted in reduction in LOS & 28-day mortality with no significant difference between both groups. Conclusions: Controlling heart rate in septic shock patients with either bisoprolol or ivabradine improves outcomes. Ivabradine is better than bisoprolol in maintaining hemodynamics and improving tissue perfusion parameters.

Background High resting heart rate (HR) is a known marker of cardiovascular outcomes for heart failure (HF) patients. Ivabradine is a new class of HR lowering drug and a specific inhibitor of the If current in the sinoatrial node. Ivabradine substantially and significantly reduces major risks associated with HF when added to guideline-based treatment for left ventricular (LV) ejection fraction ≤35% and HR ≥70 bpm in sinus rhythm. On the other hand, HF with preserved ejection fraction (HFpEF) currently accounts for roughly half of all HF cases and usually presents as LV diastolic dysfunction. However, the association between HR reduction and LV diastolic function for HFpEF patients remains uncertain. Methods/design This investigation into the effect of IVAbradine on left ventricular diastolic function of patients with heart failure with Preserved Ejection Fraction (IVA-PEF) is a multicenter, prospective, uncontrolled, open-label, single assignment, and an interventional single-arm study to investigate the effect of ivabradine on LV diastolic function of HFpEF patients. The key inclusion criterion is HFpEF with resting HR ≥75bpm in sinus rhythm. After completed informed consent forms are obtained, patients will be given 5 mg/day of ivabradine during the study. LV diastolic function is assessed in terms of mitral inflow E and mitral e’ annular velocities (E/e’). The primary endpoint will be defined as a change in E/e′ between baseline and 3 months after the start of administration of ivabradine. Conclusion The findings of our trial may provide a new perspective on ivabradine for the treatment of HFpEF.

Our previous study indicated that intravenously administered ivabradine (IVA) augmented the dynamic heart rate (HR) response to moderate-intensity vagal nerve stimulation (VNS). Considering an accentuated antagonism, the results were somewhat paradoxical; i.e., the accentuated antagonism indicates that an activation of hyperpolarization-activated cyclic nucleotide-gated (HCN) channels via the accumulation of intracellular cyclic adenosine monophosphate (cAMP) augments the HR response to VNS, whereas the inhibition of HCN channels by IVA also augmented the HR response to VNS. To remove the possible influence from the accentuated antagonism, we examined the effects of IVA on the dynamic vagal control of HR under β-blockade. In anesthetized rats (

The coronavirus pandemic showed not only an increase in levels of excess morbidity and mortality in the acute phase, but also persisting symptoms 4 weeks after the onset of the disease. A review of international studies on the prevalence and diversity of the manifestations of postcoid syndrome is presented. The data on such a manifestation of post-COVID syndrome as postural orthostatic tachycardia syndrome (POTS) are accumulating. Pathogenetic mechanisms, modern diagnostic criteria and research data on the prevalence of this syndrome are presented in the article. The Canadian Cardiovascular Society has proposed medications as a treatment for POTS, including the sinus node If channel inhibitor ivabradine. Data from several studies showing the effectiveness of this drug for POTS, including after suffering COVID-19, are presented in the article. Clinical data on the prevalence of tachycardia among patients admitted to the Sechenov University hospital are presented. About 18% of patients with hypertension and 21% of patients with normal blood pressure had a high heart rate. A clinical example of the use of ivabradine in a patient after a coronavirus infection is presented. Drug interactions and individual tolerance of ivabradine in patients after coronavirus infection are being discussed. The authors put forward the hypothesis about the further prospect of using ivabradine in the treatment of clinical manifestations of postcoid syndrome on the basis of literature data and their own experience.

Congenital junctional ectopic tachycardia is a rare and special type of supraventricular arrhythmia. Junctional ectopic tachycardia is characterized by persistently elevated heart rates that may cause an impairment in cardiac function. Junctional ectopic tachycardia is considered one of the most difficult-to-treat conditions even with a combination of antiarrhythmic medications. Ivabradine is a novel antiarrhythmic medication used to decrease the heart rate in adults with angina pectoris. We report a first case of a premature neonate with a normal heart structure who developed junctional ectopic tachycardia and was subsequently treated successfully with ivabradine.

Coronary CT angiography (CCTA) is increasing seen as a first line investigation in patients with suspected coronary artery disease. Heart-rate control improves the image quality and diagnostic accuracy of CCTA. Typically, beta-blockers are administered to induce sinus bradycardia. Sinus bradycardia may also be induced by ivabradine. We hypothesized that in a real-world population ivabradine would be an effective alternative to metoprolol at heart rate lowering for CCTA.This was a retrospective analysis of consecutive patients who were exposed to an ivabradine-based (IB) versus a metoprolol-only (MO) protocol to achieve a target heart rate/ = 65bpm. Hemodynamic responses to both strategies were compared along with differences in cost and the time expired from medication administration to CCTA.5955 consecutive patients were included in the analysis: 3211 were imaged during an era of a metoprolol only strategy (MO) and 2744 CCTA following an ivabradine based (IB) strategy. 2676 patients had heart rates65 and received heart-rate lowering medication: 1958 patients had MO, and 718 received IB protocol. Target heart rate of/ = 65bpm was achieved in 77% of MO and 89% of IB patients (p 0.01). The time from initial medication administration to CCTA was longer in the IB versus MO patients (77 versus 48 min, p 0.01).Introduction of a novel single dose ivabradine-based protocol to control heart rate for CCTA was more successful in achieving target heart rate than a metoprolol-only strategy. The use of ivabradine however incurred a 1.6-fold increase in the time delay from medication administration and imaging compared to a metoprolol only protocol.

Present investigation is based upon a new method development and validation for the simultaneous estimation of drugs comes under the classification of anti-hypertensive and anti-diabetic. For the proposed method metformin, ivabradine, metoprolol and ertugliflozin drugs were selected. The chromatographic separation was achieved by using mobile phase 0.01N potassium dihydrogen ortho phosphate buffer and acetonitrile (50:50) ratio and stationary phase of kromasil C18(250×4.6mm, 5µm) column. The retention times for metformin, ivabradine, metoprolol and ertugliflozin were found to be 2.560min, 3.116 min, 3.473 min and 5.196 min respectively. The developed method shows that all the drugs were clearly separated among each other with the system suitability. The developed method was further validated as per ICH guidelines Q2R1. It was found the method was accurate, presice with good linearity. Hence this method can be used for the routine analysis of these drugs in biological sample.

Cardiovascular diseases, especially coronary heart disease (CHD), are the leading cause of disability; various registry data show that the annual mortality rate of such patients is 2–3%. This explains the interest of practitioners in the pharmacotherapy of stable forms of coronary artery disease using current progress in the understanding of the pathogenesis of this disease and treatment compliance. Features of the pathogenesis of CHD in the form of increased myocardial oxygen demand, increased pre- and afterload on the performance of the heart necessitate the prescription of rhythm-reducing drugs such as beta-blockers, calcium channel blockers, ivabradine or their combinations, as well as nitric-containing drugs; trimetazidine, ranolazine for the purpose of myocardial cytoprotection. However, the use of hemodynamic drugs (beta-blockers, calcium channel blockers) does not always effectively relieve the symptoms of angina pectoris, even when used in combination with other drugs. This dictates the need to improve the drug effect on the ischemic myocardium with due account for the hypoxia-induced metabolic dysfunction of cardiac myocytes. In this regard, the use of trimetazidine at the initial stages of ischemia – at the level of metabolic dysfunction does not allow for the development of delayed complications: contractile disfunction of cardiac myocytes and myocardium in general. A wealth of clinical experience has been gained in the use of trimetazidine to treat stable angina pectoris in elderly patients, left ventricular dysfunction and symptoms of chronic heart failure. Drugs with a patient-friendly dosage regimen have been created to improve treatment compliance in patients with coronary artery disease. One of these drugs is once-daily modified release matrix tablets of myocardial cytoprotector Deprenorm OD, 70 mg. The creation of drugs with a patient-friendly dosage regimen will help boost patient compliance to medication and, as a result, reduce the frequency of angina attacks and improve the quality of life in this category of patients.

The combination of aspirin and clopidogrel remains the most frequent dual antiplatelet therapy in patients with acute coronary syndrome or undergoing percutaneous coronary intervention. Clopidogrel, a P2Y12 adenosine diphosphate (ADP) platelet receptor inhibitor requires transformation by cytochrome P450 (CYP) in the liver to produce an active metabolite. On the other hand, ivabradine is an effective antianginal drug that is also metabolized by the CYP enzyme, acting as a weak inhibitor. Our aim is to evaluate the impact of ivabradine on platelet reactivity in patients receiving clopidogrel and to evaluate the possible pharmacodynamic interactions between them. This is a prospective, observational, post-authorization pharmacodynamic study including patients treated with aspirin and clopidogrel and initiating ivabradine. Patients with platelet abnormalities and those treated with anticoagulants or other CYP inhibitors were excluded. A platelet aggregation test was performed at baseline before the first dose of ivabradine and repeated after 4 weeks of treatment. The primary endpoint was inhibition of platelet aggregation (IPA) after 20 mM ADP stimulation. A total of 34 patients were initially recruited; eight patients were excluded, leaving 25 patients for final analysis. All patients had chronic ischemic heart disease. The maximum ivabradine dosage of 7.5 mg twice daily was achieved in seven patients (28%). After 4 weeks of treatment with ivabradine, no significant differences were found in maximal platelet aggregation from baseline, as assessed with 20 μM ADP stimulation. In addition, no significant difference in IPA from baseline was detected after stimulation with ADP 5 μM, arachidonic acid, thrombin receptor-activated peptide 25 μM, and platelet reactivity index. Ivabradine did not alter antiplatelet response to clopidogrel in patients treated concomitantly with both drugs.

Titration of beta-blockers is a gold-standard therapy in patients with heart failure and a reduced ejection fraction but is sometimes challenging to administer, given symptomatic hypotension. Ivabradine is a recently introduced selective If channel inhibitor that purely reduces the heart rate. We encountered a patient with advanced heart failure in whom a beta-blocker could not be up-titrated given his symptomatic hypotension. Following the initiation of ivabradine, an increase in blood pressure due to heart rate optimization, probably via an improvement in the cardiac output, allowed for the further up-titration of carvedilol, followed by a successful clinical course. Ivabradine might be a novel therapeutic tool to facilitate the up-titration of beta-blockers in patients with heart failure and hypotension.

AIMS The aim of this study was to synthesize the evidence on the effect of heart failure with reduced ejection fraction (HFrEF) pharmacotherapy on health-related quality of life (HRQoL). METHODS AND RESULTS We searched MEDLINE, Embase, CENTRAL, CINAHL, ClinicalTrials.gov and the World Health Organization International Clinical Trials Registry Platform in June 2020. Randomized placebo-controlled trials evaluating contemporary HFrEF pharmacotherapy and reporting HRQoL as an outcome were included. Two reviewers independently assessed studies for eligibility, extracted data, and assessed risk of bias and GRADE certainty of evidence. The primary outcome was HRQoL at last available follow-up analysed using a random-effects model. We included 37 studies from 5770 identified articles. Risk of bias was low in 10 trials and high/unclear in 27 trials. High certainty evidence from meta-analyses demonstrated improved HRQoL over placebo with sodium-glucose co-transporter 2 (SGLT2) inhibitors [standardized mean difference (SMD) 0.16, 95% confidence interval (CI) 0.08-0.23] and intravenous iron (SMD 0.52, 95% CI 0.04-1.00). Furthermore, high certainty evidence from ≥1 landmark trial further supported improved HRQoL with angiotensin receptor blockers (ARBs) (SMD 0.09, 95% CI 0.02-0.17), ivabradine (SMD 0.14, 95% CI 0.04-0.23), hydralazine-nitrate (SMD 0.24, 95% CI 0.04-0.44) vs. placebo, and for angiotensin receptor-neprilysin inhibitor (ARNI) compared with an angiotensin-converting enzyme (ACE) inhibitor (SMD 0.09, 95% CI 0.02-0.17). Findings were inconclusive for ACE inhibitors, beta-blockers, digoxin, and oral iron based on low-to-moderate certainty evidence. CONCLUSION ARBs, ARNIs, SGLT2 inhibitors, ivabradine, hydralazine-nitrate, and intravenous iron improved HRQoL in patients with HFrEF. These findings can be incorporated into discussions with patients to enable shared decision-making.

Cardiovascular adverse effects in drug development are a major source of compound attrition. Characterization of blood pressure (BP), heart rate (HR), stroke volume (SV), and QT-interval prolongation are therefore necessary in early discovery. It is, however, common practice to analyze these effects independently of each other. High-resolution time courses are collected via telemetric techniques, but only low-resolution data are analyzed and reported. This ignores codependencies among responses (HR, BP, SV, and QT-interval) and separation of system (turnover properties) and drug-specific properties (potencies, efficacies). An analysis of drug exposure-time and high-resolution response-time data of HR and mean arterial blood pressure was performed after acute oral dosing of ivabradine, sildenafil, dofetilide, and pimobendan in Han-Wistar rats. All data were modeled jointly, including different compounds and exposure and response time courses, using a nonlinear mixed-effects approach. Estimated fractional turnover rates [h-1, relative standard error (%RSE) within parentheses] were 9.45 (15), 30.7 (7.8), 3.8 (13), and 0.115 (1.7) for QT, HR, total peripheral resistance, and SV, respectively. Potencies (nM, %RSE within parentheses) were IC 50 = 475 (11), IC 50 = 4.01 (5.4), EC 50 = 50.6 (93), and IC 50 = 47.8 (16), and efficacies (%RSE within parentheses) were I max = 0.944 (1.7), Imax = 1.00 (1.3), E max = 0.195 (9.9), and Imax = 0.745 (4.6) for ivabradine, sildenafil, dofetilide, and pimobendan. Hill parameters were estimated with good precision and below unity, indicating a shallow concentration-response relationship. An equilibrium concentration-biomarker response relationship was predicted and displayed graphically. This analysis demonstrates the utility of a model-based approach integrating data from different studies and compounds for refined preclinical safety margin assessment. SIGNIFICANCE STATEMENT: A model-based approach was proposed utilizing biomarker data on heart rate, blood pressure, and QT-interval. A pharmacodynamic model was developed to improve assessment of high-resolution telemetric cardiovascular safety data driven by different drugs (ivabradine, sildenafil, dofetilide, and pimobondan), wherein system- (turnover rates) and drug-specific parameters (e.g., potencies and efficacies) were sought. The model-predicted equilibrium concentration-biomarker response relationships and was used for safety assessment (predictions of 20% effective concentration, for example) of heart rate, blood pressure, and QT-interval.

Heart rate reduction therapy using ivabradine has demonstrated its prognostic implication in patients with heart failure with reduced ejection fraction. However, the target heart rate with optimal clinical outcomes, particularly for those with systolic dysfunction following a transcatheter aortic valve replacement (TAVR), remains unknown. Consecutive patients with left ventricular ejection fraction (LVEF) < 50% and sinus rhythm following TAVR received transthoracic echocardiography at index discharge. The ideal heart rate was calculated using a formula: 93 - 0.13 × (deceleration time [ms]). Those whose actual heart rates at discharge were within 10 bpm of the calculated ideal heart rate were assigned to the optimal heart rate group, and their prognosis was compared with those without. Twenty-four patients (83 [78, 85] years old, LVEF 41% [35%, 44%], 16 males) were included. The median difference between actual heart rate and ideal heart rate was 12 (0, 16) bpm and 11 patients were assigned to the optimal heart rate group. One year later, the optimal heart rate group achieved more improvement in LVEF (24% [15%, 28%] vs. 7% [7%, 12%], p = .003) and had lower heart failure readmission rates (0.059 vs. 0.116 events/year; p = .49). In conclusion, an optimal heart rate might be associated with cardiac reverse remodeling and prevention of heart failure recurrences in patients with systolic dysfunction following TAVR. The implication of deceleration time-guided heart rate optimization therapy for such cohorts remains the next concern.

Elevated resting heart rate in chronic heart failure (HF) patients has been associated with higher mortality and poor prognosis. Ivabradine is a new pure bradycardic agent that has been used to treat angina or heart failure reduced ejection fraction (HFrEF) with sinus heart rate above 70 beats per minute. However, the effect of ivabradine for chronic HF patients on rehospitalization and cardiac function is still inconsistent. Thus, this meta‐analysis aimed to elucidate the effect of Ivabradine in chronic HFrEF patients. We systematically searched PubMed, Medline, Clinical Trials.gov, and The Cochrane Central Register of Controlled Trials for randomized controlled trials (RCTs) of ivabradine with search terms Ivabradine (MeSH Terms), chronic heart failure and beta‐blocker. The primary endpoints of the study include the impact of Ivabradine on heart rate, left ventricle ejection fraction (LVEF), left ventricular remodeling, exercise capacity, and quality of life (QoL) in patients with chronic HFrEF. Secondary endpoints were safety analysis of Ivabradine including cardiovascular mortality, worsening HF readmission, visual disturbances, and asymptomatic bradycardia. The analysis was done by Review Manager 5.4 Analyzer, to analyze the mean differences (MD) for continuous data and risks ratio (RR) for dichotomous data. A total of six RCTs and one subgroup analysis showed add of Ivabradine to standard HF therapy was associated with greater resting heart rate reduction (MD = −9.57; 95% CI ‐11.15, −8.00), improved LVEF (MD = 3.89; 95% CI 2.61, 5.17), left ventricular reverse remodeling improvement (MD = −3.73; 95% CI ‐4.25, −3.21, LVESV; MD = −17.00, 95%CI ‐29.65, −4.35, LVEDD; MD = −1.43, 95%CI ‐2.78, −0.08, LVEDV; MD = −14.75, 95%CI ‐34.36, 4.87), increased exercise capacity (exercise duration; MD = 8.52; 95%CI 0.09, 16.94), and significant reduction on rehospitalization due to worsening HF (RR = 0.76, 95%CI 0.69, 0.84). However, Ivabradine has no significant effect on the quality of life (MD = 0.65; 95%CI ‐10.52, 11.82), and cardiovascular mortality (RR = 0.92; 95%CI 0.82, 1.03). Moreover, there were some events of visual disturbances and asymptomatic bradycardia observed in the Ivabradine group compared to the placebo group (RR = 4.76; 95%CI 3.03, 7.48; RR = 3.78; 95%CI 2.77, 5.15, respectively). Addition of Ivabradine to standard HF therapy is associated with cardiac function improvement, reduction on worsening HF readmission, greater HR reduction, and better exercise capacity in chronic HFrEF patients, although it cannot reduce cardiovascular mortality or improve the quality of life.

Purpose Ivabradine has been approved for the treatment of chronic heart failure and chronic stable angina pectoris in Europe. Based on adverse outcomes of reproductive animal studies and the lack of human data, ivabradine is considered contraindicated during pregnancy. The aim of this observational study is to analyse ivabradine use before and during pregnancy. Methods We evaluated all ivabradine-related requests to the German Embryotox Institute from 2007 to 2019. Exposed pregnancies were analysed as to their outcome. Results Off-label use for supraventricular tachycardia was frequent in women of childbearing age. Of 38 prospectively ascertained pregnancies with ivabradine exposure and completed follow-up, 32 resulted in live births, 3 in spontaneous abortions, and 3 were electively terminated. One neonate presented with major birth defects (atrial septal defect and cleft palate). In 33/38 patients, ivabradine was discontinued after confirmation of pregnancy without cardiac deterioration and 5/38 women continued ivabradine throughout pregnancy. In addition, there were 3 retrospectively reported pregnancies including one major birth defect (tracheal atresia). Conclusion This case series represents the largest cohort of ivabradine-exposed pregnancies, published so far. According to our findings, ivabradine appears not to be a major teratogen. However, established drugs of choice with strong evidence of low risk for the unborn should be preferred in women planning pregnancy. After inadvertent exposure during pregnancy or lack of treatment alternatives, fetal ultrasound for structural anomalies and growth restriction is recommended. In addition, close monitoring is necessary in pregnant women with supraventricular arrhythmias or cardiac disease.

The article provides a scientific review based on the proceedings of the 2020 American Heart Association consensus on drugs that may cause arrhythmias on a risk-sensitive basis and a guidance on strategies for monitoring, prevention methods and therapeutic approaches.The risk factors for drug-induced arrhythmias are divided into modifiable and non-modifiable. Among the non-modifiable risk factors are congenital anomalies (changes in the conduction system, ion channel polymorphism) and heart diseases (cavity dilatation, myocardial ischemia). Among the modifiable risk factors are various electrolyte disorders (hypo/hyperkalemia, hypo/hypermagnesemia, hypocalcemia). Certain drugs can lead to electrolyte disorders, which require management with potassium and magnesium supplements. The drug-induced arrhythmias can be caused by conditions leading to altered drug pharmacokinetics and increased plasma concentrations and metabolites having proarrhythmogenic effects, as well as drug-drug interactions.Beta-blockers, non-dihydropyridine calcium channel blockers, other antiarrhythmic drugs, ivabradine, digoxin, anesthetics (bupivacaine, propofol) are the most common culprits in causing drug-induced bradyarrhythmias. The drug-induced atrial fibrillation frequently occurs in patients receiving antiarrhythmics, various sympathomimetics, psychotropic and antineoplastic drugs, anti-inflammatory (NSAIDs, corticosteroids) and immunotropic agents (interleukin-2, fingolimod). Various sympathomimetics and inotropic drugs, some antipsychotic drugs can produce drug-induced atrial and nodal tachyarrhythmias.The drug-induced ventricular tachycardia can be caused by antiarrhythmics, inotropics and various sympathomimetics, antipsychotic and antineoplastic drugs, as well as herbal drugs (aconite, ginkgo biloba). The list of drugs that cause a long QT syndrome includes antiarrhythmics, antimicrobial drugs (macrolides, fluoroquinolones, aminoquinolines, fluconazole), antipsychotics, antineoplastic drugs, antiemetics, etc. For a complete list of drugs that prolong a QT interval, see the CredibleMeds website (Arizona, USA). The drug-induced arrhythmia prevention strategies include rising awareness among doctors about risk factors and potentially dangerous drugs, sufficient monitoring of patients at risk of developing arrhythmias (ECG monitoring, electrolyte balance, kidney and liver function), maintenance of electrolyte balance, primarily potassium and magnesium. The therapeutic approach includes discontinuation of a causative drug; relief and maintenance therapy are carried out based on the modern international clinical guidelines for various forms of arrhythmias.

Ivabradine is a unique agent that is distinct from beta-blockers and calcium channel blockers as it reduces heart rate without affecting myocardial contractility or vascular tone. Ivabradine is a use-dependent inhibitor targeting the sinoatrial node. It is approved for use in the United States as an adjunct therapy for heart rate reduction in patients with heart failure with reduced ejection fraction. In this scenario, ivabradine has demonstrated improved clinical outcomes due to reduction in heart failure readmissions. However, there has been conflicting evidence from prospective studies and randomized controlled trials for its use in stable ischemic heart disease regarding efficacy in symptom reduction and mortality benefit. Ivabradine may also play a role in the treatment of patients with inappropriate sinus tachycardia, who often cannot tolerate beta-blockers and/or calcium channel blockers. In this review, we highlight the evidence for the nuances of using ivabradine in heart failure, stable ischemic heart disease, and inappropriate sinus tachycardia to raise awareness for its vital role in the treatment of select populations.

Aims Ivabradine and sacubitril/valsartan are second‐line therapies for patients with heart failure and reduced ejection fraction (HFrEF) based on guideline recommendations. We aimed to evaluate the synergistic effects of these two medications. Methods and results Patients' data were extracted from a multicentre database between 2016 and 2018. Patients were classified into (1) Simultaneous group: simultaneous prescription of ivabradine and sacubitril/valsartan within 6 weeks; (2A) Sequential group, ivabradine‐first: ivabradine was prescribed first, followed by sacubitril/valsartan; and (2B) Sequential group, sacubitril/valsartan‐first: sacubitril/valsartan was prescribed first, followed by ivabradine. A total of 464 patients with HFrEF were enrolled. Cardiovascular death and/or unplanned re‐hospitalizations for HF were less frequent (28.6% vs. 44.8%, P = 0.01), and the improvement of left ventricular ejection fraction (LVEF) was significantly greater in patients from the Simultaneous group than those from the Sequential group (∆LVEF 12.8 ± 12.9% vs. 9.3 ± 12.6%, P = 0.007). Among Sequential subgroups, the ivabradine‐first treatment decreased heart rate and increased systolic blood pressure (SBP) compared with sacubitril/valsartan‐first treatment (∆heart rate −9.1 ± 12.9 b.p.m. vs. 2.6 ± 16.0 b.p.m., P

Ivabradine (Iva), a heart rate reducing agent that specifically inhibits the pacemaker I(f) ionic current, has been demonstrated to be cardioprotective in many cardiovascular diseases. Autophagy is an evolutionarily conserved metabolic process that regulates cardiac homeostasis. This study is aimed to explore whether autophagy is functionally involved in the cardioprotective effect of Iva in a rat model of myocardial infarction (MI). We observed that Iva treatment (po, 10 mg/kg/day) showed significant recovery on the hemodynamics parameters in MI rats, including left ventricular systolic pressure, left ventricular end diastolic pressure, and maximal ascending/descending rate of left ventricular pressure. Also, Iva treatment dramatically decreased infarct size, inhibited myocardial apoptosis, and reduced the levels of pro-inflammatory cytokines tumor necrosis factor (TNF)-α, interleukin (IL)-1β and IL-6 in MI rats. Moreover, Iva treatment enhanced autophagy and inhibited PI3K/AKT/mTOR/p70S6K pathway in MI rats. Simultaneously, we observed that autophagy enhancer rapamycin (ip, 10 mg/kg/day) showed similar cardioprotective effects with Iva. Furthermore, we observed that addition of autophagy inhibitor 3-methyladenine (ip, 10 mg/kg/day) counteracted the therapeutic effect of Iva, addressing that Iva attenuated post-MI cardiac injury by enhancing autophagy. In summary, these findings demonstrated that Iva attenuated MI in rats by enhancing autophagy, and PI3K/AKT/mTOR/p70S6K pathway might be involved in the process. Autophagy activation by Iva may be a potential therapeutic strategy for the treatment of MI., Graphical Abstract

We present an extreme rare case of cristal atrial tachycardia (AT) in a 23-year-old male presenting with recurrent refractory palpitation since last 1 year treated with betablocker metoprolol 50 mg twice daily. We subjected the patient for electrophysiologic study and radiofrequency ablation and A wave in the mid cristal region preceded the surface P-wave by 16 ms. Ablation here terminated the tachycardia but interestingly patient turned up with recurrent palpitation after 1 month. In view of mid cristal AT, we treated the patient with Ivabradine 5 mg twice daily after which the patient was asymptomatic in follow up. Our case is a unique demonstration of sinus node funny current inhibitor Ivabradine being effective to relieve symptoms even in failed cases of radiofrequency ablation with partial modification of mid cristal region in a case of recurrent mid cristal AT. Our take home message from this electrophysiology experience is that even in cases with partial modification of crista terminalis or failed radiofrequency ablation of Cristal atrial tachycardia Ivabradine can serve as an alternative before proceeding to 3D ablation.

Clinical assessment of drug-drug interactions (DDIs) in children is not a common practice in drug development. Therefore, physiologically-based pharmacokinetic (PBPK) modeling can be beneficial for informing drug labeling. Using ivabradine and its metabolite (both cytochrome P450 3A4 enzyme (CYP3A4) substrates), the objectives were (i) to scale ivabradine-metabolite adult PBPK/PD to pediatrics, (ii) to predict the DDIs with a strong CYP3A4 inhibitor, and (iii) to compare the sensitivity of children to DDIs using two CYP3A4 hepatic ontogeny functions: Salem and Upreti. A scaled parent-metabolite PBPK/PD model from adults to children satisfactorily predicted pharmacokinetics (PK) and pharmacodynamics (PD) in 74 children (0.5-18 years) regardless of CYP3A4 hepatic ontogeny function applied. However, using the Salem ontogeny, mean predicted parent and metabolite area under the concentration-time curve over 12 hours (AUC12h ) and heart rate change from baseline were 2-fold, 1.5-fold, and 1.4-fold higher in young children (0.5-3 years old) compared with Upreti ontogeny, respectively. Despite these differences, choice of appropriate hepatic CYP3A4 ontogeny was challenging due to sparse PK and PD data. Different sensitivity to ivabradine-ketoconazole DDIs was simulated in young children relative to adults depending on the choice of hepatic CYP3A4 ontogeny. Predicted ivabradine and metabolite AUCDDI /AUCcontrol were 2-fold lower in the youngest children (0.5-1 year old) compared with adults (Salem function). In contrast, the Upreti function predicted comparable ivabradine DDIs across all age groups, although predicted metabolite AUCDDI/ AUCcontrol was 1.3-fold higher between the youngest children and adults. In the case of PD, differences in predicted DDIs were minor across age groups and between both functions. Current work highlights the importance of careful consideration of hepatic CYP3A4 ontogeny function and implications on labeling recommendations in the pediatric population.

Introduction: One of the major complications among COVID-19 patients include cardiac arrhythmias. Commonest arrhythmia is sinus tachycardia which is usually associated with palpitation causing discomfort to patients. In this study, we present a comparative study of use of Ivabradine vs. Carvedilol for sinus tachycardia in post-COVID-19 infected patients. Method: 50 consecutive recovered COVID-19 patients with sinus tachycardia were included in this open labelled RCT. 25 patients received Ivabradine and remaining 25 received Carvedilol. Single therapy non-responders were treated with Ivabradine with Atorvastatin. Results: The mean age of all patients is 48.8±7.66 years (Males 49.5 ± 7.21 years; Females 47.68 ± 8.23 years). The mean heart rate (MHR) of all patients is 125.52 ± 9.07/min (Males 125.67 ± 8.78/min; Females 125.26 ± 9.5/min). After five days of single drug therapy the mean drop in the heart rate was 35.04 ± 10.55/min (Males 34.41 ± 9.71/min; Females 36.05 ± 11.72/min), resulting in 27.88 ± 8.11% (Males 27.38 ± 7.56%; Females 28.69 ± 8.89%) reduction in MHR. Among the two groups, the Carvedilol group showed improvement of MHR in 14(56%) patients; whereas in Ivabradine group 18(72%) patients improved out of 25 patients each (p: 0.2385). In the Carvedilol group the MHR reduced from 128.6 ± 8.44 to 95.68 ± 10.63 (p < 0.001), which is statistically significant; similarly, the Ivabradine group showed a MHR from 122.44 ± 8.62 to 85.28 ± 10.52 (p < 0.001). The monotherapy therapy non-responders were treated with dual-therapy of (Ivabradine + Atorvastatin). Discussion: Ivabradine is more effective in controlling heart rate compared to Carvedilol. Also, Ivabradine group scores very well in ‘patient-satisfaction’ with regards to symptom (palpitation) relief. Conclusion: The COVID-19 sequelae of sinus tachycardia can be better controlled with Ivabradine when compared to Carvedilol.