scholarly journals Ivabradine and endothelium: an update

2020 ◽  
Vol 14 ◽  
pp. 175394472093493
Author(s):  
Lucia Dallapellegrina ◽  
Edoardo Sciatti ◽  
Enrico Vizzardi

Ivabradine is a pure heart-rate lowering drug that is nowadays used, accordingly to the last ESC Guidelines, to reduce mortality and heart failure (HF) hospitalization in patients with HF with reduced ejection fraction and in symptomatic patiens with inappropriate sinus tachycardia. Moreover, interesting effect of ivabradine on endothelial and myocardial function and on oxidative stress and inflamation pathways are progressively emerging. The aim of this paper is to highlight newer evidences about ivabradine effect (and consequently possible future application of the drug) in pathological settings different from guidelines-based clinical practice.

2019 ◽  
Vol 89 (3) ◽  
Author(s):  
Edoardo Sciatti ◽  
Enrico Vizzardi ◽  
Ivano Bonadei ◽  
Lucia Dallapellegrina ◽  
Valentina Carubelli

Resting heart rate (HR) is considered a powerful predictor of mortality both in healthy subjects and in cardiovascular (CV) patients, including those affected by heart failure (HF). Its reduction below 70 bpm is the treatment target in chronic HF with reduced ejection fraction (HFrEF) when sinus rhythm is present. In acute HF (AHF) HR is usually elevated but its role as risk marker is still unknown. Notably, in unstable patients, beta-blockers can be reduced or stopped, thus enhancing this phenomenon. Moreover, some data in literature suggest that HR reduction during hospitalization or HR at discharge or in the vulnerable phase after it are more predictive of early-term events and may be therapeutic targets. On the other hand, ivabradine is a pure HR-lowering drug with no effects on inotropism. Its role in the AHF setting has been recently investigated and is the object of this review.


2015 ◽  
Vol 21 (4) ◽  
pp. 335-343 ◽  
Author(s):  
Rahul Chaudhary ◽  
Jalaj Garg ◽  
Parasuram Krishnamoorthy ◽  
Neeraj Shah ◽  
Gregg Lanier ◽  
...  

Heart failure affects over 5 million people in the United States and carries a high rate of mortality. Ivabradine, a new agent has been added to the current medical options for managing heart failure. It is a selective funny current ( If) inhibitor in sinoatrial node and slows its firing rate, prolonging diastolic depolarization without a negative inotropic effect. Ivabradine was only recently approved by Food and Drug administration after the results of Systolic Heart Failure Treatment with the If Inhibitor Ivabradine (SHIFT) trial, for a reduction in rehospitalizations from chronic heart failure. This trial assessed patients with stable heart failure with reduced ejection fraction and a heart rate of at least 70 beats per minute at rest on maximally tolerated beta-blocker therapy and demonstrated statistically significant reduction in heart failure hospitalization and deaths. Additionally, ivabradine has been associated with reduced cardiac remodeling, reduced heart rate variability, improvement in exercise tolerance, improved heart failure class of New York Heart Association, and better quality of life. It has also been tried in other conditions, such as inappropriate sinus tachycardia and cardiogenic shock, and is currently in phase II trial for patients with newly diagnosed multiple organ dysfunction syndrome.


2015 ◽  
Vol 70 (5) ◽  
pp. 565-572
Author(s):  
Frederik H. Verbrugge ◽  
Jeroen Vrijsen ◽  
Jan Vercammen ◽  
Lars Grieten ◽  
Matthias Dupont ◽  
...  

Circulation ◽  
2020 ◽  
Vol 142 (Suppl_3) ◽  
Author(s):  
Catherine F Notarius ◽  
Daniel A Keir ◽  
Mark B Badrov ◽  
Philip J Millar ◽  
Paul Oh ◽  
...  

Introduction: Elevated muscle sympathetic nerve activity (MSNA) both at rest and during dynamic cycling relates inversely to peak oxygen uptake (VO 2peak ) in patients with heart failure due to a reduced ejection fraction (HFrEF). We observed a drop in MSNA both rest (-6±2 bursts/min) and mild exercise (-4±2) in HFrEF patients after 6 months of cardiac rehabilitation. Hypothesis: We hypothesized that after training those HFrEF patients with LOW VO2peak (less than median 74% of age predicted) would have a larger decrease in MSNA during dynamic exercise than those with HIGH VO2peak (over 74%). Methods: In 21 optimally treated HFrEF patients (5 Female) (13 HIGH: mean VO 2peak =26 ml·kg/min; 98% of predicted; 8 LOW VO 2peak =12; 50%) we assessed VO 2peak (open-circuit spirometry), heart rate variability (HRV) and fibular MSNA (microneurography) at rest, during 1-leg cycling (2 min each of mild and moderate intensity upright 1-leg cycling, n=19) and recovery before and after 6 months of exercise training (45 min aerobic exercise, 5 days/ wk at 60-70 % of VO 2peak; and resistance training 2 days/wk). Results: HIGH and LOW groups had similar age (63±3 vs 63±4 years) , LVEF (30±2 vs 28±3%), BMI, resting heart rate (HR), blood pressure and MSNA (52±3 vs 50±3 bursts/min). Training increased VO 2peak in both groups (main effect P=0.009), with no group difference in HR response or ratings of perceived exertion. MSNA at rest tended to decrease after training in the HIGH but not LOW group (interaction P=0.08). MSNA during cycling increased in both HIGH (P=0.04) and LOW (P<0.001) groups but was blunted post-training in the HIGH group only (P=0.04 vs. 0.90 in LOW). Training-induced sympatho-inhibition during exercise recovery occurred in the HIGH but not LOW group (interaction P=0.01). In contrast, HRV was not improved by training in either group. Conclusions: Contrary to our hypothesis, the sympatho-inhibitory effect of 6 months of exercise-based cardiac rehabilitation favours HFrEF patients with an already normal VO 2peak . This suggests that increasing initially low VO 2peak may be insufficient to trigger beneficial exercise and recovery autonomic modulation and altered training paradigms may be required in such patients. Funded by Canadian Institutes for Health Research (CIHR)


Author(s):  
Amit Frenkel ◽  
Yoav Bichovsky ◽  
Natan Arotsker ◽  
Limor Besser ◽  
Ben-Zion Joshua ◽  
...  

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


2020 ◽  
Vol 2 (55) ◽  
pp. 34-38
Author(s):  
Przemysław Mitkowski

Sinus rhythm is diagnosed based on 12-lead ecg recording. Diagnostic criteria are as follows: positive P waves in limb lead I and II and negative in aVR; PR interval of at least 120 ms; the difference of consecutive P-P interval should be less than 120 ms. A sinus rate limit is between 50-100/min. Numerous factors: physiologic, pathologic, medications, drugs and stimulants could increase sinus rate. Sinus tachycardia is also observed in inappropriate sinus tachycardia and postural orthostatic tachycardia syndrome. ESC guidelines related to latter two syndrome are summarized.


ESC CardioMed ◽  
2018 ◽  
pp. 1863-1867
Author(s):  
Michel Komajda

Ivabradine slows down the heart rate through a blockade of the funny current channels in the sinoatrial node cells. The efficacy of the drug was tested in a large outcome clinical trial in stable chronic heart failure with reduced ejection fraction, in sinus rhythm, on a contemporary background therapy including beta blockers.


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