scholarly journals Resting heart rate in ambulatory heart failure with reduced ejection fraction treated with beta‐blockers

2020 ◽  
Vol 7 (5) ◽  
pp. 3049-3058
Author(s):  
Kenneth D. Varian ◽  
Xinge Ji ◽  
Justin L. Grodin ◽  
Frederik H. Verbrugge ◽  
Alex Milinovich ◽  
...  
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.


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.


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.


2020 ◽  
Vol 35 (8) ◽  
pp. 1109-1115 ◽  
Author(s):  
Sho Suzuki ◽  
Hirohiko Motoki ◽  
Yusuke Kanzaki ◽  
Takuya Maruyama ◽  
Naoto Hashizume ◽  
...  

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)


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